tag:blogger.com,1999:blog-47497038105901476762024-03-18T08:03:12.330-07:00Asthma HistoryJohn Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.comBlogger496125tag:blogger.com,1999:blog-4749703810590147676.post-58284441139110977252019-09-07T04:55:00.002-07:002019-09-07T04:55:14.708-07:00Foot pump nebulizer still on market today<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqbamyhvFGSJF1baZOx3fhrsmkXDdfLEbfcgPq7qp2cPJ060SE5kyV3_hRffz5-I05j2uJbfBeCGFE_yUIqsVKnQvo0dczyO4o-Orl0hux2iNChIuRStVtqhxw7G4BZYQ9uEWH9rjgeIY/s1600/new-design-Foot-Pump-Nebulizer.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" data-original-height="1283" data-original-width="1600" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqbamyhvFGSJF1baZOx3fhrsmkXDdfLEbfcgPq7qp2cPJ060SE5kyV3_hRffz5-I05j2uJbfBeCGFE_yUIqsVKnQvo0dczyO4o-Orl0hux2iNChIuRStVtqhxw7G4BZYQ9uEWH9rjgeIY/s400/new-design-Foot-Pump-Nebulizer.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">This is a foot pump nebulizer I found at an online store.<br />
It's still on sale for $10. </td></tr>
</tbody></table>
I also moderate Facebook pages. On one page I moderate was a discussion on nebulizers. A fellow asthmatic said she used to have a foot pump nebulizer.<br />
<br />
Here is her her comment:<br />
<blockquote class="tr_bq">
"My very first portable nebuliser was a totally useless foot pump affair! I couldn't do it myself because of the effort it took, and because it was foot pump powered it was impossible to get a constant and steady stream with anyone else doing it, plus they would tire quickly. Ixve no idea how it ever came to be on the market, such was it's uselessness, but it was my father's idea of a cost-cutting purchase without any appreciation of what it needed to be used for. I'm certain it's not what the doctor had in mind when they said we needed to get me a home nebuliser. That was back in the late 1980s, maybe 1988 or so."</blockquote>
I do know that there were foot pump nebulizers back in the 19th century. But this was back when there was no electricity. Between 1900 and 1930 there were squeeze bulb operated nebulizers. These were usually used to deliver a low dose of epinephrine. So, it was surprising to see that these types of nebs were sold in the 1980s.<br />
<br />
Interestingly, I did a Google search for "foot pump nebulizer, 1980s" and one popped up in the search. A sketchy site I wouldn't recommend clicking on. But, I wonder if those would be good for 3rd world countries where there's no power and no access to inhalers.<br />
<br />
The problem with the rubber squeeze bulb nebulziers is they were hard to operate. You could squeeze and squeeze and you only got a tiny bit of mist. I imagine the foot nebulizers may have been a step up from that. Still, they weren't very helpful.<br />
<br />
I know this because I got a rubber bulb to attach to the bottom of my first nebulizer. This was in 1985. Sometimes I would play with this. I'd attach it to the bottom of the cup and squeeze, squeeze, squeeze.<br />
<br />
As noted above, just a minor mist was ejected. I couldn't imagine using this to end an asthma attack. It would take forever. But, if it's all you had, then maybe you would make do.<br />
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} catch(err) {}</script>John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com689tag:blogger.com,1999:blog-4749703810590147676.post-78524523990928700452017-09-18T06:27:00.000-07:002017-09-18T06:27:02.097-07:001970-2000: Does rescue medicine make asthma worse?The 1970s saw a third spike in asthma related deaths, and this time the location was isolated to New Zealand. This prompted researchers to further investigate the relationship between asthma rescue medicine and asthma morbidity and mortality.<br />
<br />
According to Ann Janet Woolcock, data from death certificates were investigated from Australia, New Zealand, U.S.A., West Germany, Canada, Japan, Britain and Wales. Regarding these results, she said:<br />
<blockquote class="tr_bq">
Deaths were lowest in about 1975 in all countries and then increased somewhat (dramatically in new Zealand) until about 1985, but since then, and especially since 1990, mortality has decreased or remained steady in all the countries shown. There has been much speculation about the reasons for the fluctuations, but it is difficult to draw conclusions about these figures in the absence of accurate data about the prevalence and severity of the disease, and methods of treatment used in this age group (which was 4-34) in each country.</blockquote>
So did the same medicines that were supposed to make life better or asthmatics cause the rise in morbidity and mortality. Lawrence K. Altmon suggests that perhaps Dr. Parkinson, in 1995, may have been right on when he suggested that morbidity and mortality was negligible prior to the arrival of adrenaline (epinephrine) in 1902. (8, page 8)<br />
<br />
Altmon said:<br />
<blockquote class="tr_bq">
Dr. parkinson wrote that it is "possible that mortality from asthma first appeared when adrenaline (epinephrine) became available. It was identified in 1902. Theoretically, lethal asthma could be the result of adrenal medullary suppressoin secondary tothe exogenous administration of its own hormones." (8, page 8)</blockquote>
<blockquote class="tr_bq">
"The pattern of events of no adrenaline, no deaths; some adrenaline, some deaths; powerful adrenaline analogues prescribed generously, an epidemic of deaths; withdrawal of the more potent drugs, the epidemic disappears; and supports the thesis of iatrogenic adrenal medullary suppression. (8, page 8)</blockquote>
There was no doubt that by review trends from New Zealand, rises in asthma morbidity and mortality rates corresponded with the sales of fenoterol. Sales started to spike when the medicine was introduced to the market in the mid 1970s, and they began to decline when the product was pulled from the market in the early 1990s.<br />
<br />
The trend was similar to that of which occurred during the 1940s when asthma morbidity and mortality rates spiked in New Zealand, Australia, Britain and Wales as sales of isoprenaline forte increased. When the medicine was later pulled from the market, the death rate likewise declined.<br />
<br />
Statistics showed similar trends for the rest of the nation, although the rise in morbidity and mortality was more subtle and gradual. There was a gradual increase following the introduction of isoprenaline solution in the 1940s and again following the introduction of the the rescue inhaler in 1957.<br />
<br />
There were now two questions researchers set out to answer:<br />
<ol>
<li>Do beta adrenergics make asthma worse</li>
<li>If so, why?</li>
</ol>
<div>
The neat thing about this latest spike in asthma morbidity and mortality was, unlike those that occurred in the 1940s and 1960s, the experts now had an array of data to learn from.</div>
<div>
<br /></div>
<div>
The following were the theories to explain the rise in morbidity:</div>
<div>
<br />
1. <b>High doses of beta agonists increases the risk for cardiac arrest</b>. The was especially the case with non-specific B2 agonists such as epinephrine and isopreterenol. The high dosing provided by use of this medicine was suspected of of overworking the heart, thus causing cardiac arrest. Beasley, Pearce and Crane suspect this to be most likely to be the case in cases "relating to their overuse in the situation of a life-threatening attack of asthma, in which the cardiac side effects are likely to be particularly harmful in the presence of severe hypoxia." (1, page 20)<br />
<br />
Janet Woolcock suggests that "there is little evidence that it (fatal asthma or near fatal asthma) results from a cardiovascular event). Likewise, she also suggests that "on the other hand, drugs such as albuterol, terbutaline, and salmeterol are partial beta-agonists (specific to the lungs only), and there is no substantial evidence that they increase the risk of death from asthma." (2, page 190)<br />
<br />
2. <b>High doses use of beta agonists increase tolerance to the medicine</b>: This subject was taken up by Benoy, Fellah, and Schneider in 1975. They said that: (11)<br />
<blockquote class="tr_bq">
The longer animals were pretreated and the higher the dose of bronchodilator given (isoprenaline or adrenaline) the greater was the degree of tolerance developed in the isolated lungs. Tolerance could develop to such a degree that regardless of the dose of bronchodilator used to challenge the lungs (adrenaline, isoprenaline or aminophylline) no significant bronchodilation was produced.(11, pages 551-552)</blockquote>
<blockquote class="tr_bq">
Benson &Periman (1948) and Laurence & Moulton (1960) reported that tolerance developed in the brochodilator effect of adrenaline after excessive use of this drug in man...(11, page 552)</blockquote>
<blockquote class="tr_bq">
These results suggest that asthmatic patients who are heavy users of bronchodilators may become resistant to these drugs. the valueof these drugs in relieving mild asthmatic attacks in such patients becomes less. In an extreme case, a patient may die because the drug he is using has become completely ineffective. A young asthmatic has been found dead clutching an empty bronchodilator aerosol container (Pickvance, 1967). The same conclusion was reached by Herxheimer (1973)...(11, page 552 )</blockquote>
<blockquote class="tr_bq">
Conolly <i>et al</i>. (1971)... suggested that in asthmatic patients who use sympathomimetic pressurized aerosols excessively cross-resistance developsto both exogenous sympathomimetic amines and to the natural transmiter release by the adrenergic nerves, and that this may lead to a deterioration of the asthmatic state and explain the rise in the asthma mortality rate. The cross tolerance experiments described here may exlain the good results which were obtained only after the withdrawal of adrenergic bronchodilator therapy from some asthmatic patients (Keighley, 1966, Reisman, Friedman & Arbesman, 1968)...(11, page 553 )</blockquote>
<blockquote class="tr_bq">
The work described in this paper has demonstrated that the tolerance which developed as a result of the repeated administration of isoprenaline or adrenaline remained for periods of upto three weeks after the last administration of isoprenaline or adrenaline to guinea-pigs. (11, page 553)</blockquote>
Developing a tolerance to rescue medicine may result in worsening severity.<br />
<br />
3. <b> High doses of beta agonists increase severity of asthma</b>. Some studies showed that high doses of beta adrenergics may increase the severity of asthma. This may result from high dose beta adrenergics such as isoprenaline forte and fenoterol, or from frequent use of regular doses of beta adrenergics such as isoprenaline. Later studies showed that frequent use of epinephrine, terbulatine, metaproterenol, and albuterol also resulted in increased severity. (2, pages 189-190)(3, pages 468-470) Some experts have gone as far to suggest that albuterol should not be used on a regular frequency, and should only be used as a rescue medicine as needed.<br />
<br />
Regarding these studies, Malcolm R. Sears said the following:<br />
<blockquote class="tr_bq">
These studies suggest a class efectof regular B-agonists which is likely to be more evident if higher doses of more potent B-agonists are given, and perhaps also more evident in patients with more severe asthma. If this is so, then the natural tendency to use higher doses of B-agonist in subjects with worsening asthma, and to change to more potent B-agonists for those patients when a new drug is marketed, would escalate the adverse effects (developing a vicious circle of worsening asthma), leading to increased opportunity for a fatality in disadvantageous circumstances. (2, page 469)</blockquote>
The "more potent B-agonists" being referenced to here would be isopreterenol forte and fenoterol. Sears further notes that:<br />
<blockquote class="tr_bq">
"Strong support for the hypothesis that B-agonists increase the severity of asthma ocmes from the abrupt reversal of both morbidity and mortality in New Zealand in 1990, when, on advice from the drug regulatory agency, fenoterol was effectively withdrawn from use over a period of a few months." (2, page 469)</blockquote>
Other evidence that supports this theory is the decline in asthma morbidity and mortality following increased warnings regarding the risks of isoprenaline forte that resulted in decreased sales(1, page 18) Likewise, following warnings regarding the overuse of the medihaler epi and medihaler iso, morbidity and mortality declined as well.<br />
<br />
4. <b> Over reliance on beta agonists results in delay in seeking help</b>. Various studies showed that those asthmatics who were found dead with a rescue inhaler clutched in their grasp may have had a false sense of security, and a belief that the medicine would eventually make their asthma better. Buy the time they realized this was not true it was too late. (2, pages 471-473)<br />
<br />
5. <b>Lack of use of inhaled corticosteroids</b>: Woolcock said that some patients may develop worsening asthma and have an increased risk of death, "but the lack of inhaled coticosteroids (ICS). Where salbutamol and ICS are used otgether, there is no increased risk. One message that is clear an dcan be used in educational campaigns is that increasing frequency of use of beta-agonists such as albuterol is a sign of increasing severity of asthma and thus of increased risk of death. (2, page 190)<br />
<br />
These continue to be theories debated by the medical community. Albert L. Schefler, the editor of Fatal Asthma, sums up<br />
<blockquote class="tr_bq">
A recent study in this regard explored the effect of regular beta agonist use on the bronchoprotective effect of beta agonists. Among a small group of persons with mild, stable asthma, subjects were randomly assigned to use either albuterol or placebo 2 puffs four times daily; both groups could use as-needed albuterol for "rescue." Although the bronchodilator effect of albuterol was not changed by regular use of albuterol, the bronchoprotective effect of albuterol was reduced. Albuterol did not blunt methacholine- or allergen-induced bronchoconstriction as effectively after regular beta-agonist inhalation for two weeks as it did in the placebo group. Tolerance to the bronchoprotective effect of beta agonists may be one way in which overuse of inhaled beta agonists might contribute to fatal outcomes in asthma.</blockquote>
<blockquote class="tr_bq">
Molecular studies of the beta-agonist receptor have revealed polymorphisms in the general and asthmatic populations. Some genetically determined beta-receptor types may be more susceptible to phosporylation and thereby to down-regulation, a potential mechanism for the development of tolerance to the bronchoprotective effects of beta agonists. An estimated 5-10% of the population have this particular phenotypic expression of their beta receptor and may as a result be at increased risk for severe, potentially fatal asthma. </blockquote>
<blockquote class="tr_bq">
The message here is not that beta agonists are dangerous. Used properly, they can be life- saving. The key point is that their role in asthma is as rescue medication for relief of acute asthmatic symptoms. We do no longer prescribe albuterol for regular use on a Q.I.D. basis. Frequent use of albuterol (more than one cannister [=200 puffs]/month should be a warning sign for poorly controlled asthma requiring an intensification of anti-inflammatory therapy. (10)</blockquote>
6. <b>Rescue medicine by metered dose inhaler (MDI) causes inert bronchospasm</b>: A 1985 study by J. Yarbrough, L.E. Lansfield, and S. Ting concluded that the alupent inhaler was likely to cause bronchoconstriction in the smallest air passages of the lungs. They concluded that high doses from frequent use may worsen some cases of asthma. (12)<br />
<br />
7. <b>Socioeconomic status</b>: Some studies suggest that asthma is more likely to be uncontrolled and more severe in people who live in poor economic conditions. The following have been shown by various studies:<br />
<ul>
<li>The asthma mortality rate is 5.6 higher in blacks compared to whites (13, page 238)</li>
<li>Studies in Chicago showed that the highest mortality rates are among a city's poorest neighborhoods (13, page 238)(3, page 471)</li>
<li>The highest death rates were in the nations poorest communities (13, page 238)</li>
<li>Morbitity and mortality were highest among the nations least educated (13, page 239)</li>
<li>Impoverished people are more likely to be exposed to their asthma allergens, such as dust mites, cockroaches, etc. (3, page 472) </li>
<li>Impoverished people (including children) are more likely to be exposed to cigarette smoke</li>
<li>Studies in Philadelphia showed that that areas of the city with the highest percentage of minorities (particularly African Americans) had the greatest chance of using beta agonist medicine as the sole Treatment, as compared to beta agonists combined with inhaled corticosteroid therapy. (3, page 472)</li>
<li>Crowding increases risk of severe asthma, perhaps due to increased risk of being exposed to viruses that have been shown to worsen asthma (13, page 239, 244)</li>
<li>Impoverished people are less likely to have the educational knowledge to adequately care for their own, or their child's, asthma. (13, page 247)</li>
<li>Poor children are 40% less likely to visit a doctor, compared to non-poor children (13, page 247)</li>
<li>Poor children are 40% more likely to require hospitalization, compared to non-poor children (13, page 247)</li>
<li>Poor children are "more likely to utilize the emergency department." (13, page 247)</li>
<li>A study in Boston showed that minority children were "less likely to have been on preventative therapy prior to hospitalization, and were less likely to receive a nebulizer at discharge. These differences were not explained by source of payment. Instead, the racial diferences in outpatient medication use were attributed to practice site, with hospital-based clinics and neighborhood health centers differing from private practices." (13, page 249)</li>
</ul>
<div>
It has also been established that poverty makes it unlikely for an asthmatic to:</div>
<div>
<ul>
<li>Escape from potential asthma triggers (mainly from poorly maintained homes) (13, page 244)</li>
<li>Afford asthma medicines, either rescue or preventative</li>
<li>Afford to see a physician (i.e. family practice, internist)</li>
<li>Afford to see an asthma specialist (allergist, pulmonologist, etc.)</li>
<li>Have access to well located medical clinics, hospitals (i.e. physician), resulting in delayed treatment. This increases the risk of near fatal and fatal asthma. </li>
<li>Be educated on the proper management of asthma (i.e. have an asthma action plan, the need for </li>
<li>Escape from family conflicts, single parent families, substance abuse, crime, etc., all of whihc have been linked with worsening asthma. (13, page 245)</li>
<li>Escape inner city pollution that has been linked with worsening asthma (13, page 245)</li>
<li>Escape "psychosocial variables associated with asthma death." This is particularly true for impoverished asthma children (emotion due to family dysfunction, separation from parents or one parent, etc. (13, page 245)</li>
</ul>
<div>
So it is possible that worsening asthma morbidity and mortality due to socioeconomic status may skewer statistics, making it appear as though asthma is getting worse in a particular nation overall. </div>
</div>
<div>
<br /></div>
<div>
<b>Conclusion</b>: Keep in mind that all of these theories based on just a few studies, and further studies are definitely indicated. Experts continue to wonder whether the results from the studies listed above are isolated to particular beta adrenergic medicine studies (such as adrenaline and isopreterenol only) or if they are indicative of a class action effect of the medicine.</div>
<br />
Ann Janet Woolcock said the following:<br />
<blockquote class="tr_bq">
On the other hand, drugs such as albuterol, terbutaline, and salmeterol are partial beta agonists specific only to the lungs, and not the heart), and there is no substantial evidence that they increase the risk of death from asthma. <i>Regular use of albuterol did not increase the severity of disease in patients with mild asthma. </i>(2, page 190)</blockquote>
I added the emphasis there. Albuterol is specific to beta 2 adrenergic receptors in the lungs only, and not to beta 2 adrenergic receptors in the heart. Is it possible, therefore, that this makes albuterol exempt from all the studies mentioned above?<br />
<br />
"<i>Regular use of albuterol did not increase the severity of disease in patients with mild asthma.</i>"<br />
<br />
Albuterol is the best selling asthma medicine of all time, and part of the reason is that it relieves asthma symptoms and it comes with essentially negligible side effects. Some studies do suggest, however, that high doses due to frequent use of albuterol may increase asthma severity. Further studies are ongoing to determine if this is true, and, if so, to determine the reason why.<br />
<br />
<div>
<span style="font-size: xx-small;">References.</span></div>
<span style="font-size: xx-small;"></span><br />
<ol>
<li><span style="font-size: xx-small;">Beasley, Charles Richard William Beasley, Neil Edward Pearce, Julian Crane, authors of chapter two in the book "Fatal Asthma" edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc. Chapter two is titled "Worldwide trends in asthma mortality during the twentieth century." </span></li>
<li><span style="font-size: xx-small;">Woolcock, Ann Janet, author of chapter 14 of the book, "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 14 is titled "Natural Histor of Fatal Asthma." </span></li>
<li><span style="font-size: xx-small;">Sears, Malcolm R., "author of chapter 29 in the book "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 29 is titled "Role of B-Agonists in Asthma Fatalities." </span></li>
<li><span style="font-size: xx-small;">Jackson, Mark, "Asthma: The Biography," 2009, New York, Oxford University Press </span></li>
<li><span style="font-size: xx-small;">Bisgaard, Hans, Chris O'Callaghan, Gerald S. Smaldone, editors, "Drug Delivery to the Lung," 2001, New York, Marcel Dekker, Inc </span></li>
<li><span style="font-size: xx-small;">Mittman, Gregg, "Breathing Space," </span></li>
<li><span style="font-size: xx-small;">Speizer, F.E., R. Doll, P. Heaf, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1984843/pdf/brmedj02070-0023.pdf">Observations on Recent Increase in Mortality from Asthma</a>," British Medical Journal, February 10, 1968, 1, pages 335-339 </span></li>
<li><span style="font-size: xx-small;">Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel Dekker, Inc, pages 3 and 11 </span></li>
<li><span style="font-size: xx-small;">Speizer, F.E., R. Doll, P. Heaf, and B. Strang, "Investigation into use of drugs preceding death from asthma," British Medical Journal, 1968, 1, 339-343Sheffer, Albert L, "Partner Asthma Center's Grand Rounds," asthma.partners.org, <a href="http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html">http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html</a>, accessed 10/5/13 </span></li>
<li><span style="font-size: xx-small;">Bendy, Christine J., E.L-Fellah, R. Schneider, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1666729/?page=2">Tolerance to sympathomimetic bronchodilators in guinea-pig isolated lungs following chronic administration in vivo</a>," 1975, British Journal of Pharmacology, 55, pages 547-554 </span></li>
<li><span style="font-size: xx-small;">Yarbrough, J., L.E. Lansfield, and S. Ting, "<a href="http://www.ncbi.nlm.nih.gov/pubmed/4014786">Metered dose inhaler induced bronchospasm in asthma patients</a>," , Annals of Allergy, Asthma and Immunology," July, 1985, (55)1, pages 25-27 </span></li>
<li><span style="font-size: xx-small;">Grant, Evalyn N., Kevin B. Weiss, "Socioeconomic risk factors for asthma mortality," chapter 17 of the book, Fatal Asthma," edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc.</span></li>
</ol>
</div>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com34tag:blogger.com,1999:blog-4749703810590147676.post-77463114712880144582017-09-15T15:05:00.000-07:002017-09-15T15:05:04.101-07:001985: My Journey To To The Asthma Hospital<b>January 9, 1985</b><br />
<br />
On January 8, 1985, I boarded a plane in snowy Grand Rapids, Michigan, with my mom, and three hours later we arrived in an equally white Denver, Colorado. This was not a vacation. The purpose of the trip was for mom to have me admitted to a hospital that specialized in asthma. The estimated time of stay was 6-8 weeks.<br />
<br />
While my first ride in an airplane went great, that night at the hotel the asthma beast that I was oh too familiar with struck again.<br />
<br />
"Do you think I should take you across the street," mom said as we both stood looking out the window of the hotel room at the unfamiliar complex of the asthma hospital. Undoubtedly we could see the 7-Goodman building and the 2-May building, both future homes for me, but at this moment neither of us were aware of this.<br />
<br />
"I don't know," I said, taking a hit of my Alupent inhaler, pretending to be fine. "I think we can wait."<br />
<br />
The truth was I was very short-of-breath that night. When mom fell asleep I sat up on the edge of my bed gasping for air. "I should wake her up," I thought. Instead, I took more hits of my inhaler.<br />
<br />
The next morning mom and I walked to a nearby restaurant. I concentrated on every minute, thinking each was my last of normal life. When finished we walked back to the hotel room. Mom said, said, "They say you'll only need to be here 6-8 weeks. It's only a short time. Just think of every weekend as a marker of one more week gone by."<br />
<br />
I suppose it was mom’s optimism that kept my anxiety under wraps. I was excited about meeting other asthmatics my age, but I was nervous about the unexpected.<br />
<br />
Back in the hotel room mom grabbed one end of my trunk. I sighed and grabbed my end, and we were off. While walking across the street I looked up at the buildings wondering which one would be my new home, and what floor?<br />
***<br />
<br />
Mom was sitting in the business office filling out paperwork while I sat twiddling my thumbs on a chair in the hall. A few days ago, he called and introduced himself to me, “I will be your counselor during your stay at the asthma hospital. If you have any problems at anytime I will be available.”<br />
<br />
He appeared to be of amiable disposition, and his voice was very calm. I looked forward to meeting him. For now, though, I had to wait for mom to finish filling out papers, and “It’s taking forever,” I thought as I peered down the hall where there were several offices.<br />
<br />
I leaned forward and thought about going into the office where mom was, but mom told me specifically to stay put. I could hear the muffled sound of mom’s voice followed by the muffled sound of the secretaries, followed by shuffling of paper, and then, for what seemed like an eternity, the click clack of a typewriter.<br />
<br />
What would he look like – the social worker? Would he be as nice as he sounded on the phone? I sure hoped so, because I couldn’t handle a mean person. What would the nurses be like? What would my doctors be like? And, perhaps most important, what would it be like to meet a bunch of other asthmatics who were just like me? Would they be just like me? Who would become my friend? Will I find a friend?<br />
<br />
These thoughts rolled around in my cranium like balls on a billiards table until finally, the click clacking stopped. I stood up and peered into the crack of the door and saw the tip of mom’s jeans where they covered the knees and the front of a desk with paper scattered about. Why was she still sitting there? How much paper work could there be?<br />
<br />
The door opened and there stood mom in her blue top and blue jeans. Her dark hair set in a new perm over her beautiful phlegmatic eyes. She was a young person, only 38, but to me, she was a sagacious god, a permanent barrier to any harm and the answer to all the problems of the world. I know this wasn’t the normal mom/son relationship of your typical teenager, but I wasn’t normal by any means – I was chronically ill. Funny thing was, though, I didn’t think of myself that way. In fact, I didn’t think of myself as chronically ill until 23 years later when I’d send for, receive, and read my medical records from my stay at the asthma hospital.<br />
“He should be here any minute now,” she said, her voice soothing.<br />
<br />
“Who?” I said, shaking my head.<br />
<br />
“Ric Dexter. She called him. She said he’s a tall man with a well kempt dark beard and is really nice. She said you’d like him.”<br />
<br />
“Yeah, I know,” I said.<br />
<br />
It seemed like forever, but from around the corner appeared a man who fit the description. "<br />
Hi, I’m Ric Dexter,” he said. “I talked to you on the phone.”<br />
<br />
I looked at mom. She said, “Hi. I’m Alice Frea and this is my son, Ric.”<br />
<br />
“Hi, Rick, I hope you are as excited as I hope you are,” he said. “Let’s get rid of this trunk, and then I’ll take you on a tour. Then I’ll show you your new room and introduce you to your new room mate.”<br />
<br />
Lamely, all I could think to say was: “Okay.”<br />
<br />
He grabbed one handle of the trunk while mom and I looked on. “Normally I’d say your son should grab that other handle,” he said, “But he doesn’t look so well right now.”<br />
<br />
I took a deep breath as I watched mom grab the handle and HEAVE the trunk. I lagged behind Ric and mom. We were walking down the hall, through a door I suspected would take us back out into the cool winter air that was Denver, Colorado. But the door took us to a hallway that wended this way and that, through this door and that door until finally, we were in some sort of lobby that smelled of cooked bacon.<br />
<br />
“This is the lobby of the Goodman building,” he said. He pointed left at a set of see through doors where I could see what appeared to be a restaurant with a few people seated at many tables eating what I suspected was bacon and eggs and toast and whatever came on the early morning menu. “That’s the cafeteria,” he said. He peered down at me. “You won’t be eating here, Ric.” He looked up at mom. “But you will become really familiar with the food here, which is pretty decent for a hospital.”<br />
<br />
“I never had good hospital food before,” I wanted to say, but held my tongue.<br />
<br />
“Around this corner,” Ric said, “ ah here it is, is the elevator that will take us to the 7th floor where you will be staying.”<br />
<br />
He pushed the little round, red button. Ric continued to explain about the hospital to mom and me, and mom occasionally responded with an “uhum,” or “okay, I see.” I stood by the elevator door listening to the thump-thump of my heart in my chest. I wondered if mom and Ric could here it<br />
<br />
“This is 7-Goodman,” he said as the door swung open revealing a long hall with bright orange carpet. “This is where my office is,” he said as we passed a window revealing offices set apart by dividers. He opened the door.<br />
<br />
“Hi, Sarah,” he said. “This is Ric Frea and his mother Alice.” Sarah was a heavyset lady with dark, curly hair. She smiled pleasantly and offered a hand, which I took. “You will see her several times a week as many of your appointments will be with me and Linda.”<br />
<br />
“Who’s Linda?” I asked. “She’s one of your doctors. Her office is right next to mine.” He pointed to an office that had “Ric Dexter” printed on the door. Then he pointed to a door that had “Linda<br />
Hepper” printed on it.<br />
<br />
“Okay,” he said, “I can show you around here later. I suppose you want to meet some kids. Right” He patted me on the shoulder and he walked to the door and opened it. “Come on. It’s time to have some fun.”<br />
<br />
I felt a lump in my throat as I stepped back into the hallway and waited for mom and Ric to take the lead. I then followed Ric down the hall to a capacious room with the same bright orange carpet that filled the hall. To my right was a large nurses station. Two nurses were sitting there with their heads stuffed into charts.<br />
<br />
The majority of the room was filled with square, white tables with chairs pushed neatly in place. Straight ahead I saw a pool table. The long wall to my right was replete with several doors and windows blocked by curtains on the other side. The same scene was on the opposite, Western wall.<br />
<br />
A bulletin board on the Western wall had a head of Beetle Baily and Garfield with the words, “WELCOME TO 7-GOODMAN” neatly printed on them. Under that was written, “My way of drawing Garfield. I call him Crashfield.”<br />
<br />
While I was busy looking around the room, I didn’t notice the nurses had noticed us and had been now standing beside us. Mom and Ric set down the trunk.<br />
<br />
"This is Karen," Ric said, introducing me to the first nurse. She was a young, fine looking curly haired nurse. She bent down before me so I could see right into her pretty blue eyes. She said, "You're blue!<br />
<br />
"We better consider this a code blue," said a short, pudgy nurse in a white dress who stood behind Karen. Her nametag read Linda.<br />
<br />
Karen grabbed my hand and nearly dragged me across the room. "Have a seat," she said motioning to a chair by the wesst side of the lobby (which I later would learn was the girl's side)You need a treatment NOW."<br />
<br />
Mom followed close behind. She kept her distance as Karen took my vitals while Linda disappeared somewhere behind the nurses' station. I groaned as the pressure from the sphygmomemometer exceeded my pain threshold on my right forearm.<br />
<br />
“Sorry,” Karen said, “We like to start out high when we have new patients.”<br />
<br />
While I listened to the air leave the sphygmomanometer, I looked over Karen’s rich head of hair at mom and Ric. Ric stood there with a cool expression on his face, as though he had been through this many times. Mom looked worried.<br />
<br />
My mom recounted her anxieties in a recent email:<br />
<br />
"Here we were at the leading asthma institution in the world and they were running a code blue on you. If they were taking it that seriously, it meant you really were THAT bad."<br />
<br />
“Ric wanted to take me on a tour,” I said to the nurses, vaguely hoping it might get me out of this predicament.<br />
<br />
“Ric understands that we need to do our jobs,” Linda said. She stood beside me now holding a nebulizer. She plugged it into the compressor that sat on a table. “Right Ric?”<br />
<br />
She clicked the nebulizer on so it hummed audibly. Over the hum, I could barely hear Ric. “I certainly do. Hey, I’m going to go back to my office while you finish up here. When you are done you can call me and I’ll finish the tour. I’ll put the trunk in Ric's room.”<br />
<br />
“Great,” mom said. “Thank for—“<br />
<br />
The rest of that conversation was lost as Linda blocked my view of mom and Ric, turned on the compressor, and the nebulizer rumbled to life. She then handed me the misting nebulizer.<br />
<br />
"I feel fine," I said.<br />
<br />
"You're just used to it," Karen said.<br />
<br />
"I feel fine," I thought, forcibly preventing myself from rolling my eyes.<br />
<br />
I put the misting mouthpiece into my mouth the way I did many times before in hospitals.<br />
<br />
"Sit straight," Karen said, "Your stomach should go out when you breathe in slowly through your mouth, inhaling the white mist. Exhale slowly through your nose."<br />
<br />
"I know all that," I said.<br />
<br />
"We're going to re-teach you many things," Linda said.<br />
<br />
"Plug your nose when you inhale," Karen said, "When you inhale count to three when you exhale count to six... sit up straight... Ric, sit up straight."<br />
<br />
<em>Lots of rules for one silly treatment</em>, I thought. But these were the rules I had to follow for the next 6-8 weeks. <em>I sure so hope I'm out of here in 6-8 weeks.</em><br />
<em><br /></em> Finally, the treatment was done. "Shake it good," Karen said. "You want to get the most medicine you can out of it."<br />
<br />
Several minutes later the comperssor was off and I watched as a petite, dark haired lady in a brown dress walked up to mom. "I'm Dr. Betty," she said, "I'll be your son's doctor. We'll take good care of him."<br />
<br />
"That's what we're hoping," mom said, and she told Betty about the asthma attack I had last night<br />
<br />
"By the looks of things here," Dr. Betty said, "You should have brought him in. In fact, he should have been in a hospital the past week. She looked mom in the eyes, "Really, HE IS THAT BAD. I just want you to know you did the right thing bringing him here."<br />
<br />
Finally, after an hour with the doctor, the smell of spaghetti was in the air and a congregation of asthmatic kids of all sizes shuffled in one by one for lunch and noon meds.<br />
<br />
I barely had a chance to meet the other kids when Karen called me to the nurse’s station where Ric was standing. “Well,” he said, “I don’t see your room mate, but how about if we finish our tour now that you’re feeling better?”<br />
<br />
He took me to a door on the east side of the room. “This is the boy’s rooms,” he said.<br />
<br />
"This place is clean for a boy's dorm," mom said as she entered the room and looked around. I followed closely behind.<br />
<br />
"Well," Ric said, "We have a level system here. If the kids follow the rules they can move up to honors and get special privileges. It's a good incentive to keep your room clean." He smiled and looked at me.<br />
<br />
On the far side of the room, the eastern side, the wall was basically a huge window with a view of the city around the hospital set amid overcast skies. "If you look north," he pointed, "you can see the Rockies on a clear day."<br />
<br />
I followed him to the next room where the bed by the window was unkempt, and books and papers scattered about. "Eric is your room mate. He's a good kid, but he's kind of sloppy."<br />
<br />
There were two other beds in the room. "The one by the door is yours," he said. "You have to be close to the nurses until you move up to the next level. If you get to honors you can pick your own bed and even have a chance to get a TV."<br />
<br />
After showing me around the boy’s rooms Ric showed mom and me around the rest of the hospital. By the time we were back on 7-Goodman the other kids slowly carted into the room. A plump black kid, who would later introduce himself as Willie, was playing pool with another boy with messy black hair.<br />
<br />
“Hey, there’s your room mate,” Ric said. I looked around the room at all the kids that were now scattered about, two boys were sitting at tables involved in a project that was perhaps homework, a conglomeration of girls were standing in the far corner perhaps chattering about the latest gossip, and perhaps the topic of the day was, “Who is the new boy? Gosh, will he turn out to be a cool kid or a chump?”<br />
<br />
Ric led mom and me to the pool table to where the messy haired kid was aiming his cue at the black ball. Click. “Aha, I won!” he yelled as the black eight ball bounded into a corner pocket. “Finally I beat you.”<br />
<br />
“Ah, that’s fine,” Willie said, “We’re just having fun.”<br />
<br />
“Fun, my butt. It’s all about winning.” The messy haired boy’s grin filled his face as he twirled his pool stick over his head.<br />
<br />
“Hey, Eric, how’s it going,” Ric said. The pool stick flew out of Eric’s hand and clattered on the floor.<br />
<br />
“What? Who?” His smile instantly wiped away and filled with an expression of concern.<br />
“I want you to meat someone.” Ric motioned for me to move forward. “This is Ric Frea<br />
<br />
"This is your new roommate. Rick, this is Eric Groch.”<br />
<br />
I offered my hand, but Eric walked away. He bent down, picked up his pool stick, and leaned on the table, facing the door to his –and my—room.<br />
<br />
Beside me, mom was standing with her camera out. She tried to take a picture of Eric, but he quickly darted out of the range of the camera. Mom aimed through the camera again, but he darted, ducked under the pool table. The camera clicked. The picture of the pool stick and parts of Eric’s red shirt still show in the picture today, the only one of him I have.<br />
<br />
Only fitting, though, as he would turn out to be a big thorn in my side – a drug addict, criminal mind moron you might say. The kind of person no mom would ever want her son to meat, and here I was his roommate.<br />
<br />
Willie said, "Well, if you're not going to play pool, Rick can play."<br />
<br />
"Cool," I said, "I'll play."<br />
<br />
Eric plopped himself out from under the table, but when he saw my mom was eagerly standing by waiting to snap another picture, back under he went. An ominous sign of the chump Eric would turn out to be.<br />
<br />
Willie would turn out to be a good pal.<br />
<br />
(Dean and his mom and dad were standing nearby. Mom talked with his mother. Introduced me to Dean, who was admitted the day before. The next day mom and Dean’s parents went shopping while I participated in an array of tests.)<br />
<br />
Later that day, after a ton of appointments with doctors and testing, mom asked my doctor if she could take me to the museum. Dr. Betty said I was too unstable. I understood, but it was a disappointing none-the-less considering mom was in town five days and I couldn't do anything with her.<br />
<br />
Finally, on the 14th of January, I kissed her good-bye. I really didn’t have a lot of time those initial days to be homesick as the activities were abounding. Still, there were some dark moments.<br />
<br />
This was not a normal hospital where you sat in bed all day. It was more of an institution where you went about your normal daily activities, which were blended in with various tests and appointments. The intent was to get our asthma under control in the process of making us gallant asthmatics.<br />
<br />
The next morning I got up at 6 a.m. and walked out to the lobby in my jimmies. A short, curly haired blonde female teenager I had yet to be introduced to was taking a breathing treatment. I could hear the soft audible purr of the machine.<br />
<br />
“I can see your underwear,” Eric teased. “Hey everybody, you can see Rick's underwear through his witto jimmies.”<br />
<br />
Of course growing up with four brothers I didn’t care and proceeded to the nurse’s station. The night nurse placed three pills on the counter. “this one here tastes really bad, so you might want to take it with grape juice,” she said.<br />
<br />
The grape juice was good, but that pill tasted NASTY at the back of my throat regardless. It was the steroid pill. Even through the strong grape flavor, there was nothing I could do to prevent the pill from sliding over the sour receptors of my tongue.<br />
<br />
The other pill was Theo-Dur, a bronchodilator in pill form. That pill was relatively bulky, but I had no trouble getting it down.<br />
<br />
“Can I take my treatment now?” I asked. I was tight.<br />
<br />
“Well, you are gonna have to wait a while. Deana is taking a treatment now, and then comes Eric, Dean, Willie and then Stan. They were up before you. If you want to take a treatment first, you’re going to have to get up a lot earlier than this.”<br />
<br />
“Oh, come on. I need one now.”<br />
<br />
“Well, you should think about that before you sleep in,” she said, as she set the next kid’s meds on the counter.<br />
<br />
“But I didn’t’ sleep in. I’m up right on time.”<br />
<br />
“Well, you’ll have to reconsider.”<br />
<br />
I sat in a chair by the door of my room while I waited for my turn on the nebulizer. Finally, Stan sat in the treatment chair. Another girl was in the other treatment chair. I walked to the med room behind the nurse’s station. Here, on a counter, where several brown, glass bottles of medicine.<br />
<br />
I filed through cardboard papers in a box to the right and pulled out the one with my name on it. Listed on the card was the meds I was supposed to take in the nebulizer: Alupent 0.3cc and Atrovent 0.5mg. As I was reading the card Cathy, my head nurse, came into the room and poked her head over my shoulder. Willie was also in the room doing something with his nebulizer, but I paid him no attention.<br />
<br />
“I’ll just watch you do it today,” she said. Before this day she drew up the meds and I watched. So this was progress.<br />
<br />
To the left, on a rack hanging on the wall, were plastic bags with our nebs in them. I grabbed the one with my name, heart thumping but only because I had cute Cathy breathing down my shoulder, and dumped out the contents on to the counter. I set it up so the cup was open.<br />
<br />
I grabbed the syringe and set it in front of me. I reached for the large, brown bottle of Atrovent and twisted the cap until it was off. On the inside of the cap was a black squeeze bulb. I squeezed up the correct dose as Karen showed me the earlier, and squeezed it into the nebulizer cup. I did the same with the Alupent.<br />
<br />
The treatment now together, I walked back to the lobby. Cathy followed me out of the med room, but instead of following me to the treatment chair she went to the nurses' station. My chest was tight. I was audibly wheezing. I was huffing as I walked by the nurse’s station. Stan still had his hand over his nostrils and the neb in his mouth, but I could hear it was close to finished.<br />
<br />
“John, can I talk with you,” Cathy said.<br />
<br />
I approached her. As I did so Stan got up and another kid took his place in the treatment chair. I had missed my turn. Thank you very much, Cathy. How the heck could I miss my turn when no one came into the med room the whole time I was in there.<br />
<br />
On a table near the nebulizer three girls were seated and giggling. Al three were looking at me. One of them got up, giggling the whole way, and walked to the med room.<br />
<br />
“John,” Cathy was leaning on the counter looking at me. She whispered as I stood next to and leaned on the counter. I could not hear what she said, so I leaned in the same time she did. We were nearly face-to-face. “I didn’t want to say this in the med room in front of Willie.” She paused and held back a smile before she finished. “First of all, you really ought to wear a bathrobe over your pajamas. Either that or you should get dressed before you come out here for your meds in the morning. We can all see your underwear through your pajamas.”<br />
<br />
“You already said that,” I said.<br />
<br />
“Well, I guess you didn’t hear me. Do you hear me?”<br />
<br />
“Yes,” I said. “I hear you. Tomorrow I’ll get up earlier. What time is good?”<br />
<br />
“Well, if you want to get up before the other kids, you better be here by 5:30. You don’t have to, it’s your choice. Remember, you can take your morning treatment anytime between 5:30 and 6:30. But if you need a treatment as bad as you do, you ought to be up earlier.”<br />
<br />
“Okay,” I said. From now on the other kids are gonna wait for me.<br />
<br />
I turned and started for the nebulizer. Stan was STILL puffing on that thing. Is there anything coming out? I don’t see any mist. I turned to Cathy who was still leaning on the counter looking at me. “Cathy?”<br />
<br />
“Yes.” She let her smile show this time. You look darn good-looking for a nurse. I wonder how old you are.<br />
<br />
“How did Stan beat me to the treatment chair. I didn’t see him in the med room.”<br />
<br />
“He was up earlier and prepared his treatment so he was ready to go. You can do that to if you want.”<br />
<br />
The next day my alarm went off at 5 a.m. sharp. I leaned across my bed, hit the off button, and could hear my room mate snoring, his radio still blaring. I hopped out of bed in my pajamas, and I grabbed my green fluffy bathrobe I had set on my nightstand. As I opened the door to the lobby I saw there were no kids up yet. I had all the med room and the nebulizers to myself.<br />
<br />
When 5:30 arrived I had my butt in the nebulizer seat. From this point on the other kids had to wait for me.<br />
***<br />
It was my responsibility to know when my meds were due and to take them as instructed. If I missed one dose or used an improper technique, I would lose my allowance for the week. Without allowance, I’d have no money to spend at the weekly field trip. (Which didn't matter at this point anyway because Dr. Betty wouldn’t allow me to go even if I had the points.)<br />
<br />
The point sheet is what I used to keep track of my progress. On it was all the things I had accomplished in a day. If I lost it, that was like losing all my points. And it is pointed that determined how I moved up the levels.<br />
<br />
As I popped my pills with grape juice, I looked up at the board behind the nurse’s station. Dean’s name and mine were printed on the bottom written in blue marker, while all the other kid’s names were written in black. Next to our names was written the level we were on. My level was 2. Alongside the other names were 1, 2, 3, 4 or H for honors. The goal was to move up to honors, and the place no one wanted to go was level 1, because that meant no allowance and no privileges at all.<br />
***<br />
I followed Eric and the other kids to the elevator and down to the basement. It was time for my first day of school. I followed the other kids through the tunnels.<br />
<br />
Mr. Rose was a nice teacher. He seemed a bit obnoxious though, but I suppose when your teaching a bunch of chronically ill kids you have to be a bit different. "We have a new student, today," he said, "This is Rick Frea. Rick, tell us about yourself."<br />
<br />
"Um..." I said, "I'm from Michigan and I... uh... I have asthma and it got really bad and so now.. uh.. now I am here to get my asthma under control."<br />
<br />
"As is the case with all of us, right guys?"<br />
<br />
The class shouted in unison, "Right Mr. Rose."<br />
<br />
A short-stout kid with loose fitting clothes and long blonde hair sat in a seat right before Mr. Rose's desk. He never stopped talking for the first 30 minutes of class. Finally Mr. Rose said, "Chico, I think that bandana of yours is tied too tight over your skull and squeezing your brain because it sure doesn't seem to be working today."<br />
<br />
"That's because I'm hip," Chico said.<br />
<br />
"That's because you're a dip," Mr. Rose said. "Now stop talking a minute so we can educate the rest of the class because obviously, you don't have any interest in education. I'm not even sure it's possible to educate you."<br />
<br />
"I'm already fully educated," he chided.<br />
<br />
"We can all see how educated you are, Chicohead. Now hush."<br />
<br />
At noon I followed the other students back through the tunnels to 7-Goodman. The nurses gave me my noon meds. Karen was there. She told me I had appointments the rest of the day and wouldn't be going back to school.<br />
<br />
The second day of school, and many of the days that followed, I had to leave many times for "lots of appointments, which included a PFT," according to my personal diary.<br />
<br />
By the time I got back from testing the other kids were done with school. I was told after school was supposed to be our time to relax, do homework or socialize, but up to this day, I never had a chance to do either.<br />
<br />
After dinner, at 7.pm., it was time for aerobics. I was told I had to go down to participate, but I wasn't able to do anything physical. It surely wasn't fun standing there while the other kids were playing kickball.<br />
***<br />
<br />
The next day I talked to Dr. Betty between appointments and she said I could participate in aerobics if I wanted to that night. But, when I did, my chest got tight, I started to wheeze, and one of the kids had to show me how to get back to 7-Goodman.<br />
<br />
"Get an epinephrine ready," a pudgy nurse said as she started a breathing treatment and handed it to me. "Concentrate on your breathing. Sit straight. Concentrate on your breathing."<br />
<br />
I did as I was taught those first few days. I concentrated on my breathing, and soon I was able to take in a normal breath, but it didn't come until the treatment was almost finished. I almost bought myself my first Denver Epi that night, but it wasn't needed.<br />
<br />
The next day I had to do a barium swallow. That's a test to determine if there were any stomach abnormalities. I'm telling you, while I was there they did every test imaginable. They even did an EEG one day because I had constant headaches.<br />
<br />
For obvious reasons, I didn't do very well in school on these initial days. In my diary I kept writing, "School was boring today. I have to study for exams and I hate it." I was probably antsy about all these tests they were doing on me. Well, plus I was homesick being so far away from home.<br />
<br />
Finally, it was Friday of week two. I marked my diary: 4-6 weeks to go.<br />
<br />
Up to this point, I wasn't allowed to participate in any off campus events -- like there was any time for it anyway. Still, it was something that I was really looking forward to. I walked down to the business office during lunch break with one of the other kids and got money.<br />
<br />
Along with seeing Ric on regular basis, I also had to see a psychologist weekly. I didn't understand it then, but she was scoping me for the psychological consequences of asthma.<br />
<br />
Every night we either had aerobics or swimming. I had to go but was not allowed to participate that first week. I was wheezing and my chest remained tight.<br />
<br />
On day #13 my new friends wanted me to go to the mall with them. I "begged" Dr. Betty to let me go, and she said I could. She also said I could participate in aerobics that night.<br />
<br />
But, as I ran around the gym trying to be normal, the asthma beast struck and I became anxious and insisted that I needed a treatment. One of my friends escorted me upstairs, "where Kathy almost had to give me an epi," according to my diary.<br />
<br />
The next day school went great. At lunch, I rushed up to the bank to withdraw money to spend at the mall and rushed up to 7-Goodman to eat lunch and get my noon meds. I was wheezing.<br />
After school, and still wheezing after my treatment, Dr. Betty approached me. I had a bad feeling about this.<br />
<br />
She said, "John, I've decided you would benefit from being on steroids. We tried you on the basic meds and you don't seem to be responding. Your lips are blue as we speak. I want you to go upstairs to our hospital where we can watch you more closely."<br />
<br />
And so slipped my good mood. Here I was at the best asthma institution in the world and my Asthma wasn’t getting any better at all -- it was getting worse.<br />
<br />
To be continued.....John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com34tag:blogger.com,1999:blog-4749703810590147676.post-70490825382148827242017-09-14T07:50:00.000-07:002017-09-14T07:50:28.178-07:001979: Tedral Related Depression?I wrote about my experience with <a href="http://asthmahistory.blogspot.com/2017/02/1978-tedral-and-brondecon.html">Tedral</a> and <a href="http://asthmahistory.blogspot.com/2017/03/1979-tedral-side-effects.html">Tedral Side Effects</a>. I have come up with another side effect that I think might have been related to Tedral: Depression.<br />
<br />
I remember the first time I experienced it was in 1976 when my grandpa Howard died. He was my Great Grandfather, and he was 82-years-old. I did not know him very well, although I did visit him a few times with grandma at the nursing home, and maybe the occasional Christmas party at grandma's house.<br />
<br />
So, in November of 1976, he died. And I remember getting severely depressed. It lasted for quite some time. I remember feeling like I wanted to cry even in the days leading up to, and the days following the funeral.<br />
<br />
In fact, I remember the class singing "You Light Up My Life" in music, and I had to work hard not to cry.<br />
<br />
The same thing happened in 1977. It happened again in 1978. My Aunt Mary worked at K-Mart. They had a special "Blue Light Special" day where those who worked at K-Mart could invite their friends and relatives to this special day where they would have all sorts of deals.<br />
<br />
I remember being severely depressed every year this happened. And one year I won a radio. And that sort of ended the depression for a little while. But then it came back.<br />
<br />
I learned to dread November. I learned to dread the day of the K-Mart special party because I knew I'd get depressed.<br />
<br />
And then, one year, I think it was 1983 or 1984, the depression didn't come. I kept thinking it would, and it didn't. I remember concentrating on not letting the depression come, and it didn't. I prayed. I was so happy when it stopped.<br />
<br />
I have, to the best of my knowledge, not been depressed in November ever since.<br />
<br />
Mom said that when I was a kid I used to pace the living room for hours. She said she knew I was depressed. I do not ever remember her acknowledging it. I don't ever remember being treated for it until 1985 when I was at the asthma hospital.<br />
<br />
Recently, however, as I was thinking about this, and about Tedral, a thought occurred to me: what if I was going through withdrawal symptoms?<br />
<br />
I only took Tedral during allergy season, and then I was told (or my mom was told) to stop taking it or to have me quit. See? I probably became addicted to it over the summer. And when they took me off, probably near the end of October or early November, I went through withdrawal symptoms.<br />
<br />
No one ever noticed.<br />
<br />
Tedral contained theophylline, which is a xanthine just like caffeine. Like caffeine, you can develop both a psychological and a physical addiction to it.<br />
<br />
I think it ended because my asthma got so bad that I ended up taking theophylline year round. My doctor switched me to Theovent at some point. I probably only took it in the summer at first. But, by 1984, my asthma was so bad he just kept me on it year round.<br />
<br />
So, the depressions ended. They ended because my body developed a tolerance to it. My body expected it to always be there. It expected me to continue putting it into my body. And when I quit, my body had to readjust, hence the withdrawal symptoms; hence the depression.<br />
<br />
I know that when I forgot to take my theophylline over the years, it resulted in severe asthma episodes. So, I never experienced depression because, I think, asthma hit before the depression ever did.<br />
<br />
Anyway, this is just me thinking here. I could be wrong. There's really no way of knowing.John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com37tag:blogger.com,1999:blog-4749703810590147676.post-74123504005557855022017-09-11T04:56:00.000-07:002017-09-11T04:56:03.298-07:001968-2010: Mast Cell Stabilizers for asthma<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEigPCbzSSJrs0jlBpbolTfo3CFiKRSCS_G4LotoPuqhWGaUH9iHwQZ3Z6hE0-Quy3tBTXxmm1f5x1k0y3sgdo-0AmkXIo8aIoDhSvgKPgoB1sUYp4ycqW8DqoyW3nE6dJsIbQ-kZQyr6N8/s1600/spinhaler.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="268" nfa="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEigPCbzSSJrs0jlBpbolTfo3CFiKRSCS_G4LotoPuqhWGaUH9iHwQZ3Z6hE0-Quy3tBTXxmm1f5x1k0y3sgdo-0AmkXIo8aIoDhSvgKPgoB1sUYp4ycqW8DqoyW3nE6dJsIbQ-kZQyr6N8/s400/spinhaler.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Intal Spinhaler used by asthmatics in the 1970s, 80s and 90s</td></tr>
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In the early 1980s, my doctor introduced me to the Intal Spinhaler that crushed a capsule with a medicine called disodium cromoglycate or chromolyn. It was a white powder that was proven to improve lung function by decreasing inflammation. <br />
<br />
It was also proven to improve exercise related asthma. <br />
Each month you'll pick up a small white and yellow box from your pharmacist that contained a bunch of small capsules called Spincaps wrapped in tinfoil. You unwrapped one and set it aside. <br />
<br />
Then you the inhaler and held it so the mouthpiece was facing down. You unscrewed the cap and<br />
placed it onto a cup on the propeller, screwed the body back on the mouthpiece, and slide the outer sleeve (the blue part in the picture) down as far as it would go and then back up again. This pierces the capsule and makes the spinhaler ready for use. (1)<br />
<br />
You exhaled as much air as you could (just like using any inhaler), placed your mouth over the mouthpiece, and inhaled. As you inhaled, the powder would enter your airway, with a good portion going to your air passages. You could feel the powder as impacted in your upper airways, even taste it when it landed on your tongue. This is how you knew you did it right, I suppose<br />
<br />
This was the first mass produced dry powder inhaler that hit the market. It was a great medicine, and when used with an inhaled corticosteroid it worked great to prevent asthma.<br />
<br />
Mast cells are white blood cells that are randomly scattered around your respiratory tract. They are granulocytes, meaning they contain tiny grains. When told to do so, they release their contents, which contain histamine, leukotrienes, cytokines, and chemokines. These are tiny proteins that are responsible for airway inflammation.<br />
<br />
Mast cell stabilizers like cromolyn prevent mast cells from releasing their contents, thereby preventing them from causing inflammation. The idea was that this would result in better asthma control.<br />
<br />
There are a variety of environmental triggers that might trigger mast cells. One is when you inhale allergens, such as dust mites, pollen, animal dander, cockroach urine, mold spores, and certain foods. Another is rapidly breathing in air that is not properly warmed and humidified, such as what might occur while you are exercising. This irritates cells lining airways, causing mast cells to release their contents.<br />
<br />
So, cromolyn was prescribed for allergy and exercise induced asthma. Back then, these were essentially considered the hallmarks of all or most cases of asthma.<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjiJ5rFrsniw7Q4G2vNuB4nhhJmp68x5LJO47B5CMHzPbWWfhrZrLtzaPzEGYqZceRAc3mTM3Dk2KudT2D9gbYIfT4pHoJ01ZLegRVVE5f5U1ZydOtHMhy4mgBvlhTPMR-7VEyApgjgTEE/s1600/spinhaler.jpg" imageanchor="1" style="clear: right; cssfloat: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" gda="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjiJ5rFrsniw7Q4G2vNuB4nhhJmp68x5LJO47B5CMHzPbWWfhrZrLtzaPzEGYqZceRAc3mTM3Dk2KudT2D9gbYIfT4pHoJ01ZLegRVVE5f5U1ZydOtHMhy4mgBvlhTPMR-7VEyApgjgTEE/s1600/spinhaler.jpg" /></a></div>
When I was a kid I had what my doctors referred to as high risk asthma. I was allergic to pretty much everything outdoors, and had exercise induced asthma (EIA). Unless I was in an allergy proof bubble, my asthma was usually acting up. By the time I entered the 9th grade in September of 1984, I pretty much stopped going to gym class per my doctor's instructions.<br />
<br />
By January of 1985, I had made so many trips to the emergency room I was admitted to NJH/NAC in Denver. Once they managed to get my asthma under control, they did some pulmonary function testing on me to see what medicine might help me with my EIA.<br />
<br />
In one test I took no medicine and ran on the treadmill. My lung function dropped significantly. A week later I did another PFT, this time taking two puffs of Alupent before I ran on the treadmill. My lung function once again dropped significantly, indicating Alupent had no effect. <br />
<br />
A week later I used my Intal Spinhaler before exercise, and while my lung function declined it wasn't as steep of a decline, indicating that disodium cromoglycate prevented EIA, at least in me. (You can see my PFT tests <a href="http://www.scribd.com/doc/24307416/Pulmonary-Function-Tests">here</a>). <br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjtGFWIqzigbNf-4_EtVtxkdYaLLK6Sw_GCCVbV75wTPcyREznc-BV_qCcQDZ98b810GqHhATDIXvWQ24YlSHQIUEt08qiWr0tPxmzy65PEqAMkmHSwyFp4RCYauj2FpSt650MppJv2-xo/s1600/imagesCAHSNNAF.jpg" imageanchor="1" style="clear: left; cssfloat: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" gda="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjtGFWIqzigbNf-4_EtVtxkdYaLLK6Sw_GCCVbV75wTPcyREznc-BV_qCcQDZ98b810GqHhATDIXvWQ24YlSHQIUEt08qiWr0tPxmzy65PEqAMkmHSwyFp4RCYauj2FpSt650MppJv2-xo/s1600/imagesCAHSNNAF.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Intal Inhaler</td></tr>
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I was using this inhaler four times a day (which was a pain in the butt), so there was no need for me to use it prior to every time I exercised. I think the thought was that it would act as an asthma controller medicine to be used either in conjunction with or (ideally) as a stand alone medicine.<br />
<br />
In a way, it worked the same way inhaled steroids worked, yet apparently not as well. Prior to being at NJH/NAC my doctors had me using my Intal every day all the time, and only using my inhaled steroids as needed. Yet by the time I left NJH/NAC in July of 1985, I was using both medicines four times every day, along with a ton of other medicines as you can see <a href="http://go/">here</a>. Yes, this was a lot of medicine.<br />
<br />
Yet the Intal Spinhaler was a good medicine for asthmatics since it was introduced to the market in 1968. The medicine disodium cromoglycate was isolated by Roger Altounyan who had bad asthma himself and decided to test a variety of substances that were already proven to benefit asthma. He was working at Bengers Research Laboratories. (2)<br />
<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiiGn4rgMzd9feLIafhbxvfLOK1XARBuTCJHy-YkfZw-QSEWoqR9Fl_LxE6hiN48U7t1I501BNn2o09lm9qnInzW1MArzABrSkz-2G5vRcC7QIgojfbJMFaiyUjNNHe-S_oFXx3JuDKHaI/s1600/IVX64060.jpg" imageanchor="1" style="clear: right; cssfloat: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" gda="true" height="150" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiiGn4rgMzd9feLIafhbxvfLOK1XARBuTCJHy-YkfZw-QSEWoqR9Fl_LxE6hiN48U7t1I501BNn2o09lm9qnInzW1MArzABrSkz-2G5vRcC7QIgojfbJMFaiyUjNNHe-S_oFXx3JuDKHaI/s200/IVX64060.jpg" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Cromolyn Nebulizer Solution</td></tr>
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Khella was used by local natives living in Eastern Mediterranean countries for quite a few years to treat asthma with some success. They made various "concoctions" from the seeds of the plant <em>Amni Vasnaga</em>, from which the substance Khellin was extracted in 1879. (3)<br />
<br />
Various studies in the 1940s and 50s showed the medicine relaxed smooth muscles throughout the body, including the muscles surrounding air passages in the lungs. Yet the bronchodilating effect was less than epinephrine. The various studies showed the medicine accumulated in your system if used regularly, and was proven effective for both asthma and other lung diseases. (4)<br />
<br />
In 1953 The <em>American Journal of Physical Medicine </em>published the results of a study that showed inhaling aerosols of 7mg of Khellin improved lung function. Perhaps it was studies like this that inspired Altounyan to study this extract. (5)<br />
<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgNUapIKgFzN4tUHdQHByfHyb_-jvcf3fGVgtguxb1Ih_dKwJEJnqfeFfE9AcvGLqTzN8zj9uTfKUV7C1BprlGlgyy4wMJSix6RKXRksBrxMqdPUIp8KMInDuUD0_HxfPQg8DDosXqZG3M/s1600/Cromolyn.jpg" imageanchor="1" style="clear: right; cssfloat: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" gda="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgNUapIKgFzN4tUHdQHByfHyb_-jvcf3fGVgtguxb1Ih_dKwJEJnqfeFfE9AcvGLqTzN8zj9uTfKUV7C1BprlGlgyy4wMJSix6RKXRksBrxMqdPUIp8KMInDuUD0_HxfPQg8DDosXqZG3M/s1600/Cromolyn.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Amps of Cromolyn solution</td></tr>
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By experiments in the lab Altounyan produced a safer version of khellin called disodium chromoglycate. While his goal was to improve his own asthma, what he ended up with was a new product. It was marketed by Fisons and sold as the Intal Spincaps and Intal Spinhaler. It became yet another option for many asthmatics worldwide suffering from asthma and allergies. <br />
<br />
Along with being the first dry powder inhaler, it was also the first mast cell stabilizer.<br />
<br />
A problem with the spinhaler was that it couldn't be used during an asthma attack, and the dry powder entered your airway at such a force it was known to cause reflex bronchospasm, a fit of coughing and, thus, cause some asthma attacks. I never experienced this problem however. It was a nice option for me until modern inhaled steroids made it unnecessary.<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiVoywMNeZMyJ67ccigjrOMHDEhaTmUNj-gyEAv-gO-r7NvFXBM9qHKlBtp2j1hWzKGW8PLRV3c01EwnOVIvcz2PIIUpUqEmSYDt3cgdLwiZjveACV9hpgFpPoJJ7uXWluLaL05QxGXfVQ/s1600/imagesCAIOHI5B.jpg" imageanchor="1" style="clear: left; cssfloat: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" gda="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiVoywMNeZMyJ67ccigjrOMHDEhaTmUNj-gyEAv-gO-r7NvFXBM9qHKlBtp2j1hWzKGW8PLRV3c01EwnOVIvcz2PIIUpUqEmSYDt3cgdLwiZjveACV9hpgFpPoJJ7uXWluLaL05QxGXfVQ/s1600/imagesCAIOHI5B.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Tilade inhaler</td></tr>
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Nedicromil Sodium was approved by the FDA in 1992 as an alternative to Intal, and was marketed as the Tilade inhaler. (6) Studies showed it was equally effective in treating inflammation and reducing allergy and asthma symptoms as Intal. I never used Tilade, and I have little clinical experience educating it to patients either.<br />
<br />
By 1995, Cromolyn was available as a solution to be nebulized, and this was ultimately a good option for pediatricians to prescribe for kids with asthma. I have no recollection of ever giving this via aerosol to an adult, and rarely gave it to kids either for that matter. As of 2010, I believe we were no longer carrying it in our stock. <br />
<br />
The Intal Spinhaler was ultimately <a href="http://www.healthcentral.com/asthma/c/52325/109434/discontinued">phased out</a> in the U.S. and Europe in favor of an inhaler, and the inhaler was ultimately phased out on December 31, 2010. By a simple Google search, I see it's can still be purchased over the Internet, and may act as a viable alternative to top-line asthma medicines. <br />
<br />
Tilade was phased out on June 14, 2010. Altounyan's product was a great option for many asthmatics for many years, and for that we owe him thanks. Perhaps some form of this product will make a comeback someday and replace the need for inhaled corticosteroids. <br />
<br />
References: <br />
<ol>
<li>"<a href="http://draft.blogger.com/goog_1705273745">Intal Spincaps Powder for Inhalation, <span style="font-family: "times new roman";"><span style="font-family: "times new roman";">Sodium cromoglycate, </span></span></a><span style="font-family: inherit;"><a href="http://www.mydr.com.au/cmis/PDFs/CMI6078.pdf">Consumer Medicine Information</a>, " package insert for the Intal Spinhaler and Intal Spincaps, 2005</span></li>
<li>Jackson, Mark, "Asthma: A biography," 2009, New York, page 187</li>
<li> Kennedy, M.C.S, J.P.P. Stock, "<a href="http://thorax.bmj.com/content/7/1/43">The Bronchodilator Action of Khellin</a>," <em>Thorax,</em> 1952, 7, 43, pages 43-65</li>
<li>Kennedy, ibid, page 43</li>
<li>Braun, K, E. Eilender, "<a href="http://journals.lww.com/ajpmr/Abstract/1953/12000/Khellin_Aerosol_in_Bronchial_Asthma.15.aspx">Khellin Aerosol in Bronchial Asthma</a>," <em>American Journal of Physical Medicine</em>, Dec., 1953, Vol. 32, Issue 6, </li>
<li>"<a href="http://www.thefreelibrary.com/TILADE+APPROVED+BY+FDA%3B+FISONS+ANNOUNCES+CO-PROMOTION+AGREEMENT+WITH...-a013101159">Tilade approved by FDA; Fisons Announces Co-Promotion Agreement with Rhone-Poulenc Rorer</a>," Press Release, TheFreeLibrary.com, <a href="http://www.thefreelibrary.com/TILADE+APPROVED+BY+FDA%3B+FISONS+ANNOUNCES+CO-PROMOTION+AGREEMENT+WITH...-a013101159">http://www.thefreelibrary.com/TILADE+APPROVED+BY+FDA%3B+FISONS+ANNOUNCES+CO-PROMOTION+AGREEMENT+WITH...-a013101159</a></li>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com28tag:blogger.com,1999:blog-4749703810590147676.post-70249730385976801732017-09-05T08:41:00.001-07:002017-09-05T14:37:27.374-07:00Brief COPD HistoryDid you know that for most of history, nearly every lung disease, including COPD, was lumped under the umbrella term asthma? It’s true. In fact, it’s only been over the past 100 years that COPD has been plucked from under this asthma umbrella to become a disease entity of its own with its own remedies. That said, here is a brief history of COPD. <br /><br /><b>2697 B.C.</b>: Nei Ching Su Wen (Classics on Internal Medicine) is the oldest known medical document. In it, Huang Ti, The Yellow Emperor, is involved in dialogue with Ch'i Pai, his physician. The Emperor makes many references to asthma or COPD-like symptoms such as noisy breathing and troubled breathing.<br /><br /><b>1500 B.C</b>. Asthma and COPD-like symptoms were also described by the ancient Egyptians. The Ebers Papyrus is a medical document that describes over 700 remedies for asthma, including placing herbs on heated rocks and inhaling the smoke. <br /><br /><b>800 B.C</b>. Homer is the first to use the term asthma to define difficulty breathing after exertion in battle, or from wounds caused by battle. <br /><br /><b>400 B.C</b>.: Hippocrates defines asthma for the medical community as difficulty breathing. <br /><br />16<b>79 A.D</b>.: For the first time in history, physicians were allowed to perform autopsies to search for the true causes of diseases. A Swiss physician named <a href="http://asthmahistory.blogspot.com/2016/01/1679-term-emphysema-is-coined.html">Theophile Bonet</a> performed over 3,000 autopsies on patients of his who died and became the first to describe emphysema as a medical condition. He defined it as “voluminous lungs.” <br /><br /><b>1769</b>: Giovanni Morgagni described 19 cases of “turgis” lungs, and verified the findings of Dr. Bonet. <br /><br /><b>1784</b>: Dr. Samuel Johnson was a long-time sufferer of “asthma.” However, Dr. James Arthur Wilson, who was only 19-years-old, performed an autopsy on Dr. Johnson. Based on his description of Dr. Johnson’s lungs, later physicians determined that Johnson didn’t die of asthma, he died of emphysema. <br /><br /><b>1799</b>: Matthew Baillie, who also studied the body of Dr. Johnson, was the first to describe emphysema (“enlarged air spaces”) and publish his description in a book with pictures. <br /><br /><b>1814</b>. <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706597/#b22-copd-1-3">Charles Badham</a> became the first physician to use the term bronchitis when referring to inflammation of the mucous membrane. He referred to a chronic cough and increased mucus secretion as being caused by chronic catarrh. He also described chronic bronchitis as a disabling condition. <br /><br /><b>1819</b>: Rene Laennec, the inventor of the stethoscope, became the first physician to accurately describe emphysema and chronic bronchitis as related conditions. <br /><br /><b>1837</b>: Dr. William Stokes became the first to use the term chronic bronchitis. <br /><br /><b>1846</b>: English Surgeon John Hutchinson invented the spirometer. It was a device used to measure slow vital capacity (SVC) or the amount of air that can be exhaled after a deep inhalation. Later on, forced vital capacity (FVC) was described, or a forced exhalation after a deep inhalation. How fast can you get the air out after a deep inhalation? <br /><br /><b>1885</b>: Mendelssohn observed an increased incidence of “grinder’s asthma,” or what was often diagnosed as tuberculous among metal grinders. Before him it was believed inhaling coal dust was harmless, but he believed it was the cause of asthma. He was the first to observe a link between inhaled irritants like coal dust and smoke with lung disease. (1)<br /><br /><b>1947</b>: The ability to measure FEV1 was developed. This is the amount of air exhaled in the first second of FVC. Tiffeneau-Pinelli described inspiratory vital capacity (IVC) and created the formula FEV1/IVC This gave physicians the ability to differentiate between obstructive lung diseases (like asthma and chronic bronchitis) and restrictive diseases like emphysema and kyphosis. The formula used today is FEV1/FVC. Due to airway obstruction, FEV1 is reduced in people with COPD, resulting in a reduced FEV1/FVC. A normal FEV1 value is 80% of predicted. So, a diagnosis of COPD was determined to be a FEV1 less than 80% of predicted, along with a FEV1/FVC less than <a href="http://www.who.int/healthinfo/statistics/bod_copd.pdf">70%</a>. This is a good indicator of airflow obstruction and airflow limitation. In a restrictive lung disease, FEV1 and FVC will each equally be diminished to do lots of space for lungs to expand, and so FEV1/FVC may be close to normal or even slightly elevated. <br /><br /><b>1958</b>. American and British physicians defined the same disease differently up to this time. It was referred to as a chronic obstructive bronchopulmonary disease, chronic airflow obstruction, chronic obstructive lung disease, nonspecific chronic pulmonary disease, and diffuse obstructive pulmonary syndrome. This was confusing as it seemed as though each researcher, or each physician, was referring to something different. In order to unify efforts to learn about this disease, it was decided that a unified name must be created. The CIBA Guest Symposium, a gathering of various medical professionals, convened from Sept. 24-26. They were the first agree to use the term Chronic Obstructive Pulmonary Disease (COPD) in referring to the comorbidity of chronic bronchitis and emphysema. The results of the symposium were published in 1959. <br /><br /><b>The 1950s</b>: Antibiotics were <a href="http://www.news-medical.net/health/History-of-Chronic-Obstructive-Pulmonary-Disease.aspx">increasingly used</a> to treat lung infections (pneumonia) caused by increased secretions in airways. Potassium Chloride was used as a mucus thinner and theophylline as a bronchodilator. Epinephrine was used either as an injection or nebulized inhalant in emergency rooms. Epinephrine nebulizer solution was available for home use, and, after 1957, epinephrine inhalers were available. While systemic corticosteroids were available, they were rarely used to treat COPD. Isoprenaline nebulizer solution was also available, although used less regularly than epinephrine due to cost. An isoprenaline inhaler was also available after 1957. <br /><br /><b>The 1960s</b>: Isoprenaline was increasingly used, and corticosteroid and oxygen use continued to be <a href="http://www.news-medical.net/health/History-of-Chronic-Obstructive-Pulmonary-Disease.aspx">rarely used</a> to treat COPD. <br /><br /><b>1960</b>: Fry and Hyatt devised the flow volume loop, which displays the FVC as a graphic. This allowed physicians to physically see the difference between obstructive and restrictive disease. This made it easier to use spirometry as a means of differentiating between restrictive and obstructive diseases. <br /><b><br />1962</b>. Now researchers and physicians needed a unified definition of chronic bronchitis and emphysema. The American Thoracic Society Committee on Diagnostic Standards (Committee Diagnostic Standards for NonTuberculosos Respiratory Disease) defined chronic bronchitis as a cough lasting three months for at least three years, and emphysema as enlarged air spaces and loss of alveolar walls. Asthma was defined as airway hyperresponsiveness to a variety of stimuli. Asthmatic bronchitis was defined as a combination of asthma and COPD. For the first time, asthma and COPD were officially defined as unique diseases. <br /><br />Also, it was well known during the 1950s and 1960s that COPD was caused by cigarette smoke. So, in 1962, Donald O. Anderson and Benjamin Ferris <a href="http://www.nejm.org/doi/full/10.1056/NEJM196210182671601">reported</a> in the New England Journal of Medicine the results of a study performed in Berlin clearly linking the effects of cigarette smoke with chronic bronchitis. <br /><br /><b>1964</b>. In the November issue of American Journal of Public Health, Donald O. Anderson <a href="http://ajph.aphapublications.org/doi/pdf/10.2105/AJPH.54.11.1856">said</a>, “There seems little doubt whatever that cigarette smoking, and to a lesser extent other forms of tobacco smoking, are associated with mortality from lung cancer. This association has been amply demonstrated by both case history and cohort studies in a variety of countries and has been thoroughly summarized at countless symposia and in innumerable review articles. The controversy, instead, is whether this association has the attributes of a cause-effect relationship..” <br /><br />1965: William Briscoe became the first person to use the term COPD at the 9th Aspen Emphysema Conference. <br /><br /><b>2001</b>. Pauwels, et al, 2001, <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706597/#b22-copd-1-3">defined COPD</a> as chronic airflow obstruction, or airflow limitation, due to airway obstruction that progressively worsens over time and is only partly reversible (compared with asthma, which is considered to be completely reversible with medicine or time). This was the first time COPD was defined based on physiologic criteria, as opposed to clinical or anatomic criteria. <br /><br /><b>2004</b>: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) went with the definition of COPD as defined by Pauwels, et al, in 2001. Since then COPD has been considered a disease of airflow limitation. <br /><br /><b>2006</b>: COPD is the <a href="http://www.who.int/healthinfo/statistics/bod_copd.pdf">4th most common</a> cause of death in the United States, and, among the top five causes of death, is the only one rising in morbidity and mortality. <br /><br /><b>2013</b>: According to the <a href="http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/copd/learn-about-copd/how-serious-is-copd.html?referrer=https://www.google.com/">CDC</a>, COPD becomes the <a href="http://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm">3rd leading</a> cause of death in the United States, surpassing accidents and strokes, and close behind heart disease and cancer. <br /><br />References:: <br /><br /><ol style="margin-bottom: 0pt; margin-top: 0pt;">
<li>Klotz, Oskar, Wm. Charles White, ed., "<a href="http://books.google.com/books?id=lTXuAAAAMAAJ&pg=PA36&dq=mendelssohn,+smoke+harms+lungs&hl=en&ei=6ELQTpj_OYrDgAeZ1tifDQ&sa=X&oi=book_result&ct=result&resnum=2&ved=0CDoQ6AEwAQ#v=onepage&q=mendelssohn%2C%20smoke%20harms%20lungs&f=false">Papers on the Influence of Smoke on Health</a>," Bulletin #9, 1914, page 36</li>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com28tag:blogger.com,1999:blog-4749703810590147676.post-51925663707305642762017-09-04T04:42:00.000-07:002017-09-04T04:42:00.155-07:001968: Concerns about rescue inhalers lead to improved improved safety regulationsPrior to 1968, rescue inhalers were available over the counter (OTC) in Britain. Yet it was about this time that it was realized that the rising tide of asthma related deaths correlated with the introduction of the Medihaler Iso. As prescriptions and sales of the inhaler spiked in 1960, the death rate started to rise a year later. The link was obvious.<br />
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<br /></div>
<div style="margin: 0px;">
This revelation generated not just concern among the medical community, but among lawmakers as well. As a result of this new wisdom, in 1968 OTC sales of the inhalers were banned in Britain under Schedule 4B of the Poisons Regulations Act. (4, page 162) </div>
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<br /></div>
<div style="margin: 0px;">
At about the same time, "In June 1967, the Committee of Safety of Medicines issued a warning about the need for care in prescribing and using aerosols, emphasising their great value in treatment, but advising patients or parents to call their doctors if they failed to achieve the relief they usually experienced," according the authors of "Drug delivery to the lungs."</div>
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<br /></div>
<div style="margin: 0px;">
The death rate in Britain duly fell in the succeeding years. Furthermore, as noted by the authors of "Drug delivery to the lungs:"</div>
<blockquote class="tr_bq">
<div style="margin: 0px;">
When the changes in death rate were compared with estimates of prescriptions, it could be seen that the rise and fall of the death rates had followed the graph of sales of pressurized aerosols almost exactly." (5, <a href="https://books.google.com/books?id=F-7d9VzxMGYC&printsec=frontcover&dq=Drug+Delivery+to+the+Lung,&hl=en&sa=X&ved=0ahUKEwirsq-PycfVAhWM5yYKHdZqDkoQ6AEIKDAA#v=onepage&q=Drug%20Delivery%20to%20the%20Lung%2C&f=false">page 12</a>)</div>
</blockquote>
<div style="margin: 0px;">
Similar warnings were regulations and warnings were issued in other nations, including the United States. Gregg Mittman, in his book "Breathing Space," explains that:</div>
<blockquote class="tr_bq">
<div style="margin: 0px;">
The bronchodilator scare abroad prompted American physicians in the late 1960s to reflect critical on the therapeutic use of inhalers in Asthma treatment in the United States. As the sales of inhalers jumped form 3.3 million in 1964 to 5.1 million in 1968 in the United States, disturbing reports of patient abuse began to appear. Many asthmatic patients had become addicted to their bronchodilator inhalers, often grasping them for dear life. Some asthmatics admitted to going through an inhaler in a day. (6, page 235)</div>
</blockquote>
</div>
Physicians around the world realized that drugs alone were not going to work, that the entire environment around the patient would have to be investigated. Likewise, the patient would have to be educated not just about asthma, but about the medicines used to treat it. (6, page 236)<br />
<br />
As physicians and their patients became better aware of the risks of overuse of these inhalers, prescriptions and sales declined. The result of this was a national decline in the asthma death rate, although it still remained higher than the pre 1930s era when asthma morbidity and mortality was considered negligible.<br />
<br />
What did not fall, however, was asthma mortality. Studies performed during the 1970s would reveal that asthma morbidity trends have been gradually increasing since the introduction of rescue medicine. This would be investigated during a spike in asthma deaths that occurred in New Zealand in the 1970s.<br />
<br />
References: See "1940-1970: Asthma morbidity and mortality spikes"<br />
<br />
<div>
<span style="font-size: xx-small;">References.</span></div>
<span style="font-size: xx-small;"></span><br />
<ol>
<li><span style="font-size: xx-small;">Beasley, Charles Richard William Beasley, Neil Edward Pearce, Julian Crane, authors of chapter two in the book "Fatal Asthma" edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc. Chapter two is titled "Worldwide trends in asthma mortality during the twentieth century." </span></li>
<li><span style="font-size: xx-small;">Woolcock, Ann Janet, author of chapter 14 of the book, "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 14 is titled "Natural Histor of Fatal Asthma." </span></li>
<li><span style="font-size: xx-small;">Sears, Malcolm R., "author of chapter 29 in the book "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 29 is titled "Role of B-Agonists in Asthma Fatalities." </span></li>
<li><span style="font-size: xx-small;">Jackson, Mark, "Asthma: The Biography," 2009, New York, Oxford University Press </span></li>
<li><span style="font-size: xx-small;">Bisgaard, Hans, Chris O'Callaghan, Gerald S. Smaldone, editors, "Drug Delivery to the Lung," 2001, New York, Marcel Dekker, Inc </span></li>
<li><span style="font-size: xx-small;">Mittman, Gregg, "Breathing Space," </span></li>
<li><span style="font-size: xx-small;">Speizer, F.E., R. Doll, P. Heaf, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1984843/pdf/brmedj02070-0023.pdf">Observations on Recent Increase in Mortality from Asthma</a>," British Medical Journal, February 10, 1968, 1, pages 335-339 </span></li>
<li><span style="font-size: xx-small;">Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel Dekker, Inc, pages 3 and 11 </span></li>
<li><span style="font-size: xx-small;">Speizer, F.E., R. Doll, P. Heaf, and B. Strang, "Investigation into use of drugs preceding death from asthma," British Medical Journal, 1968, 1, 339-343Sheffer, Albert L, "Partner Asthma Center's Grand Rounds," asthma.partners.org, <a href="http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html">http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html</a>, accessed 10/5/13 </span></li>
<li><span style="font-size: xx-small;">Bendy, Christine J., E.L-Fellah, R. Schneider, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1666729/?page=2">Tolerance to sympathomimetic bronchodilators in guinea-pig isolated lungs following chronic administration in vivo</a>," 1975, British Journal of Pharmacology, 55, pages 547-554 </span></li>
<li><span style="font-size: xx-small;">Yarbrough, J., L.E. Lansfield, and S. Ting, "<a href="http://www.ncbi.nlm.nih.gov/pubmed/4014786">Metered dose inhaler induced bronchospasm in asthma patients</a>," , Annals of Allergy, Asthma and Immunology," July, 1985, (55)1, pages 25-27 </span></li>
<li><span style="font-size: xx-small;">Grant, Evalyn N., Kevin B. Weiss, "Socioeconomic risk factors for asthma mortality," chapter 17 of the book, Fatal Asthma," edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc.</span></li>
</ol>
</div>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com34tag:blogger.com,1999:blog-4749703810590147676.post-40918236238847823912017-08-18T18:20:00.000-07:002017-08-18T18:20:02.991-07:001960-1990: The asthma institutionBy the 1960s, the two asthma institutions in Denver that were opened to take care of tuberculosis patients were now mainly taking care of asthma patients, according to <a href="http://nationaljewishhealth.org/">NationalJewishHealth.org</a>. And "by this time TB patients comprised only half of the patient population and asthma patients a third." (5)<br />
<br />
It was in this decade that National Jewish Hospital opened a facility specifically for the increasing population of asthmatics with high risk asthma that was non responding to conventional therapy. It was in 1969 that a fee for service based on a patients ability to pay was begun.<br />
<br />
By 1976 Asthma was recognized as the most prominent chronic disease among children, affecting 1.5 million children in the United States, and this included myself. It produced a lot of suffering for those afflicted, and it also accounted for about one-forth of all school days lost. (4, page 164)<br />
<br />
It is a debilitating disease not only for the child who is suffering, but for parents who don't understand the disease, and fear their child might die. Yet perhaps even worse than that for the parent is the helpless feeling that there's nothing you can do, and what you do do doesn't help. Probably because most of what they did back to was based on fallacies of the past, such as putting asthmatics in a steam filled bathroom hoping that would relieve an attack.<br />
<br />
Yet for the child the suffering is even worse yet, and here I can allude to my own experience. Many nights I would stay up late, many times all night long, my wrists firmly pressed on the window sill, by face up against the cold screen with the intend on sucking in cool air and oxygen. Many nights I suffered in this way from an asthma attack.<br />
<br />
When I was little I sat up on the bed, all frogged up, gasping for air. I did this probably because I didn't know there was anything not normal about it. When I was older I'd push open the window in secrecy in the middle of the night because I didn't want to bother my busy parents. Another reason I suffered in secrecy like this was because I didn't want my parents to worry about me.<br />
<br />
Another reason may have been because of a poor self esteem exacerbated by parents who disciplined me because I underachieved, even when I was probably underachieving because of my asthma. Another reason for my low self esteem was because kids picked on me at school because I acted different from the "normal" kids. I had a runny nose and they didn't. I wasn't able to play baseball on teh dusty baseball diamond. So they picked on me. The same way my brothers sometimes picked on me when I didn't play baseball with them. I was basically fodder for the other kids.<br />
<br />
Now as I look back on all this I think I'm sometimes just saying this kind of stuff to justify why I was picked on as a kid, but based on my own medical records my counselors, my psychologist, and my medical physicians all believed this. Asthma had taken a physical and psychological toll on me. And to make matters worse my teachers and parents had no clue this was going on, and the end result was a shot self esteem and shot level of self confidence.<br />
<br />
And then I had mood changes. And many children have mood changes, so my parents and physicians probably figured I was just one of those intractable children. I became stubborn sometimes at home, and I was emotionally distraught. I remember being extremely depressed to the point my parents once grounded me from watching the news. I remember pacing the living room for hours worrying about the death of a relative, or that I was going to get old and die. Of course my parents and doctors had no clue I was depressed, or at least at the time they didn't associate it with the fact my asthma was poorly controlled. More recently my mom acknowledged to me she was aware of it, but I don't remember her ever doing anything to help me.<br />
<br />
So, again, I can understand the theory that asthma was believed to be psychological. Plus when a child is admitted to one of these hospitals the environment is controlled. By the 1970s and 1980s air conditioning was added to both the children's ward and the gymnasiums where children exercised. There was a focus on a good diet, and we were exercising all the time. Stuffed animals and items that collected dust were not allowed. Clothing was washed regularly so it was allergen free, and furniture was made of leather or other solid material that was easy to wash and didn't harbor allergens.<br />
<br />
By the 1970s there were two prominent asthma hospitals in Denver, one was National Asthma Center and the other was National Jewish Hospital at Denver. By 1978 National Asthma Center admitted financial trouble, these two great hospitals merged to create National Jewish Hospital/ National Asthma Center. The main campus was on Colfax Avenue, or the National Jewish Hospital campus. The merger resulted in the "largest treatment center for pediatric and adult asthma," according to<a href="http://www.nationaljewish.org/about/whynjh/history/clinical/clinical-history3/"> NationalJewishHealth.org</a>.(5)<br />
<br />
Once admitted the children would under go an examination by a physician, and then spend the next several days undergoing a variety of tests. I remember doing many pulmonary function tests, x-rays, electrocardiograms, sweat test (to rule out cystic fibrosis), and so many other tests I can't even recall all of them. I just remember being exhausted by the end of it.<br />
<br />
I met with a counselor on day one, and I think the main reason for my counselor was to help me deal with the day to day life at my new home, and also to help me learn to cope with life once I return home. I saw my counselor once or twice a week, and once every two weeks I saw a psychologist. I only saw a psychiatrist once that I remember, and he prescribed Xanax to help me relax. He actually prescribed an antidepressent before that, but I had an allergic reaction that gave me hives all over my body, so he must have decicded just to stick with xanax. It seemed to work pretty well (I'll tell you the story about that later).<br />
<br />
So I was admitted to the hospital in 1985, this was long after the psychosomatic theory of asthma had been proven to <em>not</em> be true. But I'm certain the doctors trained to work there, and the psychologist, were still privy to these old theories. I'm certain, especially after reading my medical records, that they believed much of my asthma was in my head. They noted the anxiety. They noted trouble when my mom visited, and how my asthma was exacerbated during these times.<br />
Travis quotes one physician as saying that "once asthma has been established, acute attacks may be triggered by emotions. There is a psychological basis for some emotionally precipitated attacks, particularly when the emotional upset is accompanied by shouting, crying and rapid breathing... it becomes impossible after a time to separate problems which are precipitating asthmatic attacks from those that are secondary to the asthma. The secondary gain can be a significant problem." (4, page <a href="http://books.google.com/books?id=6T2sAAAAIAAJ&pg=PA170&dq=Children%27s+Asthma+Research+Institute+%26+Hospital&hl=en&sa=X&ei=uI-XUI6YDOGNygHplIHYAw&ved=0CEIQ6AEwBA">169</a>)<br />
<br />
This appears to be my proof that asthma was no longer believed to be psychological by the time I was admitted in 1985, although psychological factors can still trigger asthma. Most of the asthmatics admitted by this time were on systemic corticosteroids, and the fear of side effects was paramount. Although, through the efforts of physicians at the hospital, I believe most patients went home on preventative asthma medicines, with controlled asthma, and off systemic steroids. At least that was the case with me and the children I was admitted with.<br />
<br />
It also must be noted that, even back in the 1940s I'm sure, occupational therapy was a major therapy given to asthmatic children admitted to the hospital. Children with intractible asthma, and I can attest to this, do not develop many of the skills other kids do to cope with life. This is the same for kids with other intractible diseases too. They don't develop skills that most people take for granted, such as balancing a check book or searching for an apartment. These types of basic skills that are worked on at the hospital, if the need is there.<br />
<br />
And, again, there was a major focus on education and exercise. These two were almost ingrained together at the asthma hospital. You need to understand your disease and every part of it, and you needed to exercise. Many times exercise was education, and education was exercise. You need to know your medicine, and you need to be compliant with your medicine. And you need to now why you are exercising, and how it will make you better.<br />
<br />
You need to know what aerobic exercise is, and if your legs weren't being kicked high enough in the air, you will be told this. And unless you have a good excuse, like your asthma was really acting up, you did as you were told. And for the most part you did it because you wanted to, because you were just happy you were able to exercise at all, because most of use weren't able to prior to being admitted.<br />
<br />
You will leave National Jewish educated, and if your physicians don't think you have a good grasp on your education, you will probably not be cleared for discharge.You need to take complete responsibility for your medicine, so that even if your parents back home aren't involved in your care, you know exactly what to do at all times. You need to know why you are taking your medicines and why it's so important to take them every day. And you need to exercise.<br />
<br />
You need to plan ahead on the first day of the week, and plan out what pills you will be taking and on what day and on what times during what day. You need to plan before every trip out of your house to make sure you take your medicine before hand, and that you have all the medicine you will need on the trip, such as your rescue inhaler. You cannot just take for granted someone else, even your parents, will remember your medicine when you leave the house. It is solely your responsiblity.<br />
<br />
You will have to also know when to take your rescue medicine, and when to wait. You will also have to know your asthma triggers and how to avoid them. You will also have to know what your symptoms of asthma are and what to do about them. You have to know it all, and you have to be completely responsible for your own health. That is essential, and it is engrained in your head over and over and over and over and over again until you are discharged.<br />
<br />
And also you had to exercise every day. The school I attended, the Kunsburg School, had a pool, and we swam two days a week during school. And when we weren't swimming we had gym class. Every evening after dinner we went to the gym in the school to do some form of aerobic activity. We stretched, and then we moved for 20 minutes. That was mandatory. We did kickball. We did basketball. We did baseball. We did dodge ball. And if you weren't moving, you were pestered by the PE instructor until you did just that.<br />
<br />
When you were first admitted you had a complete physical, followed by a series of tests. Your asthma was stabilited one way or another, and then you were cleared within You were then required to exercise, and you were required to attend school.<br />
<br />
And then, during the evenings, and on the weekends, you had fun just like normal kids do. You go on field trips. You go to the mall shopping and you go to movie theaters to watch the best movies. And you go to amusement parks, camping, and all sorts of fun things. Sometimes you go to video stores and rend movies to watch at home. You have parties with the other kids. You have dances. You have icecream socials. You have dance and singing competitions. You played games with the nurses and other kids.<br />
<br />
In the winter there was a basketball team, and either you joined the team or you traveled with the team and you watched the team. And in the spring there was a baseball team, and either you played or you watched. And it was much more enjoyable to play than watch. And you traveled to other institutions in the area, including those housing other sick kids, or otherwise sheltered kids. The goal is to make the hospital as much like home as possible. And, for the most part, they succeeded at this. It was a really fun experience. And all along you learned. Everything was a learning experience.<br />
<br />
At one point during my stay I wrote in my journal: "The only thing that makes this place seem like a hospital is the nurses wear stethoscopes over their shoulders." For the most part that was true. Although you were still thousands of miles away from your home, away from your parens, and you were chronically sick. So most of the kids got homesick, and that was another issues the staff there had to deal with. And, I'd assume, another reason for all the activities.<br />
<br />
In 1985, while I was a patient at NJH/NAC, the name was changed to National Jewish Center for Immunology & Respiratory Medicine. In 1995 the inpatient floors at the hospital were closed and a new pediatric outpatient program was added, and in 1997 the name was chanced again to<br />
<br />
<span style="font-size: xx-small;">References:</span><br />
<ol>
<li><span style="font-size: xx-small;">Minton, Gregg, "Breathing Space,"</span></li>
<li><span style="font-size: xx-small;">Wamboldt, Fredrick S. "Asthma Theory and Practice: It's Not Too Simple," April 2, 2008,</span></li>
<li><span style="font-size: xx-small;">Jackson, Mark, "Asthma: A Biography,"</span></li>
<li><span style="font-size: xx-small;"><span style="font-size: xx-small;">Travis, George, "</span><a href="http://books.google.com/books?id=6T2sAAAAIAAJ&pg=PA170&dq=Children%27s+Asthma+Research+Institute+%26+Hospital&hl=en&sa=X&ei=uI-XUI6YDOGNygHplIHYAw&ved=0CEIQ6AEwBA"><span style="font-size: xx-small;">Chronic Illness in Children</span></a><span style="font-size: xx-small;">," 1976, California, F</span>ord University Press</span></li>
<li><span style="font-size: xx-small;">"Clinical History," NationalJewishHealth.org, <a href="http://www.nationaljewish.org/about/whynjh/history/clinical/clinical-history3/">http://www.nationaljewish.org/about/whynjh/history/clinical/clinical-history3/</a>, accessed </span></li>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com19tag:blogger.com,1999:blog-4749703810590147676.post-51859292593691099432017-08-16T18:15:00.000-07:002017-08-16T18:15:12.775-07:001960s: Did rescue medicine cause a spike in asthma deaths? A spike in asthma related deaths forced physicians to take a closer look at this disease. Upon review of the available data, they began to surmise that the very medicines meant to make life better for asthmatics was responsible.<br />
<br />
The spike in asthma rates correlated with the releases and increased advertising of the new metered dose inhaler that was introduced to the market in 1957. The first to be released to the market were the Medihaler Epi (epinephrine) and Medihaler Iso (isoprenaline). As word got out there were devices asthmatics could carry in their pockets or purse that would give instant relief from asthma, sales of the device skyrocketed. (5, page 11)<br />
<br />
This followed a rise in the death rate. According to Speizer, Doll and Heaf in 1968:<br />
<blockquote class="tr_bq">
It is evident that an increase in mortality began to occur in about 1961 and that all ages between 5 and 64 years of age have been affected. The greatest increase in mortality has taken place at ages 10 and 14 years, the ages the rate has increased eight times, from 0.3 to 2.5 per 100,000 persons. The increase has, however, been substantial at all ages from 5 to 34 years, and at these ages the annual number of deaths increased by 308 and the death rate trebled from 0.7 to 2.2 per 100,000 persons. (7, page 336)</blockquote>
They further noted that that for the purposes of their study, the investigated only data obtained for the age group of 5-34, mainly because as asthmatics get older "mortality from bronchitis begins to exceed that from asthma." (7, page 336)<br />
<br />
<div>
Initial studies involved questioning the attending physicians of the patients who died from asthma. F.E. Speizer, Doll, Heaf and Strang in 1968 reported their findings. (9, page 342)</div>
<blockquote class="tr_bq">
Excessive use of pressurized aerosols was reported by 29 general practitioners without specific inquiry having been made. The reports ranged from a vague implication, such as "tended to use aerosols too frequently" or "suspicion of excess aerosol at death," to direct observation such as "died clutching aerosol" and a detailed account of the amount consumed. In extreme cases the use of as many as two canisters per day or two in two hours was reported. (9, page 342)</blockquote>
Investigators speculated that, perhaps, such asthmatic were victim of the false sense of security provided by the inhalers. Instead of seeking help, they continued to puff on their inhalers. By the time they called for help it was too late. (5, page 12-13)<br />
<br />
Upon further review of the data, they learned that asthma death rates remained stable in most nations where asthma death statistics were available. However, there were significant spikes in six Western countries: England and Wales, Scotland, Ireland, New Zealand, Australia, and Norway. (1, page 15) (2, pages 15-19)<br />
<div>
<br /></div>
<div>
In England, in particular, the asthma death rate was stunningly high. According to Speizer, Doll and Heaf in 1968, the asthma death rate in England "accounted for 5.7% of all deaths at ages 10 to 14 years, it ranked sixth in the list of causes of death." (7, page 336)</div>
<div>
<br /></div>
<div>
Since the sharpest rise in asthma deaths was limited to six nations, investigators searched for something that was particular to these regions. What they learned was reported by Beasley, Pierce and Crane. They noted that isoprenaline forte... contained a concentration of isoprenaline two to eight times greater than the standard isoprenaline metered dose inhaler available in other countries. Epidemics occurred only in countries where the high-dose preparation of isoprenaline was available; and in the two countries which marketed the high dose preparation and had no increase in mortality, it was introduced late into their markets per-capita sales were low." (1, page 16)</div>
<div>
<br /></div>
<div>
When the product was later pulled from these markets and the death rate declined, this proved to many researchers that this was probably the cause.<br />
<br />
References; ???<br />
<ol>
<li><span style="font-size: xx-small;">"Asthma Statistics, "AAAI.org, <a href="http://www.aaaai.org/about-the-aaaai/newsroom/asthma-statistics.aspx">http://www.aaaai.org/about-the-aaaai/newsroom/asthma-statistics.aspx</a>, accessed 9/29/13</span></li>
<li><span style="font-size: xx-small;">Beasley, Charles Richard William, Neil Edward Pearce, and Julian Crane, "Worldwide Trends in Asthma Mortality During the Twentieth Century," chapter two in the book "Fatal Asthma," edited by Albert L. Shefer, 1998, New York, Marcel Dekker, pages 13-29</span></li>
<li><span style="font-size: xx-small;">Woolcock, Ann Janet, "Natural History of Fatal Asthma," chapter 14 of the book, "Fatal Asthma," edited by Albert L. Shefer, 1998, New York, Marcel Dekker, pages 179-196</span></li>
<li><span style="font-size: xx-small;">1940s: Why did asthma morbidity and mortality increase</span></li>
<li><span style="font-size: xx-small;"><span style="background-color: white; color: #333333;">Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel </span></span><span style="background-color: white; color: #333333; font-size: xx-small;">Dekker, Inc, pages 3 and 11</span></li>
</ol>
<br />
<br />
<br />
<br />
<br />
References: See "1940-1970: Asthma morbidity and mortality spikes"</div>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com9tag:blogger.com,1999:blog-4749703810590147676.post-23654914895915815242017-08-14T18:10:00.000-07:002017-08-14T18:10:07.919-07:001950s: The first peak flow meter<div>
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<tr><td class="tr-caption" style="text-align: center;">Wrights original peak flow meters (circa 1950s)</td></tr>
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If you're an asthmatic you may not be familiar with Dr. Martin Wright, but you probably are familiar with an instrument he invented: the peak flow meter. It was a convenient, inexpensive, hand held tool that could be used by the patient at home to assess the effects of bronchitis and asthma. </div>
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It was first introduced in the 1950s by London physician, Dr. Martin Wright, of the Clinical Research Center at Northwick Park Hospital. It was an instrument specifically designed to measure 'peak flow,' or the amount of air that can be forced out of a patient's lungs after a maximum inhalation. </div>
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The original Wright was a large, heavy, clock shaped device and was too expensive for the common person to have at home. It was generally used in hospitals to assess patients. It worked by the patient blowing air into the meter, and this air rotated a pointer on a dial against the resistance of a spring. The device gave the first accurate readings of a peak flow.</div>
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<tr><td class="tr-caption" style="text-align: center;">Mini Wrights Peak Flow Meters (circa 1970s)</td></tr>
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In the 1970s Dr. Wright invented a new device that was inexpensive and portable. It's basically just a "tube with a spring inside and a calibrated scale along the outside. The puff from the patient under test pushes the spring back. A pointer registers the furthest point reached. The meter comes complete with a set of cardboard mouthpieces. Doctors recon that the instrument could be useful in home treatment. Patient's could monitor their own lung power in a simple and cheap way of determining recovery from lung ailments."</div>
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This instrument was called a "Mini Wright," although ultimately it became known as the peak flow meter. The devices were ultimately manufactured by various companies, and now you can get an array of different types. The first ones were not disposable, although they were soon thereafter manufactured for single patient use only, and the separate cardboard mouthpieces are no longer needed </div>
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<tr><td class="tr-caption" style="text-align: center;">Many peak flow meters available today</td></tr>
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I remember the "Mini Wright" from when I was an asthma patient back in the late 1970s and throughout the 1980s. I also remember having one at Shoreline when I first started working there. I believe at some point it simply became lost. Gone are the days of the Mini Wright, replaced by the even cheaper plastic models. <br />
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Can you guess how many peak flow meter brands are on the market? I couldn't even fathom a guess, although I've had over 20 in my grasp at one point or another.</div>
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<span style="font-size: xx-small;">Reference:</span><br />
<ol>
<li><span style="font-size: xx-small;">"<a href="http://books.google.com/books?id=IjlM0RhC3E4C&pg=PA675&lpg=PA675&dq=martin+wright,+peak+flow+meter&source=bl&ots=JBhxsLSXxJ&sig=O03KGKxhdbRTFu3NaLSz87msydQ&hl=en&sa=X&ei=1ulZUM-7KbT8yAGEo4FI&ved=0CDgQ6AEwAA#v=onepage&q=martin%20wright%2C%20peak%20flow%20meter&f=false">Hot Air Invention</a>," <i><a href="http://books.google.com/books?id=IjlM0RhC3E4C&pg=PA675&lpg=PA675&dq=martin+wright,+peak+flow+meter&source=bl&ots=JBhxsLSXxJ&sig=O03KGKxhdbRTFu3NaLSz87msydQ&hl=en&sa=X&ei=1ulZUM-7KbT8yAGEo4FI&ved=0CDgQ6AEwAA#v=onepage&q=martin%20wright%2C%20peak%20flow%20meter&f=false">New Scientist</a>, </i>March 1, 1979, page 675</span></li>
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<span style="font-size: xx-small;">Further reading and another picture:</span></div>
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<ol>
<li><span style="font-size: xx-small;">Check out: Wrights Peak Flow Meter, The <a href="http://medicine.nus.edu.sg/anaesthesia/virtual_museum/airmed_spirometer.htm">Virtual Museum Library</a>,
<a href="http://medicine.nus.edu.sg/anaesthesia/virtual_museum/airmed_spirometer.htm">http://medicine.nus.edu.sg/anaesthesia/virtual_museum/airmed_spirometer.htm</a></span></li>
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John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com10tag:blogger.com,1999:blog-4749703810590147676.post-73206307880855952942017-08-11T14:30:00.000-07:002019-12-13T06:45:33.349-08:001949-1969: The National Foundation for Asthmatic ChildrenOne of the main reasons National Jewish Health was able to stay afloat through the years is that it recognized the changing health needs in America. While both National Jewish Hospital for Consumptives and Denver Sheltering Home for Jewish Children opened to provide opportunities for children and adults inflicted or affected by tuberculosis.<br />
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Between the 1940s and 1960s the number of tuberculosis patients declined, and the number of asthma patients increased. Plus there as a need for taking care of patients with other diseases, including emphysema, chronic bronchitis, cystic fibrosis, bronchiectasis, silicosis, sarcoidosis, and fungal infections (1)<br />
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Yet there was also an increased emphasis on research, hence the name change of the Sheltering home to Jewish National Home for Asthmatic Children at Denver in 1953, and in 1957 to Children's Asthma Research Institute & Hospital (CARIH). The hospital also performed research into immunity, and this was a major reason for the 1985 name change of National Jewish Hospital/ National Asthma Center to National Jewish Center for Immunology & Respiratory Medicine.<br />
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There was another institution in Tuscon, Ariona, that was similar to National Jewish. People with lung ailments flocked to Arizona due to its dry climate, which was perceived to better for adults and children with breathing difficulties. The National Foundation for Asthmatic Children (NFAC) was opened in Arizona in 1949. It was actually the first "diseased based organization to launch a national campaign on behalf of the asthmatic child. (2, page <a href="http://books.google.com/books?id=WqPcB7Bzo9oC&pg=PA116&dq=Jewish+National+Home+for+Asthmatic+Children+at+Denver&hl=en&sa=X&ei=zlCaUMu2DeaPyAGi-IHQAw&ved=0CDoQ6AEwAA#v=onepage&q=Jewish%20National%20Home%20for%20Asthmatic%20Children%20at%20Denver&f=false">115</a>) During the 1950s National Jewish Home for Asthmatic Children started a similar educational campaign. (2, page 116)<br />
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Back then asthma was a little known disease, yet a massive advertising and public relations campaign by both National Jewish and NFAC increased awareness of the 2.5 million children in America with asthma. The campaigns increased awareness of the hospitals and research centers in both Denver and Tuscon. And the number of patients being referred to these hospitals increased. (2, page 116)<br />
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In 1973 CARIH changed its name to National Asthma Center, and admitted financial trouble by 1978, so it merged with National Jewish to create National Jewish Hospital/ National Asthma Center. This created the largest asthma hospital and research center in the world. Although there was an emphasis on patient care, the hospital continued to emphasize research.<br />
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While the school at NFAC closed in 1969, the hospital persisted. It was another option for children with hardluck asthma or other respiratory diseases. There was another such hospital in New York called Asthmatic Children's Foundation. In 1981 there were 15 similar residential treatment centers for asthmatics. (3)<br />
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In August of 2009 several former patients at NFAC met in Tuscon, Arizona to reminisce about their stay at the institution. The major emphasis back then about asthma was that medicine was used to treat acute symptoms, with included bronchospasm. Asthma was also a disease caused by a nervous disorder, or a suppressed cry for the mother. (4)<br />
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These kids were treated with a good course of education, exercise, and a good, healthy diet. They were also allowed to live a relatively normal life outside of that, by going on trips to town like normal kids, shopping, tours, amusement parks, parks, etc. They were also allowed to participate in games and other fun things kids do.<br />
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The kids "attend a boarding school for asthmatic children. These children can play out of doors year round and they become confident and competitive because they are competing with children on their own level," according A.B. Sieh, executive director for NFAC, in an article published in the Rotarian in August 1965. (5, page 51)<br />
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Boys and girls afflicted with bronchial asthma generally are admitted to the hospital for a one or two year stay, and this is at no charge, similar to the two asthma hospitals in Denver. The school the kids attend has a capacity of 72, and it's usually full (5, page 51)<br />
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Sieh notes that the "they come here pigeon chested with hollow eyes and sad faces... we have had children, who upon arrival, who could not walk up a single step without bringing on an asthma attack... the Arizona sun takes over and we have healthy looking children who can go home -- not cured, but rehabilitated to the point that they can cope with their asthma and live a normal life, attend public schools, and not be 'different.'<br />
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So while the main goal was to improve asthma, it wasn't like you were living in a hospital, at least not all the time. It allowed kids to get better, so they could go on to live normal lives.<br />
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References:</div>
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<ol>
<li><span style="font-size: xx-small;">"Clinical History," NationalJewishHealth.org, <a href="http://www.nationaljewish.org/about/whynjh/history/clinical/clinical-history3/">http://www.nationaljewish.org/about/whynjh/history/clinical/clinical-history3/</a>, accessed 11/7/12</span></li>
<li><span style="font-size: xx-small;">Mitman, Gregg, "Breathing Space," 2007</span></li>
<li><span style="font-size: xx-small;">Melvin, Tessa, "<a href="http://www.nytimes.com/1982/09/26/nyregion/for-36-children-hope-on-asthma.html">For 36 Children, Hope on Asthma</a>," <em>New York Times</em>, September 26, 1982</span></li>
<li><span style="font-size: xx-small;">Beal, Tom, "<a href="http://azstarnet.com/news/local/article_c1d21021-0bb3-530f-806d-d133a817af6e.html">Tuscon asthmatic kids of reunite, view latest research</a>," <i>Arizona Daily Star, </i>August 3, 2009</span></li>
<li><span style="font-size: xx-small;">"These Rotarians: <a href="http://books.google.com/books?id=qDMEAAAAMBAJ&pg=PA51&dq=national+foundation+for+asthmatic+children&hl=en&sa=X&ei=04GaUJGmAeG3yQH75IHQBQ&ved=0CD8Q6AEwAg#v=onepage&q=national%20foundation%20for%20asthmatic%20children&f=false">ABCs School</a>," <i>The Rotarian: An International Magazine, </i>August, 1965</span></li>
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John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com8tag:blogger.com,1999:blog-4749703810590147676.post-7483275388705345812017-08-07T14:26:00.000-07:002017-08-07T14:26:05.165-07:001960s: Spike in asthma death rate earns worldwide attentionA gradual rise in asthma deaths began during the 1940, although it gained little attention from the medical community, let along the general public. However, a rising tide of asthma deaths in the 1960s not only gained the attention of the medical community, it resulted in an increase in research and studies into our disease. This would have a significant impact on the millions of asthmatics around the world, and for the better.<br />
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The asthma death started to rise sharply in 1961. Then, according to Beasly, Pearce and Crane:<br />
<blockquote class="tr_bq">
In the mid-1960s, asthma mortality increased dramatically in at least six Western countries: England and Wales, Scotland, Ireland, New Zealand, Australia, and Norway. In these countries, the mortality rates increased 2-10 fold within a 2-5 year period. Other countries such as the United States, Denmark, Canada, and Germany did not experience epidemics, although in some countries such as Japan, significant increases in asthma mortality were noted within more narrowly defined age groups. (1, page 15)</blockquote>
It was the goal of researchers to discover the likely cause. A variety of theories were postulated and investigated by the experts.<br />
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A. Accuracy of physicians certifying the cause of death: This was investigated and pretty much ruled out as a probable cause (7, page 337<br />
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B. Changes in the way asthma was diagnosed: While it was determined that asthma might be misdiagnosed or under diagnosed, this was ultimately ruled out as a likely cause in an increase in asthma fatalities (7, page 335)<br />
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C. Increase in the number of cases of asthma: This was actually considered as a likely cause noted by Speizer, Doll and Heaf in 1968. They said, "In the absence of evidence t the contrary, it would seem that an increase in the case fatality rateis the most likely explanation of the increased mortality rate, and we have accepted this as a working hypothesis." ( 7, page 338),<br />
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D. Environmental factors: As noted by Speizer, Doll and Heaf in 1968:<br />
<blockquote class="tr_bq">
"Certainly the increase could not be due to smoke pollution, which has decreased in English towns over the last decade, nor could it be attributed to pollution with sulphur gases, which has remained approximately constant (Ministry of Techology, 1967). Motor traffic has increased considerably, and one of the constituents of motor fumes could perhaps have had a harmful effect. If this were the case, however, a substantial difference in mortality would be expected between urban and rural areas, and we have failed to find any evidence of this in the national mortality data for 1966. The death rate as 2.0 per 100,000 persons aged 5 to 34 in conurbations, 3.0 in urban areas of more than 100000 population, 2.2 in urban areas under 50,000 population, and 1.9 in rural districts. (7, page 338)</blockquote>
Similarly, Lawrence K. Altman said:<br />
<blockquote class="tr_bq">
We often yearn for the "good old days." For instance, it is often said that there is more pollution today than before, but that statement i snot necessarily correct. Think back to those earlier eras. Think of the stench from humans who found it dificult to keep clean when bathtubs were scarce. Imagine what it was like when horse manure constantly filled the streets. It is said that in the 1920s asthma from horses was a common affliction. Dr. Sheffer told me about how a horse trotting along the street could trigger an asthma attack inDr. Robert Cook of Roosevelt Hospital in New York City.</blockquote>
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Think also of the dust in the environment and pollution from wood-burning and coal-burning stoves. Recall the inversions that caused so much sickness and death in Pennsylvania and London, England, a few decades ago. </blockquote>
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Many ofthe offending environmental hazards have been removed. Public health campaigns and legislation have reduced the amount of tobacco smoke and dangerous chemicals in the air. Those changes have created a widespread impression that we live at a time when we breathe cleaner air (8, pages 5-6)</blockquote>
So, needless to say, environmental causes were ruled out as a factor. This is not to say that environmental factors are not likely factors in asthma morbidity in mortality. It merely rules these out as likely culprits or the spike in morbidity and mortality during the 1940s and 1960s.<br />
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E. Aging population: This was not considered an adequate reason because a majority of the data collected by the experts is generally collected for asthmatics between the ages of 5 and 35 years of age, or some similar range. The reason for this is because the older a person gets the greater the chance asthma will be complicated, or confused with, other medical conditions people normally get as they get older. Asthma under the age of 5 is difficult to diagnose. (1, page 13)<br />
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F. Improved ability to recognize and diagnose asthma: This may result in an increase in the number of people diagnosed, but it would not explain the increase in morbidity and mortality. (1, page 18)<br />
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G. Change in mode of treatment. There were actually two new modes of treatment on the market during the 1960. They were:<br />
<ol>
<li>Systemic Corticosteroids</li>
<li>Metered Dose Inhaler (MDI). This was often referred to as pressurized aerosol (asthma rescue inhaler)</li>
</ol>
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Systemic corticosteroids were never ruled out as a culprit. However, Speizer, Doll and Heaf note the following: </div>
<blockquote class="tr_bq">
Corticosteroids were introduced into the management of the disease in 1952, but the increase in mortality did not begin until nine years later. This discrepancy, however, is not sufficient to exculpate them entirely. The frequent and prolonged use of corticosteroids spread slowly, and the risk of harmful effects may be at a maximum only after patients have been under treatment for several years. </blockquote>
If patients were on a high dose of steroids and the patient suddenly stopped taking the medicine, this would result in adrenal gland suppression, which may result in death.<br />
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The asthma rescue inhaler was introduced between 1957 and 1960: According to Speizer, Doll and Heaf:<br />
<blockquote class="tr_bq">
These were introduced in England and Wales in 1960 and began to gain wide acceptance in 1961; and in the next five years their consumption is estimated to have increased more than fourfold (Ministry of Health, unpublished data). The closeness of the correlation justifies inquiry into the possible harmful effect of the preparations, but a temporal correlatoin of this sort, taken by itself, is a poor basis for drawing conclusions about cause and effect." (7, page 335)</blockquote>
Ultimately, while there were many likely causes for the spike in asthma deaths during the 1940s and 1960s, the finger was pointing at beta adrenergic medicine as the likely culprit. Whether this was the actual cause was never fully determined.<br />
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References.<br />
<ol style="font-size: x-small;"><span style="font-family: Georgia, Times New Roman, serif;">
<li>Beasley, Charles Richard William Beasley, Neil Edward Pearce, Julian Crane, authors of chapter two in the book "Fatal Asthma" edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc. Chapter two is titled "Worldwide trends in asthma mortality during the twentieth century."</li>
<li>Woolcock, Ann Janet, author of chapter 14 of the book, "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 14 is titled "Natural Histor of Fatal Asthma."</li>
<li>Sears, Malcolm R., "author of chapter 29 in the book "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 29 is titled "Role of B-Agonists in Asthma Fatalities."</li>
<li>Jackson, Mark, "Asthma: The Biography," 2009, New York, Oxford University Press</li>
<li>Bisgaard, Hans, Chris O'Callaghan, Gerald S. Smaldone, editors, "Drug Delivery to the Lung," 2001, New York, Marcel Dekker, Inc</li>
<li>Mittman, Gregg, "Breathing Space," </li>
<li>Speizer, F.E., R. Doll, P. Heaf, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1984843/pdf/brmedj02070-0023.pdf">Observations on Recent Increase in Mortality from Asthma</a>," <i>British Medical Journal, </i>February 10, 1968, 1, pages 335-339</li>
<li><span style="font-size: xx-small;"><span style="background-color: white; color: #333333;">Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel </span></span><span style="background-color: white; color: #333333; font-size: xx-small;">Dekker, Inc, pages 3 and 11</span></li>
<li>Speizer, F.E., R. Doll, P. Heaf, and B. Strang, "Investigation into use of drugs preceding death from asthma," <i style="color: #333333;">British Medical Journal, </i><span style="background-color: white; color: #333333;">1968, 1, 339-343</span><span style="background-color: white; color: #333333; font-size: xx-small;">Sheffer, Albert L, "Partner Asthma Center's Grand Rounds," asthma.partners.org, </span><span style="font-size: xx-small;"><a href="http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html">http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html</a>, accessed 10/5/13</span></li>
<li>Bendy, Christine J., E.L-Fellah, R. Schneider, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1666729/?page=2">Tolerance to sympathomimetic bronchodilators in guinea-pig isolated lungs following chronic administration <i>in vivo</i></a>," 1975, <i>British Journal of Pharmacology</i>, 55, pages 547-554</li>
<li>Yarbrough, J., L.E. Lansfield, and S. Ting, "<a href="http://www.ncbi.nlm.nih.gov/pubmed/4014786">Metered dose inhaler induced bronchospasm in asthma patients</a>," , <i>Annals of Allergy, Asthma and Immunology," </i>July, 1985, (55)1, pages 25-27</li>
<li>Grant, Evalyn N., Kevin B. Weiss, "Socioeconomic risk factors for asthma mortality," chapter 17 of the book, Fatal Asthma," edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc.</li>
</span></ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com6tag:blogger.com,1999:blog-4749703810590147676.post-79995981423259103322017-08-04T14:24:00.000-07:002017-08-08T04:52:13.403-07:001940: Asthma death rate begins a gradual riseThe 1940's was a significant decade in the history of medicine, as advances in medicine resulted in declines of morbidity and mortality from some of histories deadliest diseases, such as consumption and influenza. Our asthma history saw an opposite trend. While asthma morbidity and mortality were negligible through the 1930, they started to gradually climb during the fourth decade of the 20th century.<br />
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Considering these other diseases were in the forefront of the general public, the spike in asthma deaths nearly went unnoticed. Some experts may have seen what was going on, although they had no way of even guessing at the cause. The reason was because most of the public's attention remained on other diseases, with all public funds, therefore, not going for asthma research. For this reason there was very limited data regarding asthma available to review.<br />
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That left researchers to reviewing death certificates. However, many experts wondered if methods of certifying death certificates were even accurate. There were probably times when asthma was misdiagnosed and under diagnosed. A middle aged man with bronchitis may have been misdiagnosed with asthma. A child with asthma may have been misdiagnosed with asthma. Likewise, a child with asthma may have gone unrecognized, and therefore un-diagnosed.<br />
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It actually wasn't until the 1960s when all eyes were opened to the rising death rates that death certificates were reviewed. The experts decided to limit their research to asthmatics between the ages of 5 and 35. The reason was that the likelihood of having pure asthma was greatest among this age group. Those under five were hard to diagnose, and those over 35 had a a greater likelihood of having some other disease combined with asthma. Figuring out which one resulted in death could sometimes be difficult to determine.<br />
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Data was collected from as far as 1900 for this age group. According to Beasley, Pearce and Crane in 1968, here is what was learned:<br />
<blockquote class="tr_bq">
Those Western countries in which relevant data have been published indicate that asthma mortality was uniformly low and relatively stable between 1900 and 1940. The death rate began to increase gradually in the 1940s in a number of countries including New Zealand and Australia, in which a threefold increase over a 15-year period was observed. Mortality declined again in the late 1950s in New Zealand, England, and Wales, but not Australia. In contrast, little change in asthma mortality rates was observed in the United States during this period. Although the interpretation of death rates over such an extended period is difficult, the historical data are likely to be acceptable accuracy in this age group." (1, page 14)</blockquote>
They also made one other observation:<br />
<blockquote class="tr_bq">
It is interesting to note that isoprenaline was introduced in a nebulizer formulation during the 1940s when mortality began to increase, but whether this had a role in the increase in mortality was not examined in detail at the time. (1, page 14)</blockquote>
Trends in asthma related deaths were not significantly studied until the 1960s. When this was done, one of the theories that arose for the rise of asthma deaths in the 1940s was the availability of nebulized isoprenaline at home. Theorists sense this may have created a false sense of security among asthmatics, particularly children. Where they once would have sought help, they now simply resorted to their rescue medicine.<br />
<br />
Isoprenaline was a new line of sympaththeomimetic medicines, also known as beta adrenergic medicine, more recently as asthma rescue medicine. Regardless of what it is called, it has the tendency to provide immediate relief from an asthma attack. Having access to such medicine was a godsend for asthmatics, because it meant that they could get immediate relief in the convenience of their own homes.<br />
<br />
While physicians were happy to provide such an opportunity to asthmatics, they were not ready for the potential consequences. Allowing asthmatics to have quick access to such rescue medicine resulted in two things.<br />
<ol>
<li>Overuse of isoprenaline may have resulted in cardiac arrest. This would have resulted in suden death from isoprenaline overdose secondary to asthma. </li>
<li>Overuse of isoprenaline may have resulted in tolerence to the medicine. This would have made the asthma refractory to the isoprenaline, resulting in increased dosing. By the time the asthmatic gave up on the isoprenaline, it was too late. </li>
</ol>
<div>
These were simply theories that were never proven. It as impossible for researchers to question these asthmatics after they died, and therefore it was impossible to know how much isoprenaline they used, if any. </div>
<div>
However, in many instances, there were reports from family members and friends of these asthmatics using their rescue medicine prior to death. </div>
<div>
<br /></div>
<div>
For these asthmatics, however, such theories were trivial and too late. Although data obtained from studying how they died may have resulted in safety precautions that saved the lives of many future asthmatics. In this way, the experts made sure these asthmatics did not die in vane. </div>
<div>
<br /></div>
<div>
Another good thing that came out of the rise in asthma deaths during the 1940s, and later in the 1960s, was better recognition of our disease by the medical community. This ultimately resulted in better recognition by the public, and therefore better funding for future research. </div>
<div>
<br /></div>
<div>
However, as morbidity and mortality from asthma still remained low in comparison to other diseases, the rise in public awareness continued to pale in comparison. While it's sad to say, many asthmatics continued to suffer from their disease because the general public simply was not paying attention. <br />
<br />
<span style="font-size: xx-small;">References.</span></div>
<span style="font-size: xx-small;"></span><br />
<span style="font-size: xx-small;"><br /></span><ol>
<li><span style="font-size: xx-small;">Beasley, Charles Richard William Beasley, Neil Edward Pearce, Julian Crane, authors of chapter two in the book "Fatal Asthma" edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc. Chapter two is titled "Worldwide trends in asthma mortality during the twentieth century." </span></li>
<li><span style="font-size: xx-small;">Woolcock, Ann Janet, author of chapter 14 of the book, "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 14 is titled "Natural Histor of Fatal Asthma." </span></li>
<li><span style="font-size: xx-small;">Sears, Malcolm R., "author of chapter 29 in the book "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 29 is titled "Role of B-Agonists in Asthma Fatalities." </span></li>
<li><span style="font-size: xx-small;">Jackson, Mark, "Asthma: The Biography," 2009, New York, Oxford University Press </span></li>
<li><span style="font-size: xx-small;">Bisgaard, Hans, Chris O'Callaghan, Gerald S. Smaldone, editors, "Drug Delivery to the Lung," 2001, New York, Marcel Dekker, Inc </span></li>
<li><span style="font-size: xx-small;">Mittman, Gregg, "Breathing Space," </span></li>
<li><span style="font-size: xx-small;">Speizer, F.E., R. Doll, P. Heaf, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1984843/pdf/brmedj02070-0023.pdf">Observations on Recent Increase in Mortality from Asthma</a>," British Medical Journal, February 10, 1968, 1, pages 335-339 </span></li>
<li><span style="font-size: xx-small;">Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel Dekker, Inc, pages 3 and 11 </span></li>
<li><span style="font-size: xx-small;">Speizer, F.E., R. Doll, P. Heaf, and B. Strang, "Investigation into use of drugs preceding death from asthma," British Medical Journal, 1968, 1, 339-343Sheffer, Albert L, "Partner Asthma Center's Grand Rounds," asthma.partners.org, <a href="http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html">http://www.asthma.partners.org/newfiles/ShefferFatalAsthma.html</a>, accessed 10/5/13 </span></li>
<li><span style="font-size: xx-small;">Bendy, Christine J., E.L-Fellah, R. Schneider, "<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1666729/?page=2">Tolerance to sympathomimetic bronchodilators in guinea-pig isolated lungs following chronic administration in vivo</a>," 1975, British Journal of Pharmacology, 55, pages 547-554 </span></li>
<li><span style="font-size: xx-small;">Yarbrough, J., L.E. Lansfield, and S. Ting, "<a href="http://www.ncbi.nlm.nih.gov/pubmed/4014786">Metered dose inhaler induced bronchospasm in asthma patients</a>," , Annals of Allergy, Asthma and Immunology," July, 1985, (55)1, pages 25-27 </span></li>
<li><span style="font-size: xx-small;">Grant, Evalyn N., Kevin B. Weiss, "Socioeconomic risk factors for asthma mortality," chapter 17 of the book, Fatal Asthma," edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc.</span></li>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com8tag:blogger.com,1999:blog-4749703810590147676.post-84053502168103003382017-08-04T13:30:00.000-07:002017-08-04T13:30:15.796-07:001913: Cauterize your nose, cure your asthmaAnother interesting concept of Adams is that he denied that most asthmatics had allergies, although he associated abnormalities in the nasal cavity with asthma. He noted that Henry Hyde Salter cursorily mentioned the relevance of the nose in cases of asthma, when such knowledge was known since 1844 when Herck of Freiburg noted the association of sneezing and asthma. (1, page <a href="http://books.google.com/books?id=RLASAAAAYAAJ&printsec=frontcover&dq=asthma+and+its+radical+treatment&hl=en&sa=X&ei=-tSTUJeVH-mWywGIl4C4CQ&ved=0CDYQ6AEwAA#v=onepage&q=asthma%20and%20its%20radical%20treatment&f=false">89</a>)<br />
<br />
Later, Adams noted, Voltolini, in 1872, claimed to have "relieved eleven cases of asthma by removal of nasal polypi. This idea received further impetus when Lazarus, Brodie and Dixon and others showed that electrical stimulation of the nasal mucosa caused bronchial spasm."<br />
<br />
<span style="background-color: white; font-family: inherit;">Ernst Schmiegelow explained that Voltini noted that no other asthma physicians prior to him noted the link between nasal polypi and asthma. And while polypi are not always associated with asthma, there are noted cases where, upon removal of the polypi, the asthma disappeared. Although, if asthma has existed long enough so that it is chronic, removal of the polypi will not make the asthma disappear. Schmiegelow notes that Voltini's opinions were confirmed by Hanisch. (2, </span><a href="http://books.google.com/books?id=Fyx7rKQPzZgC&pg=PA14&lpg=PA14&dq=Voltolini,asthma&source=bl&ots=VmkSZi8Bed&sig=yjIm9UeQ1Lm0zjpRL6a2rokSj8w&hl=en&sa=X&ei=RJ48UaHuFIXayAHn7IDIAQ&ved=0CDkQ6AEwAA#v=onepage&q=Voltolini%2Casthma&f=false" style="background-color: white; font-family: inherit;">page 14</a><span style="background-color: white; font-family: inherit;">)</span><br />
<span style="background-color: white; font-family: inherit;"><br /></span><span style="background-color: white;"><span style="font-family: inherit;">Schmiegelow notes that "</span><span style="font-family: inherit;"><span style="color: #274e13;"><span style="text-indent: 13.28px;">H</span><span style="font-style: italic; text-indent: 13.28px;">anisch </span><span style="text-indent: 13.28px;">thinks that as not all nasal polypes cause </span><span class="gstxt_hlt" style="text-indent: 13.28px;">asthma, </span></span><span style="text-indent: 13.28px;"><span style="color: #274e13;">there must be a certain debility of the whole organisation or at least of the organs of breathing. In the nasal polypes themselves he finds sufficient ground for the weakened state of the organisms and lungs, as the insufficient breathing, the restless sleep, the buccal respiration, etc., must be considered capable of causing the general weakness</span>." (2, page 14)</span></span></span><br />
<span style="background-color: white;"><span style="font-family: inherit;"><span style="text-indent: 13.28px;"><br /></span></span></span><span style="background-color: white;"><span style="font-family: inherit;"><span style="text-indent: 13.28px;">B. Frankel and Weber also confirmed the findings of Voltini, and they also believed that chronic catarrh could also cause asthma. They believed irritation of the nasal mucous membrane passed a message down the pneumogastric to the pulmonary fibres, causing asthma, and "the result of the reflex was always a bronchospasm.". (2, page 15) Henry Hyde Salter previously mentioned this, and referred to is as reflex asthma. </span></span></span><br />
<span style="background-color: white;"><span style="font-family: inherit;"><span style="text-indent: 13.28px;"><br /></span></span></span><span style="background-color: white;"><span style="font-family: inherit;"><span style="text-indent: 13.28px;">Schmiegelow also mentions a Dr. Wilhelm Hack, who<span style="font-family: inherit;"> "</span></span></span></span><span style="font-family: inherit;"><span style="background-color: white; text-indent: 13.28px;">supported by casuistic observations, considered a number of different nervous diseases from the same point of view. </span><span style="background-color: white; font-style: italic; text-indent: 13.28px;">Hack's </span><span style="background-color: white; text-indent: 13.28px;">principal object was to show that in the swollen cavernous mucous membrane in the foremost end of the inferior turbinated bones, different nervous states of irritation originate, and these reflex neuroses can be caused experimentally, and they disappear entirely as soon as the places in question are operatively removed. The filling of the cavernous membrane is, according to </span><span style="background-color: white; font-style: italic; text-indent: 13.28px;">Hack, </span><span style="background-color: white; text-indent: 13.28px;">the essential in the pathogenesis of these reflex neuroses."</span></span><br />
<span style="background-color: white; font-family: inherit;"><br /></span>Adams notes that other physicians were so focused on the other theories of asthma, particularly that asthma was neurotic, that they were overlooking the true cause: that there was a problem with the patient's nasal passage causing the asthma, or that there was a toxaemia in the blood causing asthma as I discussed in this post.<br />
<br />
Adams emphasises the following: (1,<a href="http://books.google.com/books?ei=IAM1UaD_KKeBygHP9YHIAQ&dq=asthma+and+its+radical+treatment&jtp=27&id=9ssvAQAAMAAJ#v=snippet&q=septal%20tubercle&f=false"> page 89-90</a>)<br />
<blockquote class="tr_bq">
<span style="background-color: white; color: #274e13;"><span style="font-family: serif;">"I have seen patients with noses absolutely ruined, mere shells of what they should have been—their </span><span class="gstxt_hlt" style="font-family: serif;">asthma </span><span style="font-family: serif;">remaining the same, but promptly clearing up on simple antitoxaemic </span><span class="gstxt_hlt" style="font-family: serif;">treatment, </span><span style="font-family: serif;">except in the case of a poor woman who owed an opium habit to her doctor. Francis cauterises the septal tubercle of all asthmatics—sometimes a valuable temporary procedure; others would also cauterise the lower turbinals—an unnecessary addition. The value of proper nasal </span><span class="gstxt_hlt" style="font-family: serif;">treatment </span><span style="font-family: serif;">cannot be gainsaid; but that it should be subsidiary </span><span class="gstxt_hlt" style="font-family: serif;">and </span><span style="font-family: serif;">ancillary to </span><span class="gstxt_hlt" style="font-family: serif;">treatment </span><span style="font-family: serif;">of the toxaemia I have, where mouth breathing was absent, occasionally </span><span class="gstxt_hlt" style="font-family: serif;">and </span><span style="font-family: serif;">successfully proved by the experi</span><span class="gtxt_body" style="font-family: serif;">ment of carrying out the latter <span class="gstxt_hlt" style="font-family: inherit;">treatment and </span>leaving the nose alone. Apart from the experimental <span class="gstxt_hlt" style="font-family: inherit;">and </span>therapeutical evidence just mentioned, the importance of a nasal factor in <span class="gstxt_hlt" style="font-family: inherit;">asthma </span>can be gauged from several considerations."</span></span></blockquote>
Some of the ailments he observed on asthmatics, were:<br />
<br />
<ul>
<li>Nasal polypi</li>
<li>Deviated Septum</li>
<li>Hypertrophied areas in nasal passages</li>
<li>Pigeon chest (due to laboring for air so frequently)</li>
<li>Mouth breather</li>
<li>Expanded shoulders (due to years of laboring for air)</li>
<li>Expanded chest (due to emphysema if chronic)</li>
</ul>
<div>
References:</div>
<div>
<ol>
<li>Adam, James, "<a href="http://books.google.com/books?ei=IAM1UaD_KKeBygHP9YHIAQ&dq=asthma+and+its+radical+treatment&jtp=27&id=9ssvAQAAMAAJ#v=onepage&q=asthma%20and%20its%20radical%20treatment&f=false">Asthma and it's radical treatment</a>," 1913, </li>
<li><span style="background-color: white;"><span style="font-family: inherit;">Schmiegelow, Ernest, "<a href="http://books.google.com/books?id=Fyx7rKQPzZgC&pg=PA14&lpg=PA14&dq=Voltolini,asthma&source=bl&ots=VmkSZi8Bed&sig=yjIm9UeQ1Lm0zjpRL6a2rokSj8w&hl=en&sa=X&ei=RJ48UaHuFIXayAHn7IDIAQ&ved=0CDkQ6AEwAA#v=onepage&q=Voltolini%2Casthma&f=false">Asthma, considered specially in relation to nasal disease</a>," </span></span></li>
<li></li>
</ol>
</div>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com15tag:blogger.com,1999:blog-4749703810590147676.post-34048546885708720152017-08-02T13:20:00.000-07:002017-08-02T13:20:00.180-07:001913: Adam: A perfect description of an asthma attackConsider the following description of an asthma attack:<br />
<blockquote>
"<span style="color: #006600;">In marked attacks not only is the struggle for breath so severe as to make the patient sit or kneel in bed, but he may even get out of bed and stand gasping at an open window, or clutching at any support that will aid the respiratory muscles of respiration. many will not go to bed at all, but sit in a chair all night, dozing when they can.</span><span style="color: black;">" (1, <a href="https://www.blogger.com/References%20Adam,%20James,%20%22Asthma%20and%20it's%20radical%20treatment,%22%201913,%20London,%20Gasgow:%20Alexander%20Stenhouse">page 9</a>)</span><br />
<span style="color: #006600;"></span></blockquote>
<span style="color: black;">If that doesn't describe one of my typical asthma attack when I was a kid I don't know what does. </span><br />
<span style="color: black;"><br /></span>
<span style="font-size: xx-small;">References</span><br />
<ol>
<li><span style="font-size: xx-small;">Adam, James, "<a href="http://books.google.com/books?id=9ssvAQAAMAAJ&printsec=frontcover&dq=asthma+and+its+radical+treatment&hl=en&sa=X&ei=IAM1UaD_KKeBygHP9YHIAQ&ved=0CDoQ6AEwAA#v=onepage&q=asthma%20and%20its%20radical%20treatment&f=false">Asthma and it's radical treatment</a>," 1913, London, Gasgow: Alexander Stenhouse</span></li>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com13tag:blogger.com,1999:blog-4749703810590147676.post-85990114768749770302017-07-31T13:14:00.000-07:002017-07-31T13:14:00.144-07:001913: Adam: Abnormalities Associated With AsthmaDr. James Adam believed the most common cause of asthma was a toxin or poison in the blood. The other cause of asthma was lesions in the respiratory tract (published 7/10/14). While most physicians focused their attention on spasms in the lungs, he believed they should be focused more on one of these two causes of airway spasms.<br />
<br />
He observed that many asthmatics, although not all, present with one or more of the following abnormalities along their respiratory tract or amid the chest and body:(1, <a href="http://dr.%20james%20adam%20proposed%20%20that%20the%20cause%20of%20most%20cases%20of%20asthma%20was%20a%20toxin%20or%20poison%20in%20the%20blood%20that%20resulted%20from%20some%20form%20of%20error%20in%20diet%20%287/10/14).%20%20The%20other%20cause%20of%20asthma%20was%20some%20form%20of%20lesion%20in%20the%20respiratory%20tract.">page 12</a>, 35-38)<br />
<ol>
<li>Polypi</li>
<li>Septal deviations blocks air passage</li>
<li>Turgid turbinals: blocks air passage</li>
<li>Irritable turbinals (very sensitive to stimulus, causing coughing or sneezing)</li>
<li>Congestion of mucus membrane (anywhere from nose, trachea or bronchi)</li>
<li>Pigeon breast: from a lifetime of asthma the chest becomes deformed, where one sternum, or breastbone, is pushed outward</li>
<li>Emphysema during asthma attacks, becomes chronic if asthma not cured </li>
<li>Barrel chest: rounded, bulging chest that shows little movementn with respiration. It occus during a paroxysm, and becomes chronic if asthma not treated (sign of emphysema)</li>
<li>Rounded, almost stooped shoulders (sign of emphysema)</li>
<li>Unilateral nasal obstruction</li>
<li>Sputum at the end of the attack</li>
<li>Curschmann spirals in the sputum</li>
<li>Eosinophile cells in sputum, with Charcot-Leyden crystals</li>
<li>Heart Rate of 90-110</li>
<li>Blood pressure within normal limits: paroxysm does not raise the blood pressure, but adrenalyn used to treat asthma may</li>
<li>Blood pressure of 80-90 mmHg at end inspiration, and 120-130 at end expiration: decreased BP on inspiration may probably be due to impeded pulmonary circulation</li>
<li>Flatulence during the paroxysm</li>
<li>Asthmatics live long: In this, he agrees with other asthma physicians such as Salter and Berkart. (1, page 38) Adam notes this is true "so long as they don't become drug slaves)</li>
</ol>
<div>
While most other members of the medical community focused most of their attention on the spasmotic and nervous theories of asthma, Adam was focused on the Lesion Theory of Asthma and the Toxaemia theory of asthma, and for that reason his "radical treatment" would better help asthmatics as opposed to the more traditional treatment prescribed by other physicians.</div>
<br />
<span style="font-size: xx-small;">References</span><br />
<ol>
<li><span style="font-size: xx-small;">Adam, James, "<a href="http://books.google.com/books?id=9ssvAQAAMAAJ&printsec=frontcover&dq=asthma+and+its+radical+treatment&hl=en&sa=X&ei=IAM1UaD_KKeBygHP9YHIAQ&ved=0CDoQ6AEwAA#v=onepage&q=asthma%20and%20its%20radical%20treatment&f=false">Asthma and it's radical treatment</a>," 1913, London, Gasgow: Alexander Stenhouse</span></li>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com38tag:blogger.com,1999:blog-4749703810590147676.post-76164212531739483862017-07-28T13:12:00.000-07:002017-07-28T13:12:11.905-07:001913: Two types of chronic asthmaticsJames Adams explains that most cases of asthma are chronic before they are seen by a physician; that these cases are usually treated as bronchitis first (airway inflammation and increased sputum production). Bronchitis "is really the form asthma commonly takes at first." Only as time progresses, does asthma be come chronic. (1, <a href="http://books.google.com/books?ei=eaw9UbYWxO_KAaDegbAJ&id=RLASAAAAYAAJ&dq=james+adam%2C+asthma&jtp=31">page 31</a>, 33)<br />
<div>
<br /></div>
<div>
He describes two types of chronic asthma: (1, page 30)<br />
<div>
<ol>
<li>Fat: Less common; overeating can lead to asthma; chronic bronchitis</li>
<li>Lean: More common; usually as the disease becomes more chronic, a toxaemia in the blood will cause the asthmatic to become thin, with expanded shoulders and chest due to chronic laboring and emphysema. </li>
</ol>
<div>
Adam writes that the most common sign of chronic asthma is "dusky, sallow skin with chloasms round the eyes, sure token of toxaemia. There is no mistaking this asthmatic chachexia (fatigue, weakness, as in wasting away) and the first sign of improvement resulting from correct treatment is the clearing of the skin; it looks as though it has been washed from the inside -- as it has been... it takes prolonged, repeated and severe paroxysms to develop the other (signs of chronic asthma). (1, page 31)</div>
<div>
<br />
What causes the signs of chronic asthma, Adam notes, is the hyperaemia that is constantly ongoing and not treated (and it's usually not treated because most physicians don't respect the toxaemia theory of asthma.). Toxaemia that is constant acts on the "skin and bronchial mucous membrane as well as on the tissues generally, producing the cachexia and bronchitis, the stress of the dyspnea, which is the main factor in producing the other thoracic changes, is intermittent.<br />
<br />
Other signs of chronic asthma would be your distended chest and shoulders, pigeon chest, etc. These are signs that the person has a toxaemia, and that the person has been working hard to suck in air. (You can see more signs of the toxaemic effect on asthma in this post (1913: Lesions in respiratory tract cause asthma on 7/22/17)<br />
<br />
Bronchitis is generally caused by a metabolic disorder, and therefore, the treatment generally revolves around decreasing carbohydrates (sugary foods), such as "sweets cakes." (1, page 33, 35)(also see chapter on atypical asthma)<br />
<br />
References:</div>
<div>
<ol>
<li>Adam, James, "Asthma and its radical treatment," </li>
<li></li>
</ol>
</div>
<div>
</div>
</div>
</div>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com31tag:blogger.com,1999:blog-4749703810590147676.post-42919566742441475752017-07-26T13:04:00.000-07:002017-07-27T01:52:33.614-07:001913: Adam Toxaemic Theory of AsthmaBy the turn of the 20th century, the medical profession had readily accepted both the nervous theory of asthma and that spasmodic theory of asthma. The allergic theory of asthma was in its infancy, and the old toxaemic theory of asthma was no longer written about in new editions of asthma books.<br />
<br />
Yet it was the old theory, the toxaemic theory of asthma, that Dr. James Adam proposed as the most valid explanation of asthma. He understood that is was no longer accepted by the medical community, and he understood treatment based on this old theory was considered radical. This, therefore, was the reason he referred to his asthma book as "<a href="http://books.google.com/books?id=9ssvAQAAMAAJ&printsec=frontcover&dq=asthma,+berkart&hl=en&sa=X&ei=RZg0UY_KCsStygH57oGoAg&ved=0CGMQ6AEwCA#v=onepage&q=asthma%2C%20berkart&f=false">Asthma and its Radical Treatment</a>." (1, <a href="http://books.google.com/books?ei=RZg0UY_KCsStygH57oGoAg&dq=asthma,+berkart&jtp=4&id=9ssvAQAAMAAJ#v=onepage&q=asthma%2C%20berkart&f=false">pages 1-3</a>)<br />
<br />
Dr. Adam said he continued to have much respect for Dr. Henry Hyde Salter who, during a series of articles published in the 1950s, articulated support for the nervous and spasmodic theories of asthma. Yet Dr. Salter also articulated support for the toxaemic theory of asthma. Of Dr. Salter, Adams wrote:<br />
<blockquote class="tr_bq">
<span style="color: black;"><span style="color: black;">Hyde Salter’s book, written before most of us were born, must not be overlooked by anyone interested in the subject; he had probably a wider experience of <span class="gstxt_hlt">asthma, </span>and a better grip of the value of the dietetic treatment, than many twentieth-century authorities."</span> </span></blockquote>
<span style="color: black;"></span>Dr. Salter, from our own studies, was an ardent supporter of the idea that there was a direct correlation between what one puts into his body and asthma. He wrote that many of his patients, including himself, observed that upon eating too much or eating the wrong foods, often lead to a paroxysm of asthma. The prevention of asthma, therefore, was to eat healthily and eat light. The remedy was emetics and enemas.<br />
<br />
Salter believed the certain foods, or too much food, lead to some form of poison in the blood that leads to the nervous system causing bronchospasm. Dr. Adam simply refined this theory as follows: (1, <a href="http://books.google.com/books?ei=RZg0UY_KCsStygH57oGoAg&dq=asthma,+berkart&jtp=4&id=9ssvAQAAMAAJ#v=onepage&q=asthma%2C%20berkart&f=false">page 3</a>)<br />
<strong>Toxaemic theory of asthma</strong>: Asthma is a disease of the nervous system, and "all neurosis are toxaemias." A poison enters the body and this "hits the nerves of the respiratory tract."<br />
<br />
Adam suggests that asthma is caused in this way:<br />
<blockquote class="tr_bq">
<span style="background-color: white;"><span style="background-color: white; color: #274e13;">This toxaemia arises partly in the bowel, partly in the tissues; it arises partly by absorption of nitrogenous poisons resulting from intestinal puttefaction under microbic action ; but mainly is due to an error in nitrogenous metabolism, the result of imperfect oxidation or enzyme action. In short, the poison arises from Proteid food or proteid tissue.</span></span></blockquote>
<blockquote class="tr_bq">
<span style="background-color: white;"><span style="color: #274e13;">The error in proteid metabolism is closely connected with excess of carbohydrate in the diet.</span></span></blockquote>
<blockquote class="tr_bq">
<span style="background-color: white;"><span style="color: #274e13; font-size: small;">The oxidation of the excess of the simpler carbohydrate molecule seems to interfere with proper oxidation of the more complex proteid molecule. In other words, the excess of energy food interferes with the metabolism of the tissues and tissue-foods; the imperfectly metabolised products so resulting set up asthma.</span></span></blockquote>
<span style="background-color: white;">In other words, as Salter explained, the poison, or toxaemia, was the cause of some error in diet. The result, according to Adams, was as followed</span><br />
<blockquote class="tr_bq">
<span style="background-color: white;"><span style="color: #274e13;">The toxaemia, whether arising in bowel or tissues or both, tends to show itself first as catarrh, later as spasm, in the respiratory tract. This toxaemia shows itself in conditions, catarrhal and spasmodic, other than, but closely related to, <span class="gstxt_hlt">asthma.</span></span></span></blockquote>
<span style="background-color: white;">He believed there were certain prodomata (early signs) of asthma that are often overlooked, and while these signs may not be present in all cases of asthma, if one is observed it can be a sign of an impending attack, such as:</span><br />
<ul style="color: black;"><span style="background-color: white;">
<li>Polyuria (excessive urine production)</li>
<li>Oliguria (diminished urine production)</li>
<li>Anuria (no urine production)</li>
<li>Constipation (unable to have a bowel movement)</li>
<li>Formication (sensation you have insects crawling under your skin)</li>
<li>Pruritus (sensation that results in urge to scratch; itchy sensation)</li>
<li>Urticaria (hives)</li>
<li>Erythema (redness of skin)</li>
<li>Cyanosis (Blueness of skin, representative of ischemia of tissues of hand, foot, lips, etc.)</li>
<li>Petechiae (red or purple spots on the skin caused by minor hemorrhage; local bleeding due to broken capillary vessels)</li>
<li>Embarrassed breathing (asthma)</li>
</span></ul>
<span style="background-color: white;">The above will continue until something happens involving the elimination of something, which generally involves:</span><br />
<ul style="color: black;"><span style="background-color: white;">
<li>Vomiting (spitting up stomach contents)</li>
<li>Diarrhea (loose stools)</li>
<li>Polyuria (excessive urination)</li>
<li>Expectoration (sputum production)</li>
</span></ul>
<span style="background-color: white;">Due to the toxaemic effect, the following are also associated with asthma (all are associated with increases of eosinophilia in sputum): (1, page 34-35)</span><span style="background-color: white;"></span><br />
<span style="background-color: white;"></span><br />
<div>
<ul><span style="background-color: white;">
<li>Eczema: Commonest and most likely to occur in children with bronchitis. It usually shows up before asthma and disappears. Although will continue to "dog" the patient if the asthma is not "cleared up." Cause is same as asthma, and treatment therefore same too (see treatment for both asthma and eczema is generally to restrict carbohydrates)</li>
<li>Ichthyosis: Probably caused by metabolic disorder</li>
<li>Psoriasis: Adams notes it's "said to be associated with asthma, but I have never seen the combination." Restricting carbohydrates generally doesn't work, but restricting "nitrogenous intake does." The difference in treatment may prove the non-association of psoriasis with asthma.</li>
<li>Dermatitis Herpetiformis: Also associated with asthma. </li>
</span></ul>
</div>
<span style="background-color: white;">One of the reasons that he published his book was because he believed that "far too much attention has been paid (by the general practitioner) to the most striking feature of asthma, the asthmatic spasm; too little to the conditions that precede and cause the spasm, and those by which Nature cures it." Of course, the toxaemic theory of asthma provides the answer to why the spasm occurs, and thus its radical treatments would prevent and treat asthma.<br /><br />Adams also noted that his theory came at a time when other theories were more readily accepted by the medical profession. However, his idea are "put forward with the hope that it will be useful not only in the treatment of <span class="gstxt_hlt" style="color: black;">asthma </span>but also in those other diseased states whose kinship with <span class="gstxt_hlt" style="color: black;">asthma </span>is too."</span><br />
<div>
<span style="font-size: xx-small;"><br /></span></div>
<div>
<span style="font-size: xx-small;">References</span><br />
<ol>
<li><span style="font-size: xx-small;">Adam, James, "<a href="http://books.google.com/books?id=9ssvAQAAMAAJ&printsec=frontcover&dq=asthma+and+its+radical+treatment&hl=en&sa=X&ei=IAM1UaD_KKeBygHP9YHIAQ&ved=0CDoQ6AEwAA#v=onepage&q=asthma%20and%20its%20radical%20treatment&f=false">Asthma and it's radical treatment</a>," 1913, London, Glasgow: Alexander Stenhouse</span></li>
</ol>
</div>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com28tag:blogger.com,1999:blog-4749703810590147676.post-72919312150252771582017-07-24T12:58:00.000-07:002017-07-24T12:58:02.259-07:001851-1913: The history of asthma sputum<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcS_HV9QGXNhm-uDf61LSVN29pi-LmoxblEnex7iv7UZFc_7kdgaERYMVvgMkNNNZuFehHoK0nJfOyz8G8QN1sPS_PR5ChqmksUDSxGnG7jEtn7v0MCMlEfSFz4h3G6HQhGPrpDqjpNjk/s1600/220px-Ernst_Viktor_von_Leyden.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcS_HV9QGXNhm-uDf61LSVN29pi-LmoxblEnex7iv7UZFc_7kdgaERYMVvgMkNNNZuFehHoK0nJfOyz8G8QN1sPS_PR5ChqmksUDSxGnG7jEtn7v0MCMlEfSFz4h3G6HQhGPrpDqjpNjk/s1600/220px-Ernst_Viktor_von_Leyden.jpg" width="309" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Ernst Victor von Leyden (1832-1910 discovered<br />
crystals in asthmatic sputum, and suspected these<br />
to be the cause of asthma. During his era, he was<br />
the closest supporter of Dr. Robert Bree's<br />
bronchitic theory of asthma. (9, pages 14-15)<br />
He believed these crystals somehow irritated the<br />
"vagus in the mucus membrane of the bronchials,<br />
and hereby caused by reflex action a spasm<br />
of the muscles of the small bronchial tubes."<br />
(10, page 8)</td></tr>
</tbody></table>
Most people find sputum disgusting, and so will have nothing to do with it. But as far back as 400 B.C. the medical significance of it was observed by ancient Greek physicians, and probably even earlier than that. <br />
<br />
If you mention it at the dinner table your mother might smack your hand. But for the sake of gaining a complete grasp on the history of asthma and respiratory disease, we must delve into the topic of sputum. Sorry, but we must.<br />
<br />
It must have been observed at an early date in history that people with breathing issues produce sputum, sometimes consisting of a putrid smell, often consisting of many varied colors such as red, yellow, brown and white. <br />
<br />
Yet rather than being petrified by the grossness of the substance, Greek philosophers became fascinated by it. They even gave it its own classification as one of the four humors that, along with determining ones personality, also determined whether was healthy or sick. <br />
<br />
Prior to the philosophical medicine of the ancient Greeks, other ancient societies, and the primitive clans and families that roamed the lands before them, believed sputum was the production of some evil spirit, demon or god. When a person expectorated the substance, they were in essence expectorating an evil substance that caused the symptoms they were suffering from.<br />
<br />
From the ancient world to the scientific revolution there were few changes in the way physicians viewed diseases and treated their patients. In 1799 Dr. Robert Bree speculated that sputum contained a poison that it was trying to get out of the body, and asthma was the result. This theory wasn't much different than any idea Hippocrates might have postulated. <br />
<br />
Since the sputum preceded the asthmatic fit, Bree essentially speculated that asthma was essentially bronchitis, and thus created the bronchitic theory of asthma. Others, without much more evidence, speculated sputum was the effect of asthma rather than the cause.<br />
<br />
Such speculation gradually tapered off, but never really came to an end, during the scientific revolution, and mainly due to the inventions of the microscope, which allowed physicians to see that the human body was made up of substances too small to be seen by the unassisted eye, and the stethoscope, which allowed physicians to hear changes that occurred inside the chest and to diagnose diseases with accuracy prior to autopsy. <br />
<br />
The microscope allowed physicians to learn that air passages were surrounded by smooth muscle, and that it was capable of spasming when stimulated. The stethoscope allowed them to hear when sputum accumulated in the chest, and learn that it was the effect and not the cause of asthma. <br />
<br />
So, pretty much, prior to the 1850s asthma was basically considered to be a disease of excess sputum, mainly because this was all physicians could observe with the unaided eye and ear. <br />
<br />
Yet by the 1850s it was looking pretty clear that asthma was also a disease associated with spasms of the air passages, particularly by the wheezes heard by air flowing through narrowed air passages, and rhonchi heard as air flowed through sputum lined air passages. (1, pages 592-595)<br />
<br />
In 1851, Dr. Beau, along with his assistant Cozart, observed that fits of asthma usually ended with a wad of sputum being coughed up. Beau used this observation as evidence to support his theory that asthma was a disease of chronic catarrh, and that asthma was caused by increased sputum in the air passages. (3, page 31)<br />
<br />
When this sputum dried out mucus plugs formed that were capable of blocking the air passages, thus resulting in dyspnea and other symptoms of asthma, including the "sonorous and sibilant rhonchi -- their 'rales vibrants' heard upon auscultation with a stethoscope." (3, page 31)<br />
<br />
The fit, therefore, was resolved when mucus plugs were broken up with a fit of coughing. (3, page 31)<br />
<br />
Then, in 1878, at a time when most physicians had accepted the nervous and spasmotic theories, J.B. Berkart used Beau's research as evidence of the bronchitic theory of asthma. <br />
<br />
Berkart said:<br />
<blockquote class="tr_bq">
With the displacement of the mucous plug into the larger bronchus, or on its expulsion by means of a fit of coughing, the dyspnea ceases, and with it also the rales disappear. This form of bronchitis is, in their (Beau and Crozant's) opinion, due partly to an idiosyncrasy of the patient, partly to exciting causes, which greatly vary in different individuals."</blockquote>
Tiny crystals were first observed in sputum in 1851 by Jean Martin Charcot, but it wasn't until 1872 that these crystals were linked to asthma by Ernst Victor von Leyden. So history has given credit for this discovery to both men by calling the crystals Charcot-Leyden crystals.<br />
<br />
Leyden, whose asthma theories were similar to Dr Bree's bronchitic theory, believed Charcot-Leyden crystals caused asthma by irritating...<br />
<blockquote class="tr_bq">
...the peripheral extremities of the vagus nerve, and produce reflex spasm of the bronchial muscle." </blockquote>
The asthma attack, as Bree and Beau observed, ended when a wad of sputum was coughed up during a fit of coughing. (4, <a href="http://books.google.com/books?ei=3GMeUfXjI-qPyAHx6YHYAw&dq=John+Charles+Thorowgood&jtp=10&id=2QpBrMuh1NAC">page 14-15</a><br />
<br />
However, it was the discovery of these Charcot-Leyden crystals that would ultimately put an end to the bronchitic theory of asthma. This was noted by Dr. John Charles Thorowgood in 1878. He said that these crystals were found in sputum obtained from patients with "ordinary catarrh and croupus bronchitis." (4, <a href="http://books.google.com/books?id=2QpBrMuh1NAC&printsec=frontcover&dq=John+Charles+Thorowgood&hl=en&sa=X&ei=3GMeUfXjI-qPyAHx6YHYAw&ved=0CDwQ6AEwAg">page 15</a>)<br />
<br />
Thorowgood said: <br />
<blockquote class="tr_bq">
The asthmatic patient while in a fit presents abundance of symptoms distressing enough to endure or to witness; and yet, when things seem to be at their worse, and the patient well-nigh at his last gasp, a remission comes on, the spasm yields, air enters the lungs, and the attack subsides,<i> </i>coincidentally often with access of cough and mucous expectoration." (4, page 16)(9, page 1,2)</blockquote>
In 1879, bacteriologist Paul Erlich discovered the eosinophil, and it was soon discovered that elevated levels of eosinophils (eosinophilia) was commonly found in asthmatics. (5)<br />
<br />
In 1882 Heinrich Curshmann observed other spirals in asthma sputum and believed they were associated with causing asthma. He believed since Leyden's crystals didn't cause asthma, perhaps <i>his </i>crystals did. (5)<br />
<br />
Later Curshmann's crystals were determined to be fragments of mucus plugs associated with asthma, and Leyden crystals were determined to be fragments of eosinophils. Eosinophils were later learned to be a type of white blood cell that, along with mast cells, are involved in the allergic reaction.<br />
<br />
In 1911 Hermann Sahli described eosinophils in asthmatic sputum. Yet Sahli noted another author from 1891 who described eosinophils in asthmatic blood, and he concluded that these must be pathological with asthma. Yet he also noted that neither the cause of the eosinophils nor their origin was known. (7)<br />
<br />
Sahli could isolate the area where the sputum came from based on epithelial cells in it, yet he did not understand the mechanisms of its production as we do today. (7)<br />
<br />
Dr. James Adams describes asthma sputum in 1913: (8)<br />
<blockquote>
"Asthmatic sputum varies. Often there is none till the end of the attack; then it is in the typical form of small, tough pellets expelled by laborious coughing. The attack may then cease, or it may go on till a more free and profuse expectoration occurs."</blockquote>
He also wrote: (8)<br />
<blockquote>
"The sputum does not readily decompose, and is said to be wonderfully free from microbes; but this is not always so, as I have occasionally found it teeming with them."</blockquote>
The true purpose of sputum is to ball up microbes inside the lungs and haul them out, and in this way the lungs stay <i>sterile</i>. Surely asthma can be caused by inhaling a microbe, such as a bacteria, but it's also caused by asthma triggers (dust mites, smoke, fumes, chemicals, pollution, animal dander) that are innocuous to most people, and non infecting agents.<br />
<br />
So this might explain why Adams most often found asthmatic sputum without an infecting agent, and sometimes "teeming with them."<br />
<br />
Backing up a moment to 1906, Australian pediatrician Clemons van Pirquet coined the term allergy when he observed that some of his patients were hypersensitive to substances that did not bother other people (what we now refer to as allergens, or asthma triggers). This was the first time asthma was linked with allergies. <br />
<br />
By 1910 Histamine was discovered and found to be a major component in the allergic response. So some went on to speculate that finding a way to block histamine would cure both allergies and asthma.<br />
<br />
By 1946 antihystamines hit the market, and within a decade they were among the most commonly prescribed medicines. <br />
<br />
Yet as time went by, it was learned that there was more to asthma and allergies than just histamine. It was learned that asthmatic and allergic immune systems respond irrationally to allergens and asthma triggers by increasing production o<span style="background-color: white;">f eosinophils and </span>this spearheads inflammation of the bronchial muscles.<br />
<br />
Another weapon of the immune system is mast cells that line the respiratory tract and eyes, and these were discovered in 1953. .<br />
<br />
In 1967 Immunoglobulin E antibodies (IgE) were discovered. It was later learned IgE has a significant role in the asthmatic and the allergic response. The first time asthmatics are exposed to asthma triggers (allergens), say dust mites, their immune systems develop dust mite IgE antibodies that attach to mast cells that line the epithelial layer of the skin or respiratory tract.<br />
<br />
The second time that person is exposed to that allergen (dust mites in this case), a mast cell that has a dust mite IgE antibody attached to it explodes and releases its contents: the mediators of inflammation. A mediator of inflammation called histamine was discovered in 1910, and others called cytokines and leukotrienes were discovered in the 1970s.<br />
<br />
These mediators, when released into the blood stream, cause inflammation of the respiratory tract, thus causing the allergic and asthmatic responses. <br />
<br />
In the allergic person, they can also cause inflammation of the upper respiratory tract, which includes the back of the throat and nose. The offending substance (dust in our case) is recognized by the immune system, trapped in the mucus layer, absorbed by the mucus, balled up by the mucus, and sent on it's way up the respiratory track to be coughed up.<br />
<br />
So this would explain what Dr. Bree, Beau, and Berkart observed. While hacking up a wad of sputum may have been related to the fit of asthma, it was not the cause, and had nothing to do with the cure. <br />
<br />
Later it was learned that asthmatic lungs tended to produce an abnormal number of goblet cells, this results in an abnormal increase in mucus production during an asthma attack. While some of this sputum may be coughed up, some becomes trapped in obstructed air passages, dries out to form mucus plugs, and this further blocks the air passages, thus compounding the asthma response.<br />
<br />
When the fit ends, when the air passages relax and dilate, which may be a result of time or medications, the asthmatic will probably expectorate this sputum, which will usually be, if no bacteria or virus is balled up within it, white and sterile. It will also have IgE and eosinophils in it, hence your Charcot-Leyden and Curshmann crystals. <br />
<br />
So it's easy to understand how this production of sputum at the end of an attack could easily be misinterpreted as the cause, rather than the effect, of asthma.<br />
<br />
<span style="font-family: inherit; font-size: xx-small;">References:</span><br />
<ol>
<li><span style="font-family: inherit; font-size: xx-small;">Lotval, J., "<a href="http://www.ersj.org.uk/content/7/3/592.full.pdf">Contractility of Lungs and air tubes: experiments performed in 1840 by Charles J.B. Williams</a>, <i>European Respiratory Journal,</i> 1994, (7) pages 592-595</span></li>
<li><span style="font-family: inherit; font-size: xx-small;"><span style="background-color: white;">Bree, Robert, "</span><a href="http://books.google.com/books?id=ppZx4kFod34C&printsec=frontcover&dq=A+Practical+Inquiry+into+Disordered+Respiration+Distinguishing+the+Species+of+Convulsive+Asthma,+their+Causes+and+Indication+for+a+Cure&hl=en&sa=X&ei=7t-nT8_FKsTpggevqPHQAQ&ved=0CDUQ6AEwAA#v=onepage&q=A%20Practical%20Inquiry%20into%20Disordered%20Respiration%20Distinguishing%20the%20Species%20of%20Convulsive%20Asthma%2C%20their%20Causes%20and%20Indication%20for%20a%20Cure&f=false" style="background-color: white; color: #818181; line-height: 18px; text-decoration: initial;">A Practical Inquiry into Disordered Respiration Distinguishing the Species of Convulsive Asthma, their Causes and Indication for a Cure</a><span style="background-color: white;">," 4th ed, 1810, London, page pages 117-118</span></span></li>
<li><span style="font-family: inherit; font-size: xx-small;">Berkart, J.B., "On Asthma: Its Pathology and Treatment," 1878</span></li>
<li><span style="font-family: inherit; font-size: xx-small;">Thorowgood, John C., "<a href="http://books.google.com/books?id=2QpBrMuh1NAC&printsec=frontcover&dq=John+Charles+Thorowgood&hl=en&sa=X&ei=3GMeUfXjI-qPyAHx6YHYAw&ved=0CDwQ6AEwAg">Asthma and Chronic Bronchitis: A New Edition of Notes on Asthma and Bronchial Asthma</a>," 1894, London, Bailliere, Tyndall, & Cox</span></li>
<li><span style="font-family: inherit; font-size: xx-small;">Lipkowitz, Myron, Tova Navarra, "<a href="http://books.google.com/books?id=2jhkozIXfgQC&pg=PA105&sig=6y0yKKC_AoZGYLVs8S4KV5Y0ph8&hl=en#v=onepage&q&f=false">Encyclopedia of Allergies</a>," 2001</span></li>
<li><span style="font-family: inherit; font-size: xx-small;">Brenner, Barry E, "Emergency Medicine, 1998, page 10</span></li>
<li><span style="font-family: inherit; font-size: xx-small;">Sahli, Hermann, "<a href="http://books.google.com/books?id=biUSAAAAYAAJ&pg=PA701&lpg=PA701&dq=sahli,+asthma&source=bl&ots=K8_CxA8DFK&sig=_As7iryS04W1lOM_7IzMEqbyk0w&hl=en&ei=YgurTdX9N8fb0QHiwu34CA&sa=X&oi=book_result&ct=result&resnum=1&ved=0CBgQ6AEwAA#v=onepage&q=sahli%2C%20asthma&f=false">A treatise on diagnostic methods of examination</a>," 1911</span></li>
<li><span style="font-family: inherit; font-size: xx-small;">Adams, James, <a href="http://books.google.com/books?id=RLASAAAAYAAJ&printsec=frontcover&dq=asthma+and+its+radical+treatment&hl=en&ei=wPqqTfrSEefY0QHT8IWGBw&sa=X&oi=book_result&ct=result&resnum=1&ved=0CEEQ6AEwAA#v=onepage&q&f=false">Asthma and it's Radical Treatment</a>, 1913</span></li>
<li><span style="font-family: inherit; font-size: xx-small;">Thorowgood, John C., "Notes on Asthma," 1878, 3rd edition, London, J & A Churchill</span></li>
<li><span style="font-size: xx-small;">Shmiegelow, Ernst, "</span><a href="http://books.google.com/books?id=Fyx7rKQPzZgC&pg=PA4&lpg=PA4&dq=varnier,+asthma&source=bl&ots=VmkRWj2Idh&sig=94YGuyRQrOhzAC1z6D8K9R22SRw&hl=en&sa=X&ei=etooUYzEKIL-qwGHm4C4AQ&ved=0CGQQ6AEwBQ#v=onepage&q=varnier%2C%20asthma&f=false"><span style="font-size: xx-small;">Asthma, considered specially in relation to nasal disease</span></a><span style="font-size: xx-small;">," 1890, London, H.K. Lewis</span></li>
</ol>
<ol>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com41tag:blogger.com,1999:blog-4749703810590147676.post-84347176114392951412017-07-21T12:24:00.000-07:002017-07-21T21:27:20.744-07:001913: Speculation about asthma continues<div>
My mom once said that house wives today probably know more than physicians in the 19th century. As I study the history of medicine and lung diseases, I have learned this is somewhat true to a certain extent, mainly because housewives like my mom had access to greater wisdom.</div>
<div>
<br /></div>
<div>
However, there are still an amalgamate of wive's tales, excuse the pun, that wives still use to treat their children when they are sick. One of these was to place their asthmatic child in a hot and steamy bathroom. We now know this may work to make breathing easier if the diagnosis was croup, but not asthma. In fact, steam may make asthma worse because it makes the air thicker. </div>
<div>
<br /></div>
<div>
Yet as the old saying goes: we do the best given the knowledge we know today, and as we learn better we do better. So by this saying, we cannot fault our parents for trying. And as we have sick kids, we must do better.<br />
<br />
So this brings me to the topic that caught my interest today, and that is that as I read case histories the various physicians wrote in old asthma books, I realize how much more knowledge I have as an asthmatic, asthma dad, respiratory therapist, and amateur historian. </div>
<div>
<br /></div>
<div>
One of the neat things about reading an asthma history is I read a lot of case histories written by the various physicians knowing I know more than that doctor. A good example is here noted by Dr. James Adam in his 1913 book "Asthma and its radical treatment." (1, <a href="http://books.google.com/books?pg=PA36&dq=james+adam,+asthma&id=RLASAAAAYAAJ">page 33-34</a>)</div>
<blockquote class="tr_bq">
'' A boy of 26 months was sent to me by Dr Alex. Morton. He had cured him of bad generalised eczema; but asthma occurred almost every night in spite of the fact that the dietetic regimen laid down by Dr Morton was what I myself would have set for the asthma. This boy was the subject of hay fever and ichthyosis; his urine showed persistent deposit of uric acid and increased indigogens. His maternal aunt had eczema in childhood, and now has asthma; his paternal aunt has eczema and asthma; there is a history of gout and uric acid on the mother's side. Treatment freed him fromasthma for a year. He then went to stay with his grandmother who coddled him, gave him the forbidden thing, sweets and cakes, and soon brought back both eczema and asthma. Not only so, but interesting etiologically is the fact that adenoids and chronic rhinitis have developed, for which treatment has been declined; but although this injures the prognosis, the asthma has never been so bad as at first. A boy, whose father was long asthmatic but has remained well for many years, was much troubled during the first two years of life with eczema, the result largely of overfeeding. He is now five, and during the last two years he has developed 'bronchitis,' which is now taking the more typical asthmatic form."</blockquote>
<div class="gtxt_body" style="text-align: -webkit-center;">
<div class="gtxt_body" style="margin-bottom: 0.5em; text-align: left;">
<div style="font-family: inherit;">
Adams further notes that: "The association, bad feeding, eczema, bronchitis, asthma, is too frequent and too plain for anyone to doubt that a metabolic error, or at least a toxic condition, is in play."<br /><br />Given modern wisdom, I know that there was a major flaw in the analysis of Adam, and that was his decision to treat asthma and all the other maladies associated with it as a toxaemia. Surely it's a bad idea for a child to eat too many cakes, yet what might more likely cause the hay fever, asthma and eczema are allergies. The child was probably exposed to allergens near birth and at his paternal aunts. The remedy would be to not let the child go to his paternal au<span style="background-color: white; font-family: inherit;">nts. </span></div>
<div style="font-family: inherit;">
<span style="background-color: white; font-family: inherit;"><br /></span><span style="font-family: inherit;">The fact the parents were courageous enough, and perhaps wise enough, to decline treatment for </span>adenoids and rhonitis, which may have involved surgical treatment, was impressive.Adam said himself that other asthma experts were so intent on focusing on the nervous theory of asthma and the spasmodic theory of asthma that they didn't see the true cause: toxaemia in the blood. He called his theory the toxaemic theory of asthma. <br /><br />To his credit he did acknowledge his ideas would be seen as radical, of which they were. Plus, in a time when the trend was to generate theories about asthma based on science, Adam took the route of speculation. <br /><br />As my asthma history continues, I will delve in later posts more into the theories and treatments of Adams that he describes himself as radical. They would not be radical if they were proposed 100 years earlier, but, given the era he was born in, yes he was quite radical.</div>
<div style="font-family: inherit;">
<br /></div>
<div style="font-family: inherit;">
References:</div>
<ol style="font-family: serif;">
<li><span style="font-size: xx-small;">Adam, James, "</span><a href="http://books.google.com/books?id=9ssvAQAAMAAJ&printsec=frontcover&dq=asthma+and+its+radical+treatment&hl=en&sa=X&ei=IAM1UaD_KKeBygHP9YHIAQ&ved=0CDoQ6AEwAA#v=onepage&q=asthma%20and%20its%20radical%20treatment&f=false" style="font-size: x-small;">Asthma and it's radical treatment</a><span style="font-size: xx-small;">," 1913, London, Gasgow: Alexander Stenhouse</span></li>
</ol>
</div>
</div>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com35tag:blogger.com,1999:blog-4749703810590147676.post-63652658336302988892017-07-19T11:48:00.000-07:002017-07-19T11:48:10.288-07:001910-1950: Antihistamines to treat allergiesWhile some scientists and physicians studied the effects of decensitization for the treatment of hay fever (er, allergy) sufferers, others were working on other angles. This was a good thing, because one of the best selling medicines of all time was the result. <br />
<br />
In 1910 British scientists discovered a chemical called histamine that was released during an allergic reaction, and they determined it was this substance that was responsible for causing tissues to become inflamed. A year later Henry Dale proved that injecting histamine into guinea pigs and dogs would instigate the allergic response.<br />
<br />
This discovery gave scientists a lot of hope. Originally they beleived histamine was the only cause of allergies and that finding a treatment for histamine would mean allergies would be eliminated. Yet later scientists learned this was not true, that allergies were a series of complex reactions.<br />
<br />
In 2007 Gregg A. Minton explains how "in 1921 Carl Pransnitz attempted to further understand allergies by injecting into his abdomen the serum from his colleague Heinz Kustner, who had a severe allergy to fish. Prausnitz had no such allergy, but when he sat down to a fish dinner, he found that a case of the hives appeared on his body at the injection site. The experiment demonstrated that a specific immune body -- later known as an antibody -- was present in the serum of allergic patients. The substance could be passively transferred to nonallergic individuals, and it played a crucial role in the allergic reaction." (1, page 215)<br />
<br />
This experiment lead researchers to think that if they could figure out what this "antibody" was they could unlock the mystery of allergies and eliminate this annoying malady from existence. (1, page 215) So the hunt was on. <br />
<br />
<div>
In the meantime, Daniel Bovet introduced a medicine that blocked the effects of histamine in 1937, and he called this new medicine an antihistamine. It was the first truly effective medicine to treat the symptoms of allergies. By blocking the effects of histamine it therefore prevented an allergen from causing a stuffy and runny nose, itchy eyes, nose and throat, and sneezing.</div>
<div>
</div>
<div>
The next discovery was Benadryl. Minton explains it was discovered by 21 year old professor at Cincinnati University named George Rieveschi. He was trying to create an antispasmotic drug when he inadvertently discovered the "new compound in his laboratory." (1, page 216)</div>
<br />
In 1946 the first two antihistamines hit the market: Benadryl and Pryibenzamine. Minton describes how "antihistamines became, next to antibiotics and barbituates, the third most commonly prescribed class of drugs in America." (1, page 213)<br />
<br />
Minton explains that other antihistamines hit the market in 1947, but Benadryl and Prybenzamine made up the bulk of the sales. In 1947 Hydrillin hit the market, which was a product that had both an antihistamine and a bronchodilator called <span class="Apple-style-span" style="color: red;">theophylline</span>. This relieved allergy symptoms and made breathing easier, an ideal remedy for people suffering from allergic asthma (which, as it turns out, includes about 75 percent of all asthmatics)<br />
<br />
Theophylline is a medicine that was first introduced to the world in 1930 as another antispasmotic medicine for asthma. It was a medicine that relaxed the smooth muscles that lined the air passages of the lungs and made breathing easier. This new medicine provided another over the counter option for allergy and asthma sufferers. (<a href="http://hardluckasthma.blogspot.com/2012/03/theophylline-no-longer-top-line-asthma.html">I wrote about theophylline here</a>.)<br />
<br />
In 1949 Neohetramine was the first antihistamine approved by the Food and Drug Administration (FDA) as an over the counter medicine. Other antihistamines soon followed. Minton notes that "by 1950, more than 21 antihistamine compounds packaged under one hundred different trade names in tablets, nasal sprays, eye drops, and creams on the market in the United States." (1, page 216-217)<br />
<br />
References:<br />
<br />
<ol>
<li><span style="background-color: white;"><span style="font-size: xx-small;">Mittman, Gregg, "Breathing Space," 2007, New Haven and London, Yale University Press</span></span></li>
</ol>
John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com44tag:blogger.com,1999:blog-4749703810590147676.post-89902655482607481732017-07-17T11:45:00.000-07:002017-07-23T02:08:12.981-07:001909: Pituitrin tried for asthma and hay fever<div class="hw" style="background-color: white;">
<div style="font-family: Arial; font-size: 16px; font-weight: bold;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="background-color: white; float: right; font-family: arial; font-size: 16px; font-weight: bold; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjBRHwx_AWW6DaUEBcpTPBfymsEUUTY0fJhFcIUhS8oyzRCF1k6os0Sbv68PLxqd6Oa1zf4i7SZG92pRUZXGee5Yq23oA9u2_HdUBLL35ekw_XfERA_oeCz40cWefyX_Mr3-KRRu0rSQbk/s1600/pituitrin.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="223" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjBRHwx_AWW6DaUEBcpTPBfymsEUUTY0fJhFcIUhS8oyzRCF1k6os0Sbv68PLxqd6Oa1zf4i7SZG92pRUZXGee5Yq23oA9u2_HdUBLL35ekw_XfERA_oeCz40cWefyX_Mr3-KRRu0rSQbk/s400/pituitrin.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Pituitrini was an extract of the bovine pituitary gland. Along with other uses,<br />
it was trialed for asthma by various physicians, and with success, around<br />
1909 and 1910. The medicine was provided by Park-Davis & Co. out<br />
of Detroit, Michigan in one-ounce glass stopper bottles and glaseptic<br />
ampoules (ready for immediate hypodermic injection) as seen here. (2)</td></tr>
</tbody></table>
Another medicine that was trialed for asthmatics around the 1910s was a medicine called Pituitrin. It was an extract of bovine pituitary gland containing oxytocin and vasopressin, and being a relatively new medicine it garnered much attention among the medical community. As with other new medicines, it was trialed for various purposes, including asthma.<span style="font-family: "times new roman"; font-size: small; font-weight: normal;"><span style="font-family: arial;"><span style="background-color: white;"> </span></span></span></div>
<div style="background-color: white; font-family: arial; font-size: 16px; font-weight: bold;">
<span style="font-family: "times new roman"; font-size: small; font-weight: normal;"><br /></span></div>
<div style="background-color: white;">
The medicine "has been somewhat extensively used for the past two or three years," by European physicians for its Oxycontin effect on some pregnant women to help strengthen labor and reduce bleeding. (1) It does this by constricting blood vessels. It also is a bronchodilator, and for this reason, it was trialed on asthmatics.</div>
<div style="background-color: white;">
<br /></div>
<div style="background-color: white;">
In 1919 the <i>Therapeutic Notes </i>reported the following:</div>
<blockquote class="tr_bq" style="background-color: white;">
<span style="color: #274e13;"><span style="font-family: serif;">The fact that </span><span style="font-family: serif; font-style: italic;">Pituitrin </span><span style="font-family: serif;">has an Adrenalin-like action, and the fact that this action is more prolonged than that of the suprarenal active principle, has suggested its utility in the treatment of asthma and hay-fever. It has been tested clinically by leading practitioners, who pronounce it a valuable drug in these diseases. Some opinions are here given:</span></span></blockquote>
<blockquote class="tr_bq" style="background-color: white;">
<span style="color: #274e13;"> <span style="font-family: serif;">"One of my asthmatic patients has experienced great relief from the use of Pituitrin."</span>"I have used Pituitrin in two cases of hay-fever with satisfactory results. While ischemia is accomplished less slowly it seems to last much longer; one patient who experienced great irritation from the use of Adrenalin says that the Pituitrin is almost without any irritating effect.'' </span></blockquote>
<blockquote class="tr_bq" style="background-color: white;">
<span style="color: #274e13;">"I have one case of asthma which was relieved by the use of Pituitrin; it is also of a great deal of use in the treatment of hay-fever." </span></blockquote>
<blockquote class="tr_bq" style="background-color: white;">
<span style="color: #274e13;">"A case of hay-fever treated with Pituitrin in normal salt solution (1:3) showed decided relief. I found that its. action was slower, more prolonged and less irritating than Adrenalin, and no after-congestion resulted as in the case of the latter." </span></blockquote>
<blockquote class="tr_bq" style="background-color: white;">
<span style="color: #274e13;">"I used Pituitrin daily in one case of hay-fever, employing the undiluted solution so as to give the hardest possible test as to its irritation. There was no irritation and the relief was perfect.'<br />"When used in a 10-per-cent normal saline solution the results were very satisfactory."</span></blockquote>
<div style="background-color: white;">
It's very common throughout human history to find a medicine experimented with in this fashion, and this continues to this day. Also, in the 1970s a medicine called terbutaline was approved for asthma as a rescue medicine, and it was ultimately more commonly used to delay pregnancies.</div>
<div style="background-color: white;">
<br /></div>
<div style="background-color: white;">
Probably due to the success of adrenaline, pituitrin never caught on as an asthma medicine. Yet it provided another option for physicians and asthmatics when such an option was necessary.</div>
<div style="background-color: white; font-family: arial; font-size: 16px; font-weight: bold;">
<span style="font-family: "times new roman"; font-size: small; font-weight: normal;"><br /></span></div>
<div style="background-color: white; font-family: arial; font-weight: bold;">
<span style="font-family: "times new roman"; font-weight: normal;"><span style="font-size: xx-small;">References:</span></span></div>
<div style="background-color: white;">
<br /></div>
<ol style="background-color: white;">
<li><span style="font-size: xx-small;">"<a href="http://books.google.com/books?id=5lDlAAAAMAAJ&pg=PA194&dq=park,+davis+%26+Co.,+glaseptic&hl=en&sa=X&ei=moo3UbCHHcqWywG94oH4BQ&ved=0CDgQ6AEwAg#v=onepage&q=park%2C%20davis%20%26%20Co.%2C%20glaseptic&f=false">Pituitin in difficult parturition</a>," <i>Medial Review, </i>June, 1912, Volume 61, Issue 6,</span><span style="font-size: xx-small;"> Picture is from an advertisement that follows the article paid for by Park-Davis & Co.</span></li>
<li><span style="font-size: xx-small;">"<a href="http://books.google.com/books?ei=gMU1UZDUM-y6yAHViYDAAQ&dq=melland,+lancet,+adrenaline&jtp=6&id=c78CAAAAYAAJ#v=onepage&q=pituitrin%2C%20asthma&f=false">Pituitrin in Hay fever and asthma</a>," <i>Therapeutic Notes, </i>Volumes 17 and 18, Park-Davis & Co., 1909 and 1910, page 70.</span></li>
</ol>
<div style="background-color: white;">
<span style="font-family: inherit;"><span style="font-size: xx-small;">Further reading</span>: </span></div>
<div style="background-color: white;">
<br /></div>
<ol style="background-color: white;">
<li><span style="font-family: inherit; font-size: 13px;"><a href="http://books.google.com/books?id=F70CAAAAYAAJ&pg=PA77&dq=therapeutic+notes&hl=en&sa=X&ei=EE43UcyjPOTVyAGvkoGgBw&ved=0CDcQ6AEwAA#v=onepage&q=therapeutic%20notes&f=false" style="font-size: 13px;">article on pollen and hay fever</a></span></li>
</ol>
</div>
<div class="ds-single" style="background-color: white; font-size: 13px; margin-left: 1cm;">
<div style="font-family: Arial;">
<br /></div>
</div>
<div class="ds-single" style="background-color: white; font-family: Arial; font-size: 13px; margin-left: 1cm;">
<br /></div>
<div class="ds-single" style="background-color: white; font-family: Arial; font-size: 13px; margin-left: 1cm;">
<br /></div>
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<br />
The serum was written about in an editorial in the <em>Journal of the American Mecial Association </em>in October of 1904. The authors noted that there were a lot of theories as to the cause of hay fever: the heat theory, the light theory, the nervous theory, the pollen theory and the bacteria theory were just a few. Yet all that was known for sure about the disease was (1):<br />
<ul>
<li>You had to have a have a predisposition to suffer from it</li>
<li>There had to be an exciting cause to trigger it. </li>
</ul>
Dunham was a supporter of both the pollen theory and the bacteria theory. When his initial experiments found no bacteria, he ruled out the bacteria theory. His new focus was on the pollen thoery, and it was by his experiments with pollen that he would hit pay dirt. (1)<br />
<br />
He learned that when a pollen was inserted into the eyes of hay fever sufferers it caused inflammation and redness of the mucous layers around the eyes. He later discovered that it was not the pollen itself that caused this reaction, but a protein (toxalbumin) produced by pollen. When exposed to that protein, the symptoms of hay fever were present. (1)<br />
<br />
His studies were interesting in that he discovered that "as little as 1/40,000 of a milligram of the rye-pollen toxin placed in the conjunctival sac (around the eyes) will call forth in certain individuals a paroxysm of hay fever lasting several hours." (1) <br />
<br />
The serum only caused hay fever symptoms in those people with a susceptibility (or predisposition), and had no effect on any one else. His research basically confirmed the theories of Blackley, that pollen was a cause of hay fever. He, thus, proved the pollen theory of hay fever. (1)<br />
<br />
Yet Dunbar didn't stop there. By further experiments:<br />
<blockquote class="tr_bq">
<div class="gtxt_column">
<span class="gstxt_hlt"><span class="gstxt_hlt">"Dunbar </span>found on mixing the toxalbumin with the serum of animals which had been previously treated with pollen or the extracted poison that the former was rendered innocuous. Unlike diphtheria antitoxin, the hay-fever serum is not to be used subcutaneously, for subcutaneous injections give rise to unpleasant symptoms—itching, swelling and erythema. Experiments have shown that the local application of the serum to the irritated mucous membrane is more effective than its introduction hypodermically.</span></div>
</blockquote>
<span class="gstxt_hlt">
The technique he used was called passive immunization. He "injected young thoroughgbred horses with pollen toxin in increasingly large doses, (and) produced what he believed to be an antitoxin in the horse's blood that neutralized the pollen's effects," writes historian Gregg Mittman in 2007. (2, page 56)<br /><br />In one study 222 hay fever sufferers were treated with the serum, and 127 found it to be effective. The medicine was believed to be most effective if given every morning during the hay fever season, and it lasted for several hours to an entire day, even when the patient spends the day "in the open air." (1)<br /><br />Dunbar patented his serum in Germany, England and the United States as Pollantin. To treat hay fever patients the serum, a liquid or powder, must be administered frequently, such as every morning, to the mucus layers of the nasal passages and around the eyes. </span><br />
<br />
It was soon realized that Pollantin wasn't what it was cracked up to be. Not only did it not really work, it caused aniphylactic shock in some patients exposed to it. (2, page 56) So the quest was on to find a better remedy. This research would ultimately lead to the discovery of <span style="color: #660000;">desensitization</span> and <span style="color: #660000;">antihistamines</span>. <br />
<br />
<span style="font-size: xx-small;">References:</span><br />
<ol>
<li><span style="font-size: xx-small;">"</span><a href="http://books.google.com/books?id=llUcAQAAMAAJ&pg=PA1146&dq=william+dunbar,+pollantin&hl=en&sa=X&ei=jzXJUMfBGob82gX52oDIDQ&ved=0CDwQ6AEwBQ#v=onepage&q=william%20dunbar%2C%20pollantin&f=false"><span style="font-size: xx-small;">The situation in regards the serum treatment of hay fever</span></a><span style="font-size: xx-small;">," <em>The Journal of the American Medical Association, </em>Editorial, Saturday, October 15, 1904, page </span></li>
<li><span style="background-color: white;"><span style="font-size: xx-small;">Mittman, Gregg, "Breathing Space," 2007, New Haven and London, Yale University Press</span></span></li>
</ol>
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<br />
According to <a href="http://www.wellcome.ac.uk/Funding/Medical-history-and-humanities/Funded-projects/WTDV030247.htm">Mark Jackson</a> the following are the medicines Proust used during his lifetime:<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhIv916bd2WsV-zhQdh_w1yn1tp5bdavRyvu4ryIAUDchg-iY4VcwG83_b3hbVM5w0s8D1VCayaDM5eN4eizBVR7Fmw1B1mWq6VruJrZvM5Um6P6xQq6fiWrFhRN2wxnEIIf9-8M_9S8_E/s1600/Dr.+Wetzel%2527s+Cigarettes.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhIv916bd2WsV-zhQdh_w1yn1tp5bdavRyvu4ryIAUDchg-iY4VcwG83_b3hbVM5w0s8D1VCayaDM5eN4eizBVR7Fmw1B1mWq6VruJrZvM5Um6P6xQq6fiWrFhRN2wxnEIIf9-8M_9S8_E/s320/Dr.+Wetzel%2527s+Cigarettes.jpg" width="230" /></a></div>
<ol>
<li>Strammonium cigarettes (same type of medicine as atrovent and spiriva)</li>
<li>Legras powders</li>
<li>Espic powders</li>
<li>Epinepherine (adrenaline)</li>
<li>Caffeine (same family of medicine as bronchodilator theophylline, not as strong</li>
<li>Carbolic acid fumigations</li>
<li>Escouflaire powder fumigations</li>
<li>Isolation -- cork lined bedroom (staying away from allergens)</li>
<li>Opium (relaxes breathing, mild bronchodilator)</li>
<li>Morphine (relaxes, mild bronchidilator)</li>
<li>Sea, lakeside and mountain resorts (getting away from allergens, relax)</li>
</ol>
Jackson quotes Proust's journal entry to his mother:<br />
<blockquote class="tr_bq">
<span style="color: #274e13;">"Yesterday after I wrote to you I had an asthma attack and incessent running of the nose, which obliged me to walk all doubled up and light asthma cigarettes at every tobacconist's as I passed, etc. And what's worse, I haven't been able to go to bed until midnight, after endless fumigations..." (August 31, 1901)</span></blockquote>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjU0czXynk_e-yG7rXBF5oKhywCbooalS4rhhJmWBAv1gfOAjWsaDfS1AQSa4gmPL1ab-XLoqMvWqQzZ6wKgetTjDhqrp3Q050UMEQyQ9D-Lh0SJGeDHbEeHAMXWkVEwcIZzllN4AGYxU4/s1600/drawing+for+cigarettes.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="255" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjU0czXynk_e-yG7rXBF5oKhywCbooalS4rhhJmWBAv1gfOAjWsaDfS1AQSa4gmPL1ab-XLoqMvWqQzZ6wKgetTjDhqrp3Q050UMEQyQ9D-Lh0SJGeDHbEeHAMXWkVEwcIZzllN4AGYxU4/s400/drawing+for+cigarettes.jpg" width="400" /></a></div>
If the Internet were available to Mr. Proust I bet he'd be involved in an online asthma community as this blog is a part of. While he didn't have the ability to blog, at least he wrote of his asthma experience in letters. <br />
<br />
Mr. Jackson is a professor at the Center for Medical History at the University of Exeter in England. He's written books on asthma and articles on asthma and allergies and COPD. I will link to some below so you can check them out at your liking.<br />
<br />
<a href="http://hardluckasthma.blogspot.com/p/asthma-history.html">Click here for more asthma history.</a><br />
<ol>
<li><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844275/pdf/medhis5402-02-171.pdf">Divine Strammonium: The rise and fall of smoking for asthma</a></li>
<li><a href="http://www.who.int/global_health_histories/seminars/presentation21.pdf">Marcus Proust and the global history of asthma</a> (slide show)</li>
<li><a href="http://www.amazon.com/Asthma-Biography-Biographies-Mark-Jackson/dp/0199237956/ref=sr_1_1?ie=UTF8&qid=1322899923&sr=8-1">On Asthma: A Biography</a></li>
<li><a href="http://www.amazon.com/Allergy-History-Modern-Mark-Jackson/dp/1861893337/ref=sr_1_fkmr0_2?s=books&ie=UTF8&qid=1322899956&sr=1-2-fkmr0">Allergies: A history of the malady</a></li>
<li><a href="http://books.google.com/books?id=6KJ0y_oSaAsC&printsec=frontcover&dq=inauthor:%22Mark+Jackson%22&hl=en&ei=ZtrZTt71Nant0gGotrXkDQ&sa=X&oi=book_result&ct=result&resnum=8&ved=0CF8Q6AEwBw#v=onepage&q&f=false">The Oxford handbook of the history of medicine</a></li>
<li><a href="http://www.asthma.org.uk/applications/site_search/search.rm?term=asthma+timeline&searchreferer_id=3">Asthma timeline</a></li>
</ol>
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John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com384tag:blogger.com,1999:blog-4749703810590147676.post-67311809361583691572017-07-10T04:36:00.000-07:002017-07-10T04:36:14.490-07:001898: Dr. Hollopeter: What Causes Asthma? According to William Hollopeter in his 1898 book "Hay-fever and its successful treatment, there were essentially two causes of hay fever: (1, <a href="http://books.google.com/books?ei=GLwvUcuWBai_ygH_8oCIBA&id=w00EAAAAYAAJ&dq=hay+fever&jtp=47">page 47</a>)<br />
<div>
<ol>
<li>An exciting cause (heat, pollen, dust, sunlight, etc.)</li>
<li>A preexisting, underlying condition </li>
</ol>
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Provided statistics of the era, Hollopeter said that relatively few people have hay fever, which verifies that some "underlying condition, predisposition, or idiosyncrasy can hardly be doubted. Exactly what this is, or on what it depends, is unknown." (1, page 47)</div>
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Holopeter said that the first person to talk about a predisposition to developing hay fever was Dr. Abbots Smith in 1865. Likewise, Holopeter said: (1, page 47)</div>
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<span style="background-color: white; font-family: serif;">This predisposition or idiosyncrasy has generally suddenly developed without apparent reason. It has been argued that it is systematic or central, and that it is due to some local abnormality of the mucous membrane, the capillaries, or the periphery of nerves. Once acquired, however, it is seldom lost, and it apparently increases with each successive year.</span></blockquote>
The following are the major predisposing factors:<br />
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<li><b>Race</b>: English and Americans are the most susceptible. One physician went as far to suspect that sine Americans and English were the most likely to drink tea, that perhaps tea somehow affected the nervous system causing hay fever. Although the Chinese and Japanese drink tea as well, and there's a low incidence of the disease in those nations. </li>
<li><b>Geographic distribution</b>: It is rarely found in northern regions, such as Canada, Norway, Sweden and Denmark. It is most commonly seen in the U.S., Europe, and to some degree New Zealand and Australia. Even in the U.S. and England is is not commonly found along the seashore and at high elevations. It is difficult to know exactly where it's most likely to occur. (Dr. Wyman published maps for where it's most likely to occur in his 1872 book "Autumnal Catarrh." (1, pages 49-52</li>
<li><b>Heredity</b>: George Beard was the first to postulate a nervous origin of hay fever, and that it was acquired through inheritance. Various physicians have shown evidence of the malady among the various generations of the family tree (Morill Wyman, F.H. Bosworth, Morell Mackenzie) (1, page 53) </li>
<li><b>Sex</b>: Generally, "of the 433 cases cited by Phoebus, Wyman and Beard, only 143, about one-third, were females." So the tendency is that it affects males more so than females. Morell Mackenzie also noted the trend, noting he had 38 male patients with hay fever, and only 23 females. The theory is that "men are more exposed to the exciting causes such as dust, heat, pollen, etc., although females are more neurotic."(1, page 54)(2, page 96-7)</li>
<li><b>Age</b>: While occasionally occurring in people over the age of 60, it generally first appears in people under the age of 40. (1, page 55) In many cases of childhood onset hay fever, many cases are regarded as the common cold, <em>unless the parents were also afflicted with it (hence suggesting the hereditary component). </em></li>
<li><b>Education</b>: Holopeter notes pretty much the same as every other author on the subject, that: "<span style="font-family: serif;"><span style="background-color: white;">Most all writers on this subject have observed that the disease attacks the better educated classes and those of fair social position. It is rarely met with among the laboring classes. This would seem to emphasize the view that the disease is essentially a neurosis. From the notes of sixty-one cases of</span><span style="background-color: white;"> </span></span><span class="gstxt_hlt" style="background-color: white; font-family: serif;">hay-fever </span><span style="font-family: serif;"><span style="background-color: white;">i</span><span style="background-color: white;">n private practice, and the sight of many others of which no record was kept, Morell Mackenzie found all the patients persons of some education, and recalled having seen none among his hospital patients. Of fortyeight cases of Blackley, all were educated, and Wyman made the same observation. Edmund W. Holmes has shown that the ignorant classes are not so likely</span></span><span class="gtxt_body" style="background-color: white; font-family: serif;"> to recognize the disease as a distinct affection, and apply for medical aid." (1, page 55)(3, <a href="http://books.google.com/books?id=aa0DAAAAYAAJ&pg=PA200&lpg=PA200&dq=edward+holmes,+hay+fever&source=bl&ots=i21PZzRxJ2&sig=dmb73iewGDeHDZKof538e2KGrmU&hl=en&sa=X&ei=YrowUd7XJ-iqyAHfiYGIDQ&ved=0CDsQ6AEwAg#v=onepage&q=edward%20holmes%2C%20hay%20fever&f=false">page 204</a>)</span></li>
<li><b>Occupation and Mode of life</b>: The "rustic" and farmers are much more exposed to exciting causes and therefore are less susceptible to developing hay fever. Others suggest it only effects the wealthy because they have a higher intelligence. (1, <a href="http://books.google.com/books?id=w00EAAAAYAAJ&printsec=frontcover&dq=hay+fever&hl=en&sa=X&ei=GLwvUcuWBai_ygH_8oCIBA&ved=0CGMQ6AEwCA#v=onepage&q=occupation%20and%20mode%20of%20life&f=false">page 56</a>) Wyman observed, among the occupations he observed, those most likely to have hay fever have "indoor jobs requiring but little manual labor," such as merchants and manufacturers. Wyman notes that only three farmers in his little study had hay fever, and this was of interest to him. He surmised that they probably did have hay fever, " (2, <a href="http://books.google.com/books?ei=6e0tUfKbGOPtiQK40oDgBQ&id=UXQSAAAAYAAJ&dq=morrill+wyman&jtp=90">page 99</a>-100) </li>
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Of this observation regarding the low number of farmers with hay fever and the high number of merchants and manufacturers, Wyman writes the following: (2, page 100)<br />
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"It is not a little remarkable that of those who must make up the largest class in the community, so few should be reported as subjects. It may be that the disease with them is light, and therefore overlooked entirely, or not thought of sufficient importance to apply for medical aid. This, to a certain degree, is not improbable, for we find that physicians to whom application is made, do not all recognize it sufficiently to ask whether the disease has recurred annually, nor do the patients think it worth mentioning, even if it has been observed and remembered. It is by no- means infrequent for a person to experience several pretty severe annual attacks before it occurs to him that probably these are returns of one and the same disease. Still, the mechanics and farmers of New England are too intelligent and too well educated to allow the disease to escape their observation entirely. If many applied for treatment at the <span style="font-style: italic;">dispensaries </span>of the large cities, the fact would appear in their annual reports. No such disease is mentioned.</blockquote>
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I am inclined to think, therefore, that the disease is less severe or less frequent with those that labor, than with those whose employments are attended with less muscular exertion. The result, perhaps, of a life more in accordance with the rules of health, in this respect, for the mechanics and farmers of New England, as a general rule, are as well housed, clothed, and fed, so far as health is concerned, as those who are among the richer and in some respects more favored classes. This question, however, can only be satisfactorily settled when a knowledge of the disease becomes more general."</blockquote>
The following are theories as to what might cause hay fever:<br />
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1. <b>Pollen Theory</b>: It is the most generally recognized as the cause of hay fever, and while it was a speculated cause prior to the 1860s, experiments by Dr. Charles Blackley proved it during experiments he performed between 1866 and 1878. He proved that contact with pollen to the mucus membrane causes inflammation and redness, and hay fever symptoms. He wrote that there is a direct relationship between the amount of pollen in the air and hay fever symptoms. For more on Blackley's pollen theory of hay fever you can click here. </div>
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2. <b>The Neurotic Theory</b>: Holopeter basically refers to George Beard, who in 1876 postulated the nervous theory of hay fever, and made light to allay the "misconception" that nervous meant "debility and emaciation." Holopeter notes that Beard explains the truth to be more along the lines that the nervous system is full of full of "great strength and endurane." In those with hay fever, some exciting cause "excites" the nervous system to cause the symptoms of hay fever. Beard explains that the the disease and the tendency to be transferred from one generation to another was all based on this nervous theory. No evidence has yet been shown of how the nervous system causes the hay fever symptoms. (You can read more about Beard's Nervous Theory of Hay Fever by clicking here)(1, page 57-60) </div>
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<li><b>Vasomotor susceptibility</b>: Vasomotor refers to the nervous systems ability to regulate dilation and contraction of blood vessels. In hay fever it has a tendency to cause dilation of the blood vessels lining the respiratory tract and eyes, hence hyperaemia and inflammation (catarrh) and your hay fever symptoms. That this happens "indicates a neurotic tendency." Some suspect it may or may not be due to lesions. A similar event occurs with asthma, only the dilation and hyperaemia occurs in among the air passages of the lungs. (<a href="http://medical-dictionary.thefreedictionary.com/hyperaemia">Hyperaemia</a> refers to increased blood flow to a certain region of the body) Hollopeter notes that "Bosworth is inclined to think a peculiar lack of vasomotor control characterizes the neurotic manifestations." (1, page 57-60)</li>
<li><b>Idiosyncracy</b>: The fact hay fever has idiosyncratic means it's neurotic. By this, the body of the hay fever sufferer is oversensitive to some exciting cause. </li>
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3. <b>Local Disease Theory</b>: Some sort of local disease (polyp, deviated septum, rhinitis, obstructed nasal passages, etc.) may be the cause of the disease. When the polyp is removed, the hay fever may be cured. Hollopeter quotes Mackenzie: <span style="font-family: inherit;"><span style="background-color: white;"> </span><span style="background-color: white;">"there exists in the nose a well-defined sensitive area whose stimulation through a local pathologic process, or through an extra irritation, is capable of producing an excitation which finds its expression in a reflex act or in a series of reflected phenomena."</span></span> Bosworth suggested these were generally the effect rather than the cause of hay fever. Some physicians propose such local agents cause both hay fever and asthma. (1, page 62-64)</div>
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4. <b>The Uric Acid Theory</b>: In 1893, Dr. Seth S. Bishop, as quoted by Hollopeter, wrote: "an excess of uric acid in the blood causes hay fever, or nervous catarrh." Hollopeter notes that excess uric acid in the blood "causes certain disturbances of a vascular and neurotic character. Haig wrote that excess uric acid causes contraction of arterioles and capillaries, and this opinion was verified by Thomas J. Mays. Murchison, Conklin, Ebstein, Quinquad, and others. Bishop in 1894 speculated that regulation of uric acid should be regarded as a treatment for hay fever. Mays believed that while uric acid was the cause, hay fever was still nervous and, therefore, still hereditary. Although Dr. Capp suggests that the presence of excess uric acid may actually cause "a central nervous irritation." This results in "nerve currents" that are uncontrolled by the normal functions of the body, and result in the abnormal response of hay fever. (1, pages 64-71)</div>
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References:</div>
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<ol>
<li><span style="font-size: xx-small;">Hollopeter, William Clarence, "</span><a href="http://books.google.com/books?id=w00EAAAAYAAJ&printsec=frontcover&dq=hay+fever&hl=en&sa=X&ei=GLwvUcuWBai_ygH_8oCIBA&ved=0CGMQ6AEwCA" style="font-size: x-small;">Hay-fever and its successful treatment</a><span style="font-size: xx-small;">," 1898, Philadelphia, P. Blakiston's Son and Co.</span></li>
<li><span style="font-size: xx-small;">Wyman, Morill, "<a href="http://books.google.com/books?id=UXQSAAAAYAAJ&printsec=frontcover&dq=morrill+wyman&hl=en&sa=X&ei=6e0tUfKbGOPtiQK40oDgBQ&ved=0CC0Q6AEwAA#v=snippet&q=the%20climate%2C%20the%20soil&f=false">Summer Catarrh</a>," 1876 (first edition was published in 1872), New York, Hurd and Houghton</span></li>
<li><span style="font-size: xx-small;">Holmes,</span></li>
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John Bottrellhttp://www.blogger.com/profile/05107035756753427035noreply@blogger.com31