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Emergent Asthma : Endogenous, Exogenous, or Iatrogenous

Constantine John Falliers, MD
Author and Funding Information

Affiliations: Denver, CO
 ,  Dr. Falliers is Clinical Professor, Pediatrics and Internal Medicine, University of Colorado Health Science Center.

Correspondence to: Constantine John Falliers, MD, Director, Allergy & Asthma Clinic, P.C., Suite 670, 360 South Garfield, Denver, CO 80209; e-mail: cj.FalliersMD@att.net



Chest. 2005;127(2):427-429. doi:10.1378/chest.127.2.427
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In search for the possible causes of the emerging and persistent increase in the prevalence of asthma, Eneli et al in this issue of CHEST (see page 604) consider the evidence that the occasional, frequent, or prolonged intake of the analgesic acetaminophen (N-acetyl-p-aminophenol [APAP], or paracetamol) might be a contributing etiologic factor. As the authors speculate, APAP could account for pulmonary glutathione depletion, oxidative stress, T-helper type 2 (Th-2) vs T-helper type 1 dominance, leukotriene C4 and D4 formation, or cyclooxygenase-2–induced prostaglandin E2, which favors a Th-2 response and thus an allergic tendency. But whatever the case might be, it must be recognized that this “reversible” or variable obstructive intrabronchial disease1 is a clinical manifestation of diverse etiology, course, and prognosis. To study all “asthmatics” as a single set, either for basic research or for epidemiologic surveys, would be incorrect and potentially misleading. The results of any long-term risk assessment will have to be interpreted in the perspective of the spectrum of specific circumstances and of known or suspected influences.2

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