Aspirin asthma from

The term refers to a distinct clinical syndrome characterized by aggressive and continuous inflammatory disease of the airways with chronic eosinophilic rhinosinus-itis, asthma and often nasal polyposis [6-8]. Aspirin and other NSAIDs that inhibit COX-1 exacerbate the condition, precipitating violent asthmatics attacks. This is a hallmark of the syndrome. The prevalence of aspirin hypersensitivity in the general population ranges from 0.6 to 2.5%, but is much more frequent in adult asthmatic subjects where it reaches 10-15%, although it is often underdiagnosed. 

Aspirin, cyclooxygenase, and the provocation of asthma A few people with asthma suffer from a unique syndrome in which the ingestion of 40 to 300 mg of aspirin produces rhinorrhea and acute bronchoconstriction. All cyclooxygenase inhibitors will precipitate bronchospasm in patients with aspirin-evoked asthma. 

Allergy. Aspirin is a common cause of allergic or pseudoallergic symptoms and signs. Patients exhibit severe rhinitis, urticaria, angioedema, asthma or shock. Those who already suffer from recurrent urticaria, nasal polyps or asthma are more susceptible. 

Aspirin hypersensitivity is relatively common in adults (about 20%). Estimates of the prevalence of aspirin-induced asthma vary from 3.3 to 44% in different reports (SEDA-5,169), although it is often only demonstrable by challenge tests with spirometry, and only 4% have problems in practice. Patients with existing asthma and nasal polyps or chronic urticaria have a greater frequency of hypersensitivity (76), and women appear to be more susceptible than men, perhaps particularly during the childbearing period of life (77). Acute intolerance to aspirin can develop even in patients who have taken the drug for some years without problems. 

Most people tolerate aspirin well, but not patients with asthma, of whom there is a subgroup in whom aspirin precipitates asthmatic attacks (61,62). This is a distinct clinical syndrome, called aspirin-induced asthma, which affects about 10% of adults with asthma (63). Aspirin-induced asthma is usually accompanied by naso-ocular symptoms and can be triggered not only by aspirin, but by several NSAIDs, a fact that makes immunological cross-reactivity most unlikely. The propensity of an NSAID to precipitate an attack of asthma is probably related to inhibition of COX (63). There is evidence that potent inhibitors of COX-1 (such as ibuprofen, indometacin, and naproxen) are more likely to precipitate bronchoconstriction than NSAIDs that inhibit COX-2 preferentially (such as meloxicam and nime-sulide) (64,65). A widely accepted hjrpothesis is that in patients with asthma and aspirin intolerance, NSAJD-induced COX inhibition results in increased products from the 5-lipoxygenase pathway, the leukotrienes, which are both potent bronchoconstrictors and also inducers of... 

In the third stndy, 27 patients with stable chronic asthma in whom inhalation of lysine aspirin cansed a 20% fall in FEVi were challenged with increasing doses of oral cele-coxib (from 10 to 200 mg/day) they do not develop bronch-oconstriction or other extrapulmonary reactions (68). 

Consequently, Zyflo was thoroughly evaluated in a number of clinical trials for effects on models of asthma and in the treatment of chronic asthma. Challenge models of asthma with a variety of stimuli (allergen, exercise, cold dry air, or aspirin) were successful. Results in aspirin-induced asthma were dramatically effective, indicating that leukotrienes are the primary mediators of this response. Zyflo also shows remarkable anti-inflammatory effects, as predicted from animal studies (137). Eosinophil influx and albumin leakage were reduced and the urinary increase in LTE, was blocked (86%)(141,142). 

All aspirin-sensitive asthmatics do not fit the classic aspirin triad picture, and not all patients with asthma and nasal polyps develop sensitivity to aspirin. In most cases, aspirin-sensitive asthmatics are clinically indistinguishable from the general population of asthmatics except for their intolerance to aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin-induced asthmatics are not at higher risk of having fatal asthma if aspirin and other NSAIDs are avoided. ... 

From the first study in patients with local IgE against SEs [10] it appeared that the highest IgE concentrations were obtained from samples of aspirin-sensitive subjects. We therefore extended our observations in a nonallergic, but severely inflamed subgroup of patients, who also suffered from asthma. Subjects with nasal polyposis from Poland were classified as aspirin-sensitive (ASNP) or aspirin-tolerant (ATNP) asthmatics, based on a bronchial aspirin challenge test [47], Homogenates prepared from NP tissue were analyzed for concentrations of eosinophilic markers, total IgE and IgE antibodies to enterotoxins (SEA, SEC, TSST-1) [22], and compared to inferior nasal turbinates from healthy subjects. 

Suh YJ, Yoon SH, Sampson AP, et al Specific immunoglobulin E for staphylococcal enterotoxins in nasal polyps from patients with aspirin-intolerant asthma. Clin Exp Allergy 2004 34 1270-1275. Perez-Novo CA, Watelet JB, Claeys C, van Cauwenberge P, Bachert C Prostaglandin, leukotriene, and lipoxin balance in chronic rhinosinusitis with and without nasal polyposis. J Allergy Clin Immunol 2005 115 1189-1196. 

Certain individuals display hypersensitivity to aspirin and NSAIDs, as manifested by symptoms that range from vasomotor rhinitis with profuse watery secretions, angioedema, generalized urticaria, and bronchial asthma to laryngeal edema, bronchoconstriction, flushing, hypotension, and shock. Aspirin intolerance is a contraindication to therapy with any other NSAID because cross-sensitivity can provoke a life-threatening reaction. 

Aspirin intolerance has been described in a few families (Starr 1971 Lockey et al. 1973 Von Maur et al. 1974 Delaney 1973). A family aggregation, however, appears to be very rare (Falliers 1974). In our population of 500 patients with proven AIA, we found only two cases of familial intolerance to aspirin. One was a 19-year-old male, whose only brother, also asthmatic, as known to have died after taking aspirin. The other was a 21-year-old asthmatic female, whose father had never suffered from asthma but gave a history of angioedema and urticaria without dyspnea following aspirin ingestion this was confirmed in a challenge test. 

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