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Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most prevalent drugs inducing hypersensitivity reactions. The aim of this analysis was to estimate the prevalence of NSAID-induced respiratory symptoms in population across Europe and to assess its association with upper and lower respiratory tract disorders.The GAThe mean prevalence of NSAID-induced dyspnea was 1.9% and was highest in the three Polish centers [Katowice (4.9%), Krakow (4.8%), and Lodz (4.4%)] and lowest in Skopje, (0.9%), Amsterdam (1.1%), and Umea (1.2%). In multivariate analysis, the prevalence of respiratory reactions to NSAIDs was higher in participants with chronic rhinosinusitis symptoms (Odds Ratio 2.12; 95%CI 1.78-2.74), asthma symptoms in last 12 months (2.7; 2.18-3.35), hospitalization due to asthma (1.53; 1.22-1.99), and adults vs children (1.53; 1.24-1.89), but was not associated with allergic rhinitis.Our study documented significant variation between European countries in the prevalence of NSAID-induced respiratory hypersensitivity reactions, and association with chronic airway diseases, but also with environmental factors.

Drugs which block the action or formation of the cysteinyl leukotrienes (LTC4, LTD4 and LTE4) inhibit asthmatic responses evoked by allergen, exercise and cold dry air. The purpose of this study was to determine whether the specific leukotriene-receptor antagonist MK-0679 could block the airway obstruction induced by aspirin (acetylsalicylic acid (ASA)) in aspirin-intolerant asthmatics. Eight asthmatics (mean age 45 yrs), with an average history of asthma and ASA-sensitivity of about 10 yrs duration, were subjected to bronchial provocation with lysine-ASA. Baseline ASA-sensitivity was first determined in an open prestudy session by inhalation of cumulative doses of lysine-ASA to establish the dose of ASA decreasing forced expiratory volume in one second (FEV1) by 20% (PD20). Rechallenge with lysine-ASA was performed on two different occasions, 1 h after oral administration of placebo, or 750 mg of MK-0679, under double-blind conditions, in a randomized, cross-over design. Leukotriene formation was estimated by the measurement of urinary LTE4. The lysine-ASA challenge was highly reproducible (geometric mean for group PD20 being identical for the open prestudy and the placebo session), and was associated with a post-challenge increase in urinary LTE4. In contrast, after MK-0679, there was a rightward shift in the dose response relationship for all eight subjects (median shift being 4.4 fold), with three of the subjects failing to produce a 20% decrease in FEV1 despite inhalation of the highest dose of lysine-ASA feasible to deliver.(ABSTRACT TRUNCATED AT 250 WORDS)

Oral challenge with acetylsalicylic acid was compared with inhalation of Lysine acetylsalicylic acid (L-ASA) as a means to diagnose aspirin-idiosyncrasy in the airways. On the basis of history and/or clinical findings (asthma, rhinorrhea, nasal polyposis) 22 consecutive patients were challenged by both routes. Ten of these developed significant bronchoconstriction (greater than or equal to 20% drop in forced expiratory volume in one second (FEV1)) during either challenge, with the same absolute sensitivity for both tests (9/10). During the bronchial provocations, the reactions developed more promptly (20 min vs 1 h after provocation dose) and were limited to the airways. In contrast, the reactions evoked by the oral provocations were often more pronounced, longer lasting and occurrence of generalized symptoms was more common. Accordingly, the oral tests required more extensive drug treatment for reversal, whereas the bronchial provocations always were reversed by inhalation of bronchodilators. The bronchial method thus resulted in considerably shorter test sessions (4 h vs 8 h). The specificity of the bronchial test was indicated by the observation that a control group of 19 asthmatics with comparable severity of disease failed to bronchoconstrict in response to L-ASA. In conclusion, we have found the bronchial provocation method to be easy to interpret and to control, even in severely asthmatic patients. Consequently, bronchial provocation with L-ASA appears particularly useful in the out-patient office or for research on airway responses to ASA in ASA-sensitive asthmatics.