Clinically, aspirin induced adverse skin reactions resemble true immunologically mediated allergic reactions. However, it is well accepted that aspirin intolerance is not mediated by specific IgE antibodies. The exact mechanisms involved are far from clear1 2 and therefore no reliable diagnostic in vitro tests exist, and risky and time consuming provocation tests are regarded as the diagnostic gold standard. Most studies of pathophysiological mechanisms deal with nasal polyps or asthma. However, compared with asthma and nasal polyps, aspirin intolerance is very common in chronic urticaria.3-7 The reason for the preferred organ manifestation is unknown. Several lines of evidence point to a potent disturbance in the eicosanoid balance (cyclo-oxygenase theory) resulting in a shift towards increased production of leukotrienes.8-12 Our previous studies have shown that aspirin induced adverse skin reactions proved by positive oral provocation tests are common in chronic urticaria13 and can be characterised by enhanced sulfidoleukotriene production in IL-3 primed leucocyte suspensions after stimulation with C5a.14 15 This study was undertaken to define the rate of positive oral challenge tests in patients with chronic urticaria and a history of adverse skin reactions to aspirin. We also wanted to investigate the sensitivity and specificity of enhanced sulfidoleukotriene production induced by different basophil agonists …
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Bettina Wedi (2000) studied this question.
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