Eicosanoids, aspirin-intolerance and the upper airways--current standards and recent improvements of the desensitization therapy.

In 1922, Widal et al. were the first to describe intolerance reactions to acetylsalicylic acid (ASA, e.g. in aspirin) and to other nonsteroidal anti-inflammatory drugs (NSAIDs). The full clinical picture reveals a classic triad of symptoms (Samters Triad): aspirin induced bronchial asthma (with severe acute asthma attacks), aspirin-sensitivity and chronic rhinosinusitis with nasal polyps. In many cases, nasal polyps reveal as the first symptom of ASA sensitivity indicating that the upper airways are predominantly involved in the pathogenetic process. Therefore, emphasis of this article mainly focuses on the upper airways in ASA-intolerant patients. In the last decade, clear evidence has been pointed out that ASA-intolerance is related to the abnormal metabolism of arachidonic acid leading towards excessive leukotriene (LTs) production. The resulting dysbalance of the eicosanoids leukotrien and prostaglandin might be the crucial pathophysiologic keypoint of the disease. The incidence of aspirin hypersensitivity in the general population ranges from 0.6 % to 2.5% and in adult asthmatics from 4,3 % to 11%. Besides the patients history, challenge tests with Lysin-aspirin are performed as the diagnostic tool of choice. Apart from surgical or pharmacological therapy, ASA desensitization therapy is the only specific treatment of choice. As first described by Stevensson et al. in the early 1984, oral administration by means of an initial desensitization with gradually ascending doses of aspirin is followed by a daily maintenance-dose. In the last years, many publications on various desensitization protocols and routes of administration have been worked out. Recently, the intravenous route for the inititial increment desensitization has been described which might offer new therapeutical possibilities in the treatment of ASA-intolerant patients.