NSAID-induced urticaria and angioedema: a reappraisal of its clinical management.

摘要: Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs), resulting in urticaria and angioedema, is being observed with increasing frequency. Prevalence rates range from 0.1–0.3%, which partly due the large size of exposed (at risk) population. Some predisposing factors for these cutaneous reactions have been identified, among them atopic diathesis, female sex, young adulthood, a history chronic use NSAID relief acute pain. The description two different arachidonic acid cyclo-oxygenases (COX) about decade ago, designated COX-1 COX-2, incorporation into therapeutic armamentarium more selective enzyme inhibitors control inflammation pain, has led an improved understanding pathogenesis adverse NSAIDs. This allowed investigators study ‘sensitive’ individuals see if they can safely receive new pharmaceutical compounds. reasons why some people react NSAIDs are not completely clarified. prevalent theory angioedema cross-reactive patients assumes that inhibition leads shunting metabolism towards 5-lipoxygenase pathway, results increased synthesis release cysteinyl leukotrienes. Although COX-2 well tolerated by majority classic NSAID-sensitive patients, highly described individuals, casting doubts relevance such hypotheses. On other hand, who single chemically similar products (single-reactors), specific immunoglobulin E antibodies haptenated metabolites suspected, although easily demonstrated means routine vivo or vitro techniques. Facial (periorbital) constitutes most common form clinical presentation, one-third show mixed pattern (urticaria and/or angioedema) respiratory symptoms include upper tract edema, rhinorrhea, cough, breathlessness tearing. When necessary, diagnosis confirmed controlled peroral drug challenges done experienced physicians hospital setting test helpful management, will be based on strict avoidance, alternative medications. approach specially indicated hypersensitive medical conditions require continuous therapy, as those arthritis coronary heart disease.