ABSTRACT
Hippocrates used salicylates in the fonn of willow bark for its antipyretic and analgesic effects. The word aspirin comes from a, acetyl, and spirin, spiric acid, from the bark of the willow tree. Aspirin was introduced into medicine in 1899 for the treatment of fever and inflammatory disorders. The first report of an aspirin-induced reaction was that in 1903 by Dr. Franke in Gennany (1 ), who himself took 1 g aspirin and within 15 min experienced angioedema of his face and larynx, tachycardia, and choking. The symptoms settled after 2 hr. This was followed by a number of similar reports in patients in whom acute angioedema, generalized urticaria, or rhinoconjunctivitis developed after ingestion of 5 grains of aspirin {2-4). In 1905 Barnett published the frrst case reports of two patients who experienced "difficulty in respiration" after ingesting 7.5 and 15 grains of aspirin, and this probably represents the first reported case of aspirin-induced bronchospastic reactions {5). Fifteen years later the first report of deaths from a therapeutic dose of aspirin was published (6). In 1919, Francis reported the association between aspirin sensitivity and nasal polyps and suggested that antipyrin and oxyquinothein could produce similar reactions and that phenacetin was safe in these patients (7). Three years later Widal reported the association of
aspirin sensitivity, asthma, and nasal polyps (8). This association was rediscovered in 1968 by Samter and Beers and named the "aspirin triad" (9). Since that time, much has been learned about the epidemiological, clinical, and pathophysiological features of intolerance of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs), although why some asthmatics are sensitive to aspirin and others not remains unanswered.
