The incidence of asthma is increasing throughout the world, which presents both public health and economic concerns. It is widely recognized that in some adult patients with asthma, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX)-1 exacerbate the condition. This is a distinct clinical syndrome called aspirin-induced asthma (AIA). The disease develops according to a characteristic pattern of symptoms. Persistent eosinophilic rhinosinusitis precedes development of nasal polyposis, aspirin hypersensitivity, and asthma. There is no in vitro test, and diagnosis can only be established by provocation tests with aspirin. At the biochemical level, AIA is characterized by a chronic overproduction of cysteinyl leukotrienes. The key enzyme, leukotriene C4 synthase, is overexpressed in bronchi, and its messenger RNA is upregulated in peripheral blood eosinophils. This can be partly related to the genetic polymorphism of the enzyme. The disease runs a protracted course, even if COX-1 inhibitors are avoided. The course of AIA is often severe, and at least half of the patients need systemic corticosteroids to control their asthma. To prevent life-threatening reactions, patients with AIA should avoid aspirin and other analgesics that inhibit COX-1. The incidence of cross-sensitivity to paracetamol in AIA patients is low and, when a reaction does occur, the symptoms experienced are shorter and milder than if the reactions were evoked by an NSAID. Rapidly growing evidence indicates that highly specific COX-2 inhibitors, known as coxibs, are well tolerated and can be safely used by AIA patients.