The protective effects of leukotriene modifiers in aspirin-induced asthma

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase activity and, in aspirinintolerant patients, can precipitate life-threatening asthma attacks. In aspirin-sensitive asthmatic patients, exposure to aspirin results in a dramatic increase in cysteinyl leukotriene production, the precise mechanism of which remains unclear. However, clinical studies of the 2 types of leukotriene modifiers--the leukotriene synthesis inhibitors and the leukotriene receptor antagonists (LTRAs)--have established the critical pathogenic role played by leukotrienes in aspirin-induced asthma (AIA). Zileuton, the only leukotriene synthesis inhibitor now available, increased pulmonary function and alleviated the cardinal signs of AIA. Montelukast, a potent LTRA, blocked the airway obstruction induced by lysine-aspirin inhalation in aspirin-sensitive asthmatic patients. Pulmonary function improved significantly, and both ss-agonist use and frequency of nocturnal awakening decreased. Pranlukast, a LTRA available only in Japan, produced results similar to those reported for montelukast. Despite these agents' protective effects, aspirin-sensitive asthmatic patients should be cautioned to avoid the use of any drug that inhibits cyclooxygenase activity.