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.