Pulmonary side effects are relatively rarely observed with analgesics and anti-inflammatory drugs. However, some patients react to the ingestion of such drugs with bronchoconstriction and asthmatic attacks. In only a small percentage of these patients is a true allergic mechanism underlying the pulmonary reaction to the drugs. In most of the patients the basis for the pulmonary side effects is pseudoallergic. The molecular mechanism of pseudoallergy is not completely understood. However, several hypotheses have been put forward, such as drug-induced stimulation of kinin receptors, activation of the complement system or interference with eicosanoid biosynthesis. The last hypothesis is attractive, since it could explain the similar sensitivity of such patients to drugs which are completely different chemically. It is not known, however, if the crucial drug effect on arachidonic acid metabolism is inhibition of synthesis of a bronchodilator eicosanoid such as prostaglandin E2 or increased synthesis of bronchoconstrictor eicosanoids such as leukotrienes.