Peskar B A
Med Toxicol. 1986;1 Suppl 1:10-3.
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.
镇痛药和抗炎药相对较少出现肺部副作用。然而,一些患者在摄入此类药物后会出现支气管收缩和哮喘发作。在这些患者中,只有一小部分肺部对药物反应的真正机制是过敏。在大多数患者中,肺部副作用的基础是假过敏。假过敏的分子机制尚未完全了解。然而,已经提出了几种假说,如药物诱导的激肽受体刺激、补体系统激活或对类花生酸生物合成的干扰。最后一种假说很有吸引力,因为它可以解释此类患者对化学结构完全不同的药物具有相似敏感性的原因。然而,尚不清楚药物对花生四烯酸代谢的关键作用是抑制支气管扩张类花生酸如前列腺素E2的合成,还是增加支气管收缩类花生酸如白三烯的合成。