Bonne C, Moneret-Vautrin D A, Wayoff M, Descharmes A, Gazel P, Legrand A, Kalt C
Ann Allergy. 1985 Feb;54(2):158-60.
Exaggerated inhibition of cyclooxygenase has been proposed as a mechanism of drug-induced bronchospasm in aspirin-intolerant patients. This study, using platelets, shows that inhibition of prostaglandin biosynthesis by aspirin is unmodified in patients when compared with healthy subjects. The ratio of cyclooxygenase:lipoxygenase products is similar in platelets from patients and control subjects. We conclude that the cyclooxygenase alteration observed in cells from the respiratory tract is not generalised to other cells such as platelets. We also propose that the major abnormality in NSAID-intolerant patients would affect receptivity to lipoxygenase products more than their biosynthesis.
有人提出，环氧合酶的过度抑制是阿司匹林不耐受患者药物诱导支气管痉挛的一种机制。本研究利用血小板表明，与健康受试者相比，阿司匹林对患者前列腺素生物合成的抑制作用没有改变。患者和对照受试者血小板中环氧合酶与脂氧合酶产物的比例相似。我们得出结论，在呼吸道细胞中观察到的环氧合酶改变并未扩展到其他细胞，如血小板。我们还提出，非甾体抗炎药不耐受患者的主要异常对脂氧合酶产物的反应性影响大于其生物合成。
