Amery W K, Davies P T, Caers L I, Heykants J, Steiner T J, Woestenborghs R, Rose F C
Janssen Pharmaceutica N.V., Beerse, Belgium.
Cephalalgia. 1988 Jun;8(2):71-4. doi: 10.1046/j.1468-2982.1988.0802071.x.
Hepatic cytochrome P450-dependent oxidation is deficient in 5% to 10% of the Caucasian population. A similar percentage seems to suffer from migraine. The hypothesis was tested that an oxidation deficiency possibly relevant to potential dietary triggers plays a role in the pathogenesis of migraine. In 37 migraine sufferers and 26 controls age- and sex-matched to 26 of these patients, debrisoquine hydroxylation following an oral dose of 10 mg was employed as a marker of oxidation status, determined by calculating the metabolic ratio (MR): urinary debrisoquine/urinary 4-hydroxydebrisoquine. MR was similarly distributed in migraineurs and controls. Three subjects in each group were poor metabolizers (MR greater than 30, versus normal range, 0.1-12). MR in patients did not depend on type of migraine (common versus classic), attack frequency, the presence of trigger factors, smoking or a history of adverse reactions or sensitivity to medicines.
5%至10%的白种人存在肝脏细胞色素P450依赖的氧化缺陷。患偏头痛的比例与此相似。有一个假说得到了验证，即一种可能与潜在饮食诱因相关的氧化缺陷在偏头痛的发病机制中起作用。在37名偏头痛患者以及与其中26名患者年龄和性别匹配的26名对照者中，口服10毫克异喹胍后，异喹胍羟基化作为氧化状态的标志物，通过计算代谢率（MR）来确定：尿异喹胍/尿4-羟基异喹胍。MR在偏头痛患者和对照者中的分布相似。每组中有3名受试者是代谢缓慢者（MR大于30，正常范围为0.1 - 12）。患者的MR并不取决于偏头痛的类型（普通型与典型型）、发作频率、触发因素的存在、吸烟情况或不良反应史或对药物的敏感性。
