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吉尔伯特综合征患者的N-乙酰化和异喹胍羟基化多态性

N-acetylation and debrisoquine hydroxylation polymorphisms in patients with Gilbert's syndrome.

作者信息

Siegmund W, Fengler J D, Franke G, Zschiesche M, Eike O, Eike E, Meisel P, Wulkow R

机构信息

Department of Clinical Pharmacology, University of Greifswald, Germany.

出版信息

Br J Clin Pharmacol. 1991 Oct;32(4):467-72. doi: 10.1111/j.1365-2125.1991.tb03932.x.

Abstract
  1. N-acetylation and debrisoquine hydroxylation phenotypes were determined in 54 patients with Gilbert's syndrome and in 247 (sulphamethazine) and 76 (debrisoquine) non-related healthy volunteers. 2. Forty (74.1%) of the patients and 135 (54.7%) of the healthy volunteers were slow acetylators (chi 2 = 6.87). In the patients, the cumulative urinary excretion of sulphamethazine up to 6 h (Ae(0,6)) was significantly lower. No differences in the frequency of debrisoquine poor metabolizers were observed: Gilbert's syndrome 5/54 (9.3%), healthy volunteers 5/76 (6.6%). The metabolic ratios were similar in both groups as well as the urinary recoveries of debrisoquine and its 4-hydroxy metabolite. 3. Gilbert's syndrome seems to be related in some way to N-acetylation but not to the debrisoquine hydroxylation polymorphism.
摘要
  1. 对54例吉尔伯特综合征患者以及247名(涉及磺胺二甲嘧啶)和76名(涉及异喹胍)无关健康志愿者测定了N - 乙酰化和异喹胍羟基化表型。2. 患者中有40例(74.1%)以及健康志愿者中有135例(54.7%)为慢乙酰化者(卡方 = 6.87)。患者中,磺胺二甲嘧啶至6小时的累积尿排泄量(Ae(0,6))显著更低。在异喹胍代谢不良者的频率上未观察到差异:吉尔伯特综合征患者5/54(9.3%),健康志愿者5/76(6.6%)。两组的代谢率以及异喹胍及其4 - 羟基代谢物的尿回收率相似。3. 吉尔伯特综合征似乎在某种程度上与N - 乙酰化有关,但与异喹胍羟基化多态性无关。

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Hepatic uptake defect in patients with "Gilbert's disease".
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