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[酒精摄入与高尿酸血症]

[Alcohol ingestion and hyperuricemia].

作者信息

Yamanaka H

机构信息

Institute of Rheumatology, Tokyo Women's Medical College.

出版信息

Nihon Rinsho. 1996 Dec;54(12):3369-73.

PMID:8976122
Abstract

Purine nucleotide degradation during ethanol catabolism, inhibition of renal excretion of urate by lactic acid, and high purine content of certain kinds of beverage are responsible for the elevation of serum uric acid level following alcohol drinking. It is well documented that rapid consumption of ATP produces uric acid via purine nucleotide degradation. Since individuals with ALDH21 can catalyze ethanol readily, they consume large amount of ATP, and thus produce more hypoxanthine than those with ALDH22. Thus, daily drinker and heavy drinker tend to readily induce hyperuricemia after alcohol ingestion. A high purine content in beer may contribute to the increasing frequency of hyperuricemia. Restriction of any kind of alcohol beverages, especially beer, is necessary in the medical control of patients with gout or hyperuricemia.

摘要

乙醇分解代谢过程中的嘌呤核苷酸降解、乳酸对尿酸肾脏排泄的抑制以及某些饮料的高嘌呤含量,是饮酒后血清尿酸水平升高的原因。有充分的文献记载,ATP的快速消耗通过嘌呤核苷酸降解产生尿酸。由于携带ALDH21的个体能够轻易催化乙醇,他们消耗大量ATP,因此比携带ALDH22的个体产生更多次黄嘌呤。因此,每日饮酒者和酗酒者在摄入酒精后往往容易诱发高尿酸血症。啤酒中的高嘌呤含量可能导致高尿酸血症的发病率增加。在痛风或高尿酸血症患者的医学管理中,限制任何种类的酒精饮料,尤其是啤酒,是必要的。

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