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非甾体抗炎药诱导家族性腺瘤性息肉病患者息肉消退

NSAID-induced polyp regression in familial adenomatous polyposis patients.

作者信息

Giardiello F M

机构信息

Deparment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

出版信息

Gastroenterol Clin North Am. 1996 Jun;25(2):349-62. doi: 10.1016/s0889-8553(05)70251-x.

Abstract

NSAIDs inhibit prostaglandin synthesis. In 1983, Waddell et al first reported that sulindac, a NSAID (Clinoril), caused regression of rectal adenomatous polyps in several patients with familial adenomatous polyposis, an inherited form of colorectal cancer. Subsequently, NSAIDs have been used as chemopreventive agents in animal carcinogenesis models and adenoma regression had been confirmed in human trials with sulindac. This article summarizes these developments and describes possible mechanisms of colorectal neoplasia chemoprevention.

摘要

非甾体抗炎药可抑制前列腺素的合成。1983年,沃德尔等人首次报告称,一种非甾体抗炎药舒林酸(商品名奇诺力)可使数名家族性腺瘤性息肉病(一种遗传性结直肠癌)患者的直肠腺瘤性息肉消退。随后,非甾体抗炎药已被用作动物致癌模型中的化学预防剂,并且在舒林酸的人体试验中已证实腺瘤可消退。本文总结了这些进展,并描述了结直肠肿瘤化学预防的可能机制。

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