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胆结石的发病机制。

Pathogenesis of gallstones.

机构信息

Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, The Netherlands.

出版信息

Gastroenterol Clin North Am. 2010 Jun;39(2):171-83, vii. doi: 10.1016/j.gtc.2010.02.010.

DOI:10.1016/j.gtc.2010.02.010
PMID:20478481
Abstract

Cholesterol gallstone formation is a complex process and involves phase separation of cholesterol crystals from supersaturated bile. In most cases, cholesterol hypersecretion is considered the primary event in gallstone formation. The sterol is transported through the hepatocytic canalicular membrane by ABCG5-G8. Expression of this transport protein is regulated by transcription factor Liver X Receptor-alpha, which may be responsible for biliary hypersecretion. Hydrophobic bile salt pool, bile concentration, excess pronucleating mucin, and impaired gallbladder and intestinal motility are secondary phenomena in most cases but nevertheless may contribute to gallstone formation.

摘要

胆固醇结石的形成是一个复杂的过程,涉及胆固醇晶体从过饱和胆汁中的相分离。在大多数情况下,胆固醇分泌过多被认为是胆石形成的主要事件。固醇通过 ABCG5-G8 经肝细胞管腔膜转运。这种转运蛋白的表达受转录因子肝 X 受体-α调节,它可能是胆汁分泌过多的原因。疏水性胆盐池、胆汁浓度、过量的始核粘蛋白以及胆囊和肠道运动功能障碍在大多数情况下是次要现象,但仍可能促成胆石形成。

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