van Erpecum K J, van Berge Henegouwen G P
Department of Gastroenterology, University Medical Center Utrecht, PO Box 85500, 3508GA Utrecht, The Netherlands.
Dig Liver Dis. 2003 Jul;35 Suppl 3:S8-11. doi: 10.1016/s1590-8658(03)00086-0.
Apart from biliary cholesterol supersaturation, crystallization-promoting proteins and impaired postprandial gallbladder motility, the intestine may be an important factor in the pathogenesis of cholesterol gallstones. Prolonged intestinal transit could increase gallstone risk by enhancing formation in the intestinal lumen of the secondary hydrophobic and pro-lithogenic bile salt deoxycholate. Furthermore, in normal subjects there is an intimate relationship between gallbladder and intestinal motility in the fasting (interdigestive) state. In gallstone patients we found disordered intestinal motility, absent gallbladder contraction and abnormal release of the hormone motilin in the interdigestive state. These disturbances could contribute to gallstone formation.
除了胆汁胆固醇过饱和、促结晶蛋白以及餐后胆囊运动功能受损外,肠道可能是胆固醇胆结石发病机制中的一个重要因素。肠道运输时间延长可通过增强次级疏水性且促结石形成的胆盐脱氧胆酸盐在肠腔内的形成来增加胆结石风险。此外,在正常受试者中,禁食(消化间期)状态下胆囊与肠道运动之间存在密切关系。在胆结石患者中,我们发现在消化间期肠道运动紊乱、胆囊无收缩以及胃动素激素释放异常。这些紊乱可能促使胆结石形成。