20160531UDCA胆石症__培训课件.pptVIP

Anatomical abnormalities causing bile stasis might be major risk factors. Parasitic infection is also associated with primary duct stones as well as intrahepatic bile duct stones, particularly in Asia 胆管结石形成机制 Stone core formation is initiated by bacterial infection and subsequent bilirubin deconjugation Bile composition may eventually change to precipitate cholesterol Similarly, such precipitates and/or microcalculi can act as nuclei to induce bacterial colonization, which may in due course enhance precipitation of calcium bilirubinate or modify original cores. 胆管结石形成机制 a single gene defect causes bile duct and gallbladder stones in a defined subgroup – young, predominantly female patients with a recurring form of extrahepatic and intrahepatic cholelithiasis spontaneous occurrence of extrahepatic and intrahepatic gallstones in the Abcb4 knockout mouse model Gilbert variant of UDP glucuronosyltransferase 1A1 (UGT1A1) was also associated with pigment bile duct stones carriers might benefit from prevention with UDCA 遗传因素 The average risk of developing symptomatic gallstones is 2.0% to 2.6% per year The yearly incidence of complications is low (0.3%) The annual risk for gallbladder cancer is as low as 0.02% Treatment of asymptomatic patients with gallstones, is not routinely recommended 无症状胆囊结石 有症状胆囊结石 需要治疗：手术、ESWL或者（和）药物 连续5年没有症状的等同于没有症状的患者 微结石和胆泥更容易引起胆绞痛、胰腺炎等并发症 胆绞痛 早期非随机安慰剂对照研究提示UDCA可以减少胆绞痛发作【 Ann Intern Med 1982;97(3):351–6. 】【 Gut 1982;23(5):382–9 】 非随机的队列分析（n=527）提示UDCA可以明显减少无症状胆石症患者胆绞痛发作【 Hepatology 1999;30:6–13 】 随机双盲安慰剂对照研究提示UDCA不能减少有症状胆石症患者的胆绞痛发作【 Hepatology 2006;43(6):1276–83 】 溶石适应症 大约15%有症状的胆石症患者 直径小于0.5cm X线阴性 胆固醇含量超过80% 胆囊功能良好 1873年最早报道，1937年完全溶石报道 Chances of dissolution are higher if gallstones are small (less than 0.5 cm in size), not calcified (radiolucent on radiograph, including a computed tomography [CT] scan), cholesterol-enriched (ie, more than 80%), and contained within a functioning gallbladder with a patent cystic duct. Oral UDCA (at least