【2017年整理】20160531UDCA胆石症.ppt

UDCA在胆石症中的应用进展;西方国家：10%~15%，中国：0.9%~10% 美国2000年60亿美元，中国：？ 欧美胆固醇结石75%，中国：52%~79% ;易感因素;The complex pathogenesis of cholesterol gallstones depends on the concurrent existence of hepatic hypersecretion of cholesterol into bile, leading to bile supersaturation with cholesterol, accelerated nucleation/crystallization of cholesterol in gallbladder bile, impaired gallbladder motility leading to gallbladder stasis, and increased cholesterol availability from the small intestine;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;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.;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;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% ;有症状胆囊结石;胆绞痛;溶石适应症;Oral UDCA (at least 10 mg/kg/d) results in an increased proportion of biliary UDCA in bile (from less than 8%–10% of biliary bile acid pool to about 40%). Increasing biliary UDCA, in turn, results in a decreased hepatic secretion of biliary cholesterol and the formation of unsaturated gallbladder bile (ie, containing less cholesterol in solution) with