20160531UDCA胆石症.pptVIP

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 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 a cholesterol saturation index of less than 1 cholesterol crystallization can be prevented because more cholesterol can be transported within vesicles that contain mainly phospholipids and cholesterol and little bile acid reduction of intestinal absorption of cholesterol a better contractility of the stimulated gallbladder smooth muscle Excess biliary cholesterol might provide the basis for stimulation of inflammatory cells in the gallbladder Following complete dissolution, UDCA should be continued for another 3 mo in order to confirm decomposition of microscopic stones that may not be detected by ultrasonography. Absence of, or minimal, change in gallstone diameter within 6 to 12 mo of UDCA treatment represents a poor prognostic sign for dissolution UDCA administration within 3 to 6 mo prevented gallstone recurrence and more episodes of pancreatitis over a follow-up of 44 mo in idiopathic acute pancreatitis 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 compositio