Pathogenesis of human cholesterol cholelithiasis.
The pathogenesis of cholesterol cholelithiasis in humans has been studied by means of three techniques. The cholesterol-solubilizing capacity of bile may be determined by estimation of the relative composition of the three major lipid constituents of bile. Consistent reduction in the cholesterol-carrying capacity of gallbladder bile of persons with gallstones when compared with normal subjects has not been shown. Normal subjects frequently have supersaturated bile. Secretion rates of biliary lipids have been estimated by two methods; with the method that appears to be more physiologic no change in lipid secretion rates was found in gallstone patients. Bile acid pool size has been measured by isotope dilution techniques; it is reduced in patients with gallstones. It is not clear whether this reduction is important in the pathogenesis of cholesterol cholelithiasis, for the bile acid secretion rate is normal because of an increased rate of cycling of the pool through the enterohepatic circulation. The role of the gallbladder in the genesis of cholesterol cholelithiasis may be more important than has been realized.
D001646:Bile / Q000032:analysis; D001647:Bile Acids and Salts / Q000032:analysis / Q000096:biosynthesis / Q000378:metabolism; D002769:Cholelithiasis / Q000209:etiology* / Q000378:metabolism; D002784:Cholesterol / Q000032:analysis; D005260:Female; D005704:Gallbladder / Q000503:physiopathology; D006801:Humans; D007422:Intestines / Q000098:blood supply; D008099:Liver / Q000378:metabolism; D008102:Liver Circulation; D008297:Male; D008722:Methods; D010713:Phosphatidylcholines / Q000378:metabolism; D010743:Phospholipids / Q000032:analysis; D011865:Radioisotope Dilution Technique; D012995:Solubility
D001647:Bile Acids and Salts; D010713:Phosphatidylcholines; D010743:Phospholipids; D002784:Cholesterol