MODE OF ACTION OF URSODEOXYCHOLIC ACID: In cholestasis, the impaired biliary secretion of toxic bile acids causes their accumulation in the liver and a subsequent hepatic failure. This bile acid-induced liver damage can be treated successfully with the atoxic ursodeoxycholic acid (UDCA). This bile acid is formed by 7-beta-epimerization of chenodeoxycholic acid by intestinal bacteria. It represents 1-3% of the total human bile acid pool. The hepatocellular content of toxic bile acids is reduced by UDCA. This protects the liver cell from injury by toxic bile acids. THERAPEUTIC RESULTS: The therapeutic effect of UDCA in primary biliary cirrhosis has been demonstrated. Furthermore, numerous other cholestatic liver diseases benefit from UDCA treatment. The autoimmune pathogenesis of cholestatic liver diseases, e.g., primary biliary cirrhosis, might reveal an additional beneficial effect of a combination therapy with UDCA and immunosuppressive substances.
The clinical-biochemical syndrome of cholestasis is characterized by an alteration in bile constituents. As a consequence, the concentrations of bilirubin, bile acids, phospholipids and cholesterol are elevated. The main clinical symptoms of cholestasis are icterus and pruritus, and in severe cases xanthelasma and xanthoma. Primary intrahepatic cholestasis, caused by impaired bile secretion in the liver, should be separated from the extrahepatic secondary cholestasis which is a consequence of a biliary obstruction. This paper evaluates the therapy of liver diseases which developed as consequence of a primary disturbance in bile secretion.
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