Gatzen Markus, Pausch Jürgen
Medizinische Klinik I, Klinikum Kassel.
Med Klin (Munich). 2002 Mar 15;97(3):152-9. doi: 10.1007/s00063-002-1139-7.
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.
在胆汁淤积症中，有毒胆汁酸的胆汁分泌受损导致它们在肝脏中蓄积，进而引发肝衰竭。这种胆汁酸诱导的肝损伤可用无毒的熊去氧胆酸（UDCA）成功治疗。这种胆汁酸是由肠道细菌将鹅去氧胆酸进行7-β-差向异构化形成的。它占人类总胆汁酸池的1-3%。UDCA可降低有毒胆汁酸的肝细胞含量。这保护肝细胞免受有毒胆汁酸的损伤。治疗结果：已证实UDCA在原发性胆汁性肝硬化中的治疗效果。此外，许多其他胆汁淤积性肝病也受益于UDCA治疗。胆汁淤积性肝病，如原发性胆汁性肝硬化的自身免疫发病机制，可能显示出UDCA与免疫抑制物质联合治疗的额外有益效果。
