Nakashima T, Sano A, Seto Y, Nakajima T, Shima T, Sakamoto Y, Okuno T, Kashima K, Hasegawa T
Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
Hepatology. 1990 Feb;11(2):255-60. doi: 10.1002/hep.1840110215.
Urinary bile acids from 20 patients treated with chenodeoxycholate, 18 treated with ursodeoxycholate, 15 treated with rifampicin and 8 patients with advanced cirrhosis were analyzed by gas-liquid chromatography and gas-liquid chromatography-mass spectrometry. Occurrence rates and amounts of three so-called unusual trihydroxy bile acids, hyocholate, ursocholate and omega-muricholate, were increased in patients treated with chenodeoxycholate, ursodeoxycholate or rifampicin and decreased in cirrhotic patients as compared with those in untreated healthy adults. These data suggest that chenodeoxycholate and ursodeoxycholate are hydroxylated to produce unusual trihydroxy bile acids in bile acid-loaded humans and that this metabolism may be related to the induction of hepatic microsomal enzymes by rifampicin. In contrast, the hydroxylation of chenodeoxycholate and ursodeoxycholate may be impaired by severe hepatic damage. Because the urine is a secretory pathway for internal bile acids, the occurrence of unusual trihydroxy bile acids in the urine may be used as an indicator of hepatic ability to metabolize "hydrophobic" dihydroxy bile acids to their secretory forms.
采用气液色谱法和气液色谱 - 质谱联用法分析了20例接受鹅去氧胆酸治疗的患者、18例接受熊去氧胆酸治疗的患者、15例接受利福平治疗的患者以及8例晚期肝硬化患者的尿胆汁酸。与未治疗的健康成年人相比，接受鹅去氧胆酸、熊去氧胆酸或利福平治疗的患者中，三种所谓的异常三羟基胆汁酸，即猪胆酸、熊胆酸和ω-鼠胆酸的发生率和含量增加，而肝硬化患者中则降低。这些数据表明，在胆汁酸负荷的人体内，鹅去氧胆酸和熊去氧胆酸被羟基化以产生异常的三羟基胆汁酸，并且这种代谢可能与利福平诱导肝微粒体酶有关。相比之下，严重的肝损伤可能会损害鹅去氧胆酸和熊去氧胆酸的羟基化。由于尿液是内源性胆汁酸的分泌途径，尿液中异常三羟基胆汁酸的出现可用作肝脏将“疏水性”二羟基胆汁酸代谢为其分泌形式能力的指标。
