Bremmelgaard A, Ranek L, Bahnsen M, Andreasen P B, Christensen E
Scand J Gastroenterol. 1983 Sep;18(6):797-802. doi: 10.3109/00365528309182097.
In 33 patients with acute hepatic encephalopathy due to toxic or viral hepatitis the following analyses were performed: (24-14C)cholic acid conjugation and sulfation, plasma phenazone clearance, galactose elimination capacity, and concentrations of glycocholic acid and glycolithocholic acid sulfate in plasma. The (24-14C)cholic acid conjugation in patients with viral hepatitis was significantly lower in fatal cases than in patients who survived (p less than 0.002). In these patients the galactose elimination capacity and the plasma phenazone clearance were insignificantly lower. Tauro-(24-14C)cholic acid was the predominant metabolite of (24-14C)cholic acid in six patients, but in four patients with toxic hepatitis this metabolite was only found in trace amounts. Sulfation after 3 h of (24-14C)cholic acid accounted for 0-8.2% of the administered dose. The sulfate of glycolithocholic acid was found in the plasma of all patients. No survival limit with regard to the capacity for the (24-14C)cholic acid conjugation could be defined.
对33例因中毒性或病毒性肝炎导致急性肝性脑病的患者进行了以下分析:(24-¹⁴C)胆酸结合与硫酸化、血浆非那宗清除率、半乳糖清除能力以及血浆中甘氨胆酸和甘氨石胆酸硫酸盐的浓度。病毒性肝炎患者中,致命病例的(24-¹⁴C)胆酸结合显著低于存活患者(p<0.002)。这些患者的半乳糖清除能力和血浆非那宗清除率略低。牛磺-(24-¹⁴C)胆酸是6例患者中(24-¹⁴C)胆酸的主要代谢产物,但在4例中毒性肝炎患者中,仅微量发现该代谢产物。(24-¹⁴C)胆酸3小时后的硫酸化占给药剂量的0-8.2%。所有患者血浆中均发现甘氨石胆酸硫酸盐。无法确定(24-¹⁴C)胆酸结合能力的生存极限。