Holm E, Sedlaczek O, Grips E
Department of Pathophysiology, Medical Clinic I Mannheim, University of Heidelberg, Germany.
Curr Opin Clin Nutr Metab Care. 1999 Jan;2(1):47-53. doi: 10.1097/00075197-199901000-00009.
The impairment of transsulphuration during methionine degradation in hepatic failure can be counteracted by treatment with S-adenosylmethionine. Regarding the pathogenesis of hepatic encephalopathy, no convincing evidence exists for tryptophan, glutamine or glutamate being involved. Portal-systemic shunting-induced hyperammonaemia may reduce plasma branched-chain amino acids. The glucose effect on urea synthesis does not exist in cirrhosis.
肝衰竭时蛋氨酸降解过程中跨硫化作用的损害可通过用S-腺苷甲硫氨酸治疗来抵消。关于肝性脑病的发病机制，没有令人信服的证据表明色氨酸、谷氨酰胺或谷氨酸参与其中。门体分流引起的高氨血症可能会降低血浆支链氨基酸水平。肝硬化时不存在葡萄糖对尿素合成的影响。
