Zeneroli M L, Venturini I, Avallone R, Farina F, Miglioli L, Cosenza R, Amedei R, Ardizzone G, Centanaro M, Arrigo A, Baraldi M
Department of Internal Medicine, University of Modena, Italy.
Ital J Gastroenterol Hepatol. 1997 Oct;29(5):456-8.
The pathogenetic agents which cause encephalopathy due to fulminant hepatic failure are still under debate. Ammonia and benzodiazepine-like compounds are two of the most important agents considered, so far. Herein, we report the levels of benzodiazepine-like compounds in serum and in urine and of venous ammonia measured during the course of the disease (30 days). The patient rapidly developed stage IV encephalopathy with high levels of ammonia and with only a slight increase of benzodiazepine-like compounds. At that moment, the levels of these compounds were similar to those recorded in the blood when the patient regained full consciousness 28 days later. During the course of the disease, there was a 10-fold increase of benzodiazepine-like compounds in serum which was recorded in parallel with an impaired excretion due to oliguria. This observation seems to indicate that encephalopathy may develop in the absence of significantly increased levels of these compounds and that their episodic increase during fulminant hepatic failure may be an epiphenomenon linked with several factors such as impaired renal function.
导致暴发性肝衰竭所致肝性脑病的致病因素仍存在争议。氨和苯二氮䓬类化合物是目前认为最重要的两种因素。在此，我们报告了疾病过程（30天）中血清和尿液中苯二氮䓬类化合物的水平以及静脉血氨水平。该患者迅速发展为IV期肝性脑病，血氨水平很高，而苯二氮䓬类化合物仅略有升高。当时，这些化合物的水平与患者28天后完全恢复意识时血液中记录的水平相似。在疾病过程中，血清中苯二氮䓬类化合物增加了10倍，这与少尿导致的排泄受损同时出现。这一观察结果似乎表明，在这些化合物水平未显著升高的情况下也可能发生肝性脑病，并且它们在暴发性肝衰竭期间的间歇性增加可能是一种与肾功能受损等多种因素相关的附带现象。
