Gonadal function in male patients with alcoholic and non-alcoholic liver disease.

Gonadal function in male patients with various liver disease has been evaluated by basal plasma testosterone level and a response of plasma testosterone to human chorionic gonadotropin. Compared with healthy male subjects of similar age, gonadal function was not reduced in chronic hepatitis, but in alcoholic liver disease without cirrhosis and in alcoholic and non-alcoholic cirrhosis. Gonadal dysfunction in patients with chronic hepatitis and cirrhosis was correlated with abnormal liver tests. It may be concluded that gonadal function in chronic liver disease is reduced either by alcohol abuse or disturbances of hepatic function and/or hepatic hemodynamics.

Acute and chronic effect of ethanol on hepatic albumin synthesis in rat liver in vitro.

To study the effects of ethanol and its metabolite on albumin metabolism, we examined the hepatic albumin synthesis and secretion in male Wistar rats in vitro, following acute and chronic ethanol administration. After acute ethanol administration, proalbumin synthesis in rat liver in vitro, declined to 47% of the control level at 4 hrs, the lowest level, and increased thereafter to slightly higher than the control level at 16 hrs. On the other hand, chronic ethanol administration for 4 weeks, increased proalbumin synthesis to 1.5 times that of the control level. In the acute ethanol group, a significant negative correlation was observed between proalbumin radioactivity and the concentration of hepatic ethanol and acetaldehyde. The variation between proalbumin radioactivity and hepatic ethanol concentration was wider than the variation between proalbumin and hepatic acetaldehyde. In the chronic ethanol group, ethanol was not detected in the liver. No significant differences from the proalbumin/albumin ratio were seen at any time point after acute or chronic ethanol administration. These findings suggest that the effects of ethanol on hepatic albumin synthesis differ with the method of ethanol administration, and acetaldehyde and/or ethanol is involved in the reduction in albumin synthesis, however, proalbumin-albumin conversion is not disturbed.

Intravenous dehydrocholate tolerance test in patients with liver disease.

The disappearance of intravenously administered dehydrocholate was studied in 13 healthy subjects and 23 patients with chronic liver disease. Serum dehydrocholate was determined by the enzymatic method using 3 alpha-hydroxysteroid dehydrogenase. Following the loading dose of dehydrocholate, serum dehydrocholate and 3 alpha-hydroxy bile acid were assayed at five minute intervals for 15 minutes. During this 15 minute period, dehydrocholate decreased and 3 alpha-hydroxy bile acid increased. The disappearance of the dehydrocholate was delayed in patients with chronic liver disease, and the 5-minute retention value was significantly high in cirrhosis patients.

Mechanism of the protective action of thiol compounds in ethanol-induced liver injury.

The protective action of cysteine or mercaptopropionylglycine (MPG) in acute ethanol-induced liver injury has been investigated in the rat. Cysteine accelerated clearance of ethanol and acetaldehyde from blood and liver and prevented an increase in hepatic content of triglyceride and serum ornithine carbamoyl transferase activity. MPG accelerated clearance of ethanol and acetaldehyde less efficiently but prevented an increase in these variables to the same degree. The mode of action of thiol compounds in acute ethanol-induced liver injury has been discussed.

[Radioimmunoassay of cholylglycine in serum (author's transl)].

Serum levels of cholylglycines (CG) were determined by radioimmunoassay and that of total bile acids (TBA) by enzymatic method. In normal subjects, serum levels of CG, TBA and CG/TBA ratio were 0.6 +/- 0.4 micronM, 7 +/- 2 micronM and 0.08 +/- 0.06, respectively. They were increased markedly in acute hepatitis and moderately in chronic hepatitis and cirrhosis. Thus, measurement of serum CG as compared with serum TBA appears to be a sensitive liver test.