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Excessive ethanol ingestion induces hypoandrogenism in male subjects. To confirm its presence and to study its relationship with the degree of liver damage and alcohol abstinence, plasma sex hormones were measured in alcoholic patients without liver failure, after two different abstinence periods. Patients were 30 male chronic alcoholics admitted to the Alcoholism Ward for treatment of their addiction. On admission, we measured: testosterone (T), estradiol (E), follicle stimulating hormone (FSH), luteinizing hormone (LH) and sex-hormone binding globulin (SHBG). A liver biopsy was also performed. These measurements were repeated at discharge and were also done in 15 normal volunteers. On admission (mean abstinence 1.9 +/- 1.7 days) total T was similar to controls, FSH was lower (p0.02) and high levels of SHBG were found (3.5 fold increase, as compared to controls). Histologically, 9 patients had normal liver; 14 had moderate alterations and 7 showed marked alterations. Hormonal values were not different in these 3 groups. At discharge, 11.1 +/- 4.7 days after admission, T, E and FSH did not show significant changes but LH decreased (8.2 +/- 5.2 mIU/ml vs 12.9 +/- 4.1, p0.001); SHBG also decreased (65.4 +/- 21.6 nmol/l vs 117.2 +/- 33.3, p0.001) to values that still were twice those of controls. It is concluded that alcoholic patients without clinical signs of liver failure have normal plasma testosterone levels, irrespective of their histologic liver alterations and high plasma SHBG levels that decreased significantly after a short abstinence. The concomitant LH decrease suggests that hypoandrogenism is likely in these patients. Fast changes in SHBG levels rise the possibility that this protein is candidate marker of alcoholism.

The rate of ethanol metabolism (EMR) was determined in alcoholic patients with or without hepatic necrosis, steatosis, and/or cirrhosis. Fifty six cases were studied after 9-25 days of abstinence (mean 15 days). A significant increase in EMR (P less than 0.01) was found in alcoholics with hepatic necrosis (265 +/- 20.5 mg/kg/hr) compared with alcoholics with normal liver histology (154 +/- 17) and nonalcoholic controls (159 +/- 15). In alcoholics with liver steatosis but without necrosis a lesser increase in EMR (207 +/- 20, P less than 0.05 was also observed. Patients with slight fibrosis but without other abnormalities in their liver biopsies and cirrhotics with overt liver failure (jaundice, ascites) showed EMR similar to controls.