The present review summarizes the pathogenic mechanisms leading to variation of plasma
testosterone concentrations, consequences of hypoandrogenization and hyperoestrogenization, and effects of oral
testosterone treatment in men with
alcoholic cirrhosis. These patients have normal median plasma
testosterone concentrations, but 20% have values above and 20% have values below the normal limits. The majority of patients have raised
sex hormone binding globulin (SHBG) concentrations. This increase accounts for the supranormal plasma
testosterone concentrations. With decreasing liver function, plasma
testosterone concentrations decrease significantly. The combination of increased SHBG levels and decreasing liver function leads to low or subnormal plasma concentrations of non-
protein bound and non-SHBG bound
testosterone. This decrease, together with raised oestrogen concentrations, may explain the increased prevalence of
gynecomastia and testicular
atrophy which raises with decreasing liver function. Oral
testosterone treatment of alcoholic cirrhotic men produces an increase in the plasma concentrations of
testosterone,
androstenedione and
dihydrotestosterone, but oestrogen concentrations increase as well. Oral
testosterone treatment significantly reduces the prevalence of
gynecomastia, but is without significant effects on liver biochemistry, morphology, haemodynamics, and function, general well being, sexual dysfunction and survival of alcoholic cirrhotic men. A pooled estimate of the mortality risk of cirrhotic patients treated with
anabolic-androgenic steroids does not disclose any significant difference compared with placebo treatment (relative risk 0.98; 95% confidence limits 0.77-1.22). Seldom, but serious, side-effects of oral
testosterone treatment can not be excluded.