Testosterone and alcoholic cirrhosis. Epidemiologic, pathophysiologic and therapeutic studies in men.

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.