Androgeninduced liver disorders

A consistent adverse feature of pharmacological androgen therapy, regardless of indication, is the risk of androgen-induced liver disorders (Ishak and Zimmerman 1987). These involve biochemical effects on hepatic function, hepatotoxicity (hepatitic or cholestatic) and liver tumor development (benign or malignant) and peliosis hepatis. These risks are a class-specific adverse effect of 17a-alkylated androgens, especially when used orally but no reliable estimates of the incidence or prevalence are available. The East German national sports doping programme involving oral 17a-alkylated androgens resulted in deaths from liver failure and chronic liver disease (Franke and Berendonk 1997). Every marketed 17a-alkylated androgen is associated with hepatotoxicity, whereas other androgens (1-methyl androgens, nandrolone, testosterone, dihydrotestosterone) are not hepatotoxic. Cholestasis and functional impairment of liver function (BSP retention, antipyrine clearance) are consistently impaired by oral 17a-alkylated androgens. Androgen-induced hepatitis and tumours are less frequent but unpredictable. If claims that low-dose methyltestosterone used in post-menopausal women has minimal hepatotoxicity risk (Gelfand and Wiita 1997; Gitlin etal. 1999; Simon 2001) are correct, then the therapeutic index is low and such safer doses would be ineffective in men. Blood SHBG concentrations are significantly reduced by any oral androgen as well as supra-physiological circulating testosterone concentrations in peripheral or portal blood (Conway etal. 1988). This indicates that SHBG can serve as a useful, sensitive index of hepatic androgen over-dosage.

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