Drug-induced chronic active hepatitis is an important lesion. In any patient with the syndrome of chronic active hepatitis, the possibility of a drug as the cause should be a foremost consideration. No drug, taken regularly, should be dismissed as possible etiology, without testing the effects of withdrawal and readministration. Indeed, progression of chronic active hepatitis after withdrawal of the presumably responsible drug probably should be interpreted as exonerating the drug. Drug-induced chronic cholestasis differs in several regards from the syndrome of chronic activje hepatitis. In most of the reported cases, exposure prior to development of overt hepatic injury had been relatively brief (less than 1 month), and the drug had been stopped with the appearance of jaundice. Continued administration in the face of jaundice may be an important factor in worsening the injury, but the severity of illness shows little or no abatement on withdrawal of the drug in most cases, and the syndrome may persist for years. The non-neoplastic chronic lesions have acute counterparts. Drugs that can lead to the syndrome of chronic active hepatitis can cause hepatocellular as an acute lesion. Drugs that lead to the syndrome of primary biliary cirrhosis produce cholestatic injury as the acute lesion. Cirrhosis may be the end result of steatosis, acute necrosis, chronic active hepatitis, subacute hepatic necrosis, or phospholipidosis. The ultimate significance of the apparent tumorigenic effects of the contraceptive and anabolic steroids remains to be evaluated. In the opinion of this author, it is a clear expression of the impropriety of the use of anabolic steroids for trivial purposes such as improved muscular performance. Its relevance to the contraceptive use of steroids must be considered in the light of the many millions of women who have used these agents and the relatively small number of tumors identified thus far.
