The clinical spectrum of isoniazid-induced liver injury seems to be clinically, biochemically, and histologically indistinguishable from viral hepatitis, except that the injury occurs primarily in persons older than 35 years. A possible relation between susceptibility of patients to isoniazid liver injury and rapid metabolism (acetylation) of the drug has been found. Examination of isoniazid metabolites showed that patients with rapid acetylator phenotype hydrolyze much more isoniazid to isonicotinic acid and the free hydrazine moiety than do slow acetylators. The hydrazine moiety liberated from isoniazid is primarily acetylhydrazine, and studies in animals show this metabolite to be converted to a potent acylating agent that produces liver necrosis. It seems likely that formation of chemically reactive metabolites is also the biochemical event initiating isoniazid liver injury in man. Recognition of the seriousness of isoniazid hepatic injury, not readily accepted at first, has led to revisions in the uses of isoniazid prophylaxis.

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We tested the hypothesis that donor blood containing antibody to hepatitis B core antigen (anti-HBc) but lacking detectable hepatitis B surface antigen (HBsAg) and antibody (anti-HBs)might transmit Type B hepatitis by examining donor and recipient serums from a Veterans Administration study of post-transfusion hepatitis. Donor blood was available from three patients with Type B hepatitis and from one patient with hepatitis B virus infection (development of anti-HBs and anti-HBc) without symptomatic disease. All four had received 1 unit of blood with high titer of anti-HBc but lacking HBsAg and anti-HBs. In contrast, no such units had been transfused into nine patients with "immunization-like" response (development of anti-HBs without anti-HBc) or into 26 control patients. These data stress the importance of anti-HBc as an indicator of hepatitis B virus infection and support the hypothesis that high-titer anti-HBc-positive blood might be infectious.

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