Circulating immune complexes appearing in Goodpasture's syndrome.

Recently Bartoli et all described a patient with acute hepatic necrosis that occurred two days after treatment with hydrallazine 50 mg daily. The diagnosis was supported by biopsy and rechallenge with the drug. The patient was definitely jaundiced and complained of right upperquadrant pain with nausea and vomiting. We think that our case is important because it provides corroborative evidence of an acute hepatitis-like reaction caused by hydrallazine, in this instance without symptoms. Liver function tests may not routinely be performed during follow-up of patients taking hydrallazine, and the long-term effect of this otherwise unsuspected biochemical disturbance is unknown. The recent findings of unrecognised hydrazine metabolites in the urine of patients receiving hydrallazine2 indicates a possible aetiology in this case. Hydrazine and acetylhydrazine are known to be involved in hepatotoxic reactions-the latter is thought to be responsible for mediating isoniazid-induced liver damage via microsomal oxidation to a reactive hepatotoxic intermediate.3 Our patient was a rapid acetylator, which may have increased the risk of acetylhydrazineinduced hepatic necrosis, although this is presently disputed in the case of isoniazid.4 Exposure to microsomal enzyme inducers may also increase the risk, although our patient was not exposed to any such drugs. Further evaluation of abnormal liver function tests in asymptomatic patients receiving hydrallazine is indicated.