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Sera from 40 patients with a clinical diagnosis of halothane-associated hepatitis were tested for the presence of antibodies to the trifluoroacetate (TFA) halothane metabolite hapten using an ELISA assay, with TFA-albumin as the antigen. Positive results were obtained in 30% of cases of which 3/4 with encephalopathy were positive and 9/36 non-fulminant cases were positive. Antibody specificity to the TFA hapten was confirmed in each positive result by a 'hapten inhibition' experiment in which TFA albumin binding was blocked by preincubation of serum with TFA-lysine. Most probably this assay detects a relatively low affinity cross-reaction with the TFA hapten of antibodies in the patients' sera which are directed against specific TFA-labelled liver proteins. Anti-TFA-albumin antibodies were not detected in 28 normal subjects, 5 subjects with fulminant hepatic failure secondary to other causes, 6 subjects with a history of 2 or more exposures to halothane but with no evidence of liver disease and 28 patients with a variety of chronic liver diseases. It is concluded that ELISA testing using trifluoroacetylated rabbit serum albumin (TFA-RSA) as antigen is a quick and convenient assay for the confirmation of halothane-associated hepatitis in fulminant hepatic failure secondary to halothane, but is less sensitive when the illness follows a milder course.

Five chronic carriers of hepatitis B virus developed a fulminant hepatitis-like picture when immunosuppression or cytotoxic treatment, given for unrelated disorders, was withdrawn. Viral replication at the time of the final illness was confirmed in three of the five cases by measurement of serum HBV DNA or the presence of HBc antigen on liver biopsy. A cytoplasmic and nuclear pattern of HBc was seen in histological material during life, but at post-mortem was limited to a nuclear distribution, suggesting greater destruction of hepatocytes containing cytoplasmic HBc. In two of the cases, chronic liver disease was found at post-mortem, there being no previous clinical or laboratory abnormality, but it is unlikely that this was a factor in the development of the superimposed fulminating hepatitis-like illness. Immunosuppressive and cytotoxic agents must be used with extreme caution in any hepatitis B carrier, as withdrawal can precipitate acute decompensation regardless of whether or not there is underlying chronic liver disease.