Is Halothane Hepatitis Chronic Active Hepatitis?

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Abstract
Several corollaries stem from the alternative hypothesis that halothane hepatitis is actually chronic hepatitis. Review of the current status of the 4 challenged individuals, and of the literature, should provide evidence that will either support or not support the corollaries and, therefore, the alternative hypothesis. If any of the 4 challenged individuals had chronic active hepatitis when they were challenged, they should continue to show evidence of this usually steadily progressive disease. If the nonspecific stress of either a short, deliberate non-clinical exposure or an occupational exposure to anesthetic agents can exacerbate chronic active hepatitis within 24 h, it might be expected that the inordinately greater nonspecific stress of clinical anesthesia and operation would commonly produce a similar immediate exacerbation. If psychic trauma can contribute to exacerbation of chronic active hepatitis, additional evidence and opinion to support the existence of such psychosomatic hepatitis should be available. If the alternative hypothesis is true, one might expect evidence of patients who, having had unexplained hepatitis after exposure to halothane, had chronic active hepatitis, and when exposed subsequently to nonhalothane anesthesia were observed to have postoperative hepatitis again. If the alternative hypothesis is true, one might also expect evidence of health-care workers with chronic active hepatitis in whom hepatitis developed upon occupational exposure to anesthetic agents other than halothane. Follow-up of the 4 challenged individuals through personal communications reveals that all 4 remain in good health, 9, 7 and 5 yr and 12 mo. after challenge, and that 3 have recently had hepatic function tests, with results within normal limits. The physicians who attended the challenged individuals, 3 of whom had undergone liver biopsy, do not believe that their patients have chronic active hepatitis. One of the anesthetists underwent liver biopsy 4 yr after his challenge. This revealed a remarkable regression of the fibrosis and nodule formation that had been seen in the multiple liver biopsies obtained during his illness, while evidence of scarring had developed. The test for HBSAg (Australia antigen) was negative at the time of the illness in 2 of the individuals and was negative 9 yr after the challenge in a third. The test was also performed on 6 stored frozen serum samples taken from the fourth individual during and after his illness, and was negative in each.

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