To the Editor.—
The failure by Walton et al (225:494, 1973) to demonstrate lymphocyte stimulation in subjects considered to have halothane hepatitis is predictable. Although the hepatic failure following halothane has been attributed to a hypersensitivity reaction by authorities,1,2 arguments for an immunological basis of halothane hepatitis are not convincing based on such observations as an increased incidence of repeated exposure, eosinophilia, fever, granuloma formation, arthralgia, rashes, and circulating antimitochondrial antibodies. These are all nonspecific signs and have not been helpful in elucidating a mechanism of hepatic cell damage following halothane.Halothane hypersensitivity has not been well documented. In only two cases have positive provocation studies been reported,3,4 and although temporal relationship of halothane administration to exacerbation of symptoms is suggestive, immunological studies demonstrating an immediate or delayed hypersensitivity reaction have not been documented.
Reves JG. Halothane Hepatitis. JAMA. 1973;226(5):565. doi:10.1001/jama.1973.03230050043017
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