Drug Metabolism and Genetic Polymorphism in Subjects with Previous Halothane Hepatitis

L. Ranek Dept. of Internal Medicine A, Dept. of Clinical Chemistry, and Dept. of Clinical Immunology, Rigshospitalet, and Dept. of Pharmacology, Medical Faculty, University of Copenhagen, Copenhagen, Denmark; Dept. of Clinical Pharmacology, University of Odense, Odense, Denmark

K. Dalhoff Dept. of Internal Medicine A, Dept. of Clinical Chemistry, and Dept. of Clinical Immunology, Rigshospitalet, and Dept. of Pharmacology, Medical Faculty, University of Copenhagen, Copenhagen, Denmark; Dept. of Clinical Pharmacology, University of Odense, Odense, Denmark

H. Enghusen Poulsen Dept. of Internal Medicine A, Dept. of Clinical Chemistry, and Dept. of Clinical Immunology, Rigshospitalet, and Dept. of Pharmacology, Medical Faculty, University of Copenhagen, Copenhagen, Denmark; Dept. of Clinical Pharmacology, University of Odense, Odense, Denmark

K. Brøsen Dept. of Internal Medicine A, Dept. of Clinical Chemistry, and Dept. of Clinical Immunology, Rigshospitalet, and Dept. of Pharmacology, Medical Faculty, University of Copenhagen, Copenhagen, Denmark; Dept. of Clinical Pharmacology, University of Odense, Odense, Denmark

H. Flachs Dept. of Internal Medicine A, Dept. of Clinical Chemistry, and Dept. of Clinical Immunology, Rigshospitalet, and Dept. of Pharmacology, Medical Faculty, University of Copenhagen, Copenhagen, Denmark; Dept. of Clinical Pharmacology, University of Odense, Odense, Denmark

S. Loft Dept. of Internal Medicine A, Dept. of Clinical Chemistry, and Dept. of Clinical Immunology, Rigshospitalet, and Dept. of Pharmacology, Medical Faculty, University of Copenhagen, Copenhagen, Denmark; Dept. of Clinical Pharmacology, University of Odense, Odense, Denmark

P. Wantzin Dept. of Internal Medicine A, Dept. of Clinical Chemistry, and Dept. of Clinical Immunology, Rigshospitalet, and Dept. of Pharmacology, Medical Faculty, University of Copenhagen, Copenhagen, Denmark; Dept. of Clinical Pharmacology, University of Odense, Odense, Denmark

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Abstract

To test the hypothesis that halothane hepatitis is caused by a combination of altered drug metabolism and an immunoallergic disposition, the metabolism of antipyrine, metronidazole, sparteine, phenytoin, and racemic R- and S-mephenytoin was investigated in seven subjects with previous halothane hepatitis. The HLA tissue types and the complement C3 phenotypes were also determined. The metabolism of antipyrine and metronidazole was within normal range in all subjects, and they were all fast or extensive metabolizers of sparteine, mephenytoin, and phenytoin. HLA tissue types were unremarkable. Five of the seven subjects had complement C3 phenotypes F or FS. In the general population phenotype S is the most common, but the difference in complement C3 phenotypes is not statistically significant (p = 0.07). We conclude, although in a limited number of patients, that subjects with previous halothane hepatitis do not appear to be different from controls with regard to drug metabolism and HLA tissue type. The possibility of a higher frequency of complement C3 phenotype F and FS needs further investigation.

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Drug Metabolism and Genetic Polymorphism in Subjects with Previous Halothane Hepatitis

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Drug Metabolism and Genetic Polymorphism in Subjects with Previous Halothane Hepatitis

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