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Isoniazid hepatotoxicity

Authors
Anne M Larson, MD, FACP, FAASLD, AGAF
Amy L Graziani, PharmD
Section Editor
C Fordham von Reyn, MD
Deputy Editor
Elinor L Baron, MD, DTMH

INTRODUCTION

Isoniazid (INH; isonicotinylhydrazide or isonicotinic acid hydrazine) is a synthetic antibiotic that is potently bactericidal against replicating Mycobacterium tuberculosis. INH has since been associated with two syndromes of hepatotoxicity: mild INH hepatotoxicity and INH hepatitis [1-3].

Issues related to INH hepatotoxicity will be reviewed here. The clinical use of INH is discussed separately. (See "Treatment of latent tuberculosis infection in HIV-uninfected adults" and "Treatment of drug-susceptible pulmonary tuberculosis in HIV-uninfected adults".)

MILD INH HEPATOTOXICITY

Mild isoniazid (INH) hepatotoxicity refers to hepatic injury that is typically subclinical and evidenced only by mildly elevated serum aminotransferases (usually <100 international units/L) [4-6]. It occurs in up to 20 percent of patients treated with isoniazid [7-11].

Adults are more likely to be affected than children; men and women appear to be equally vulnerable. There is no relationship to race or the rate of hepatic acetylation of the drug.

Most cases are self-limited; in general, INH therapy can be continued with careful monitoring in the absence of dose adjustment. Typically aminotransferase levels return to normal within several weeks after discontinuation of INH [12,13].

           
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Literature review current through: Sep 2017. | This topic last updated: Feb 09, 2017.
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