Increased risk of antituberculosis drug‐induced hepatotoxicity in individuals with glutathione S‐transferase M1 ‘null’ mutation

Background: Pathogenesis and genetic factors influencing predisposition to antituberculosis drug (ATD)‐induced hepatotoxicity are not clear. Polymorphism at the genetic locus of a drug and xenobiotic compound metabolizing enzyme, N‐acetyltransferase type 2 (NAT2), is reported to be associated with the excess generation of toxic reactive metabolites. Polymorphisms at the glutathione S‐transferase (GST) loci (GSTM1 and GSTT1) are involved in the detoxification of these toxic metabolites in the human body to a lesser extent. We have examined whether polymorphisms at these loci are associated with the risk of ATD‐induced hepatotoxicity.

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