Pharmacogenetics of isoniazid-induced hepatotoxicity

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Isoniazid metabolism and hepatotoxicity

Isoniazid (INH) is highly effective for the management of tuberculosis. However, it can cause liver injury and even liver failure. INH metabolism has been thought to be associated with INH-induced liver injury. This review summarized the metabolic pathways of INH and discussed their associations with INH-induced liver injury.

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Association of isoniazid-metabolizing enzyme genotypes and isoniazid-induced hepatotoxicity in tuberculosis patients.

BACKGROUND Isoniazid (INH), a key drug of antituberculosis therapy, is metabolized by arylamine N-acetyltransferase2 (NAT2), cytochrome P450 2E1 (CYP2E1) and glutathione S-transferase (GST). We studied the possible influence of genetic polymorphisms of INH-metabolizing enzymes on serum concentrations of INH and its metabolites, as well as on the incidence of hepatotoxicity. PATIENTS AND METHO...

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Antituberculosis Drug-Induced Hepatotoxicity in Iranian Tuberculosis Patients: Role of Isoniazid Metabolic Polymorphism

The aim of this study was to determine the association of n-acetyltransferase-2 polymorphisms and anti-tuberculosis drug-induced hepatotoxicity in Iranian pulmonary tuberculosis patients. Acetylating phenotypes was studied in 50 Iranian pulmonary tuberculosis patients using metabolic ratio of plasma acetyl-Isoniazid to Isoniazid. The association between hepatotoxicity and the n-acetyltransferas...

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Antituberculosis Drug-Induced Hepatotoxicity in Iranian Tuberculosis Patients: Role of Isoniazid Metabolic Polymorphism

The aim of this study was to determine the association of n-acetyltransferase-2 polymorphisms and anti-tuberculosis drug-induced hepatotoxicity in Iranian pulmonary tuberculosis patients. Acetylating phenotypes was studied in 50 Iranian pulmonary tuberculosis patients using metabolic ratio of plasma acetyl-Isoniazid to Isoniazid. The association between hepatotoxicity and the n-acetyltransferas...

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Isoniazid hepatotoxicity with clinical and histopathology correlate.

A fifteen-year-old girl was treated with isoniazid (INH) for latent tuberculosis infection (LTBI), and subsequently developed epigastric pain, vomiting, and jaundice after three months of treatment. Acute fulminant hepatic failure was diagnosed. INH was stopped, and she received N-acetyl cysteine and Vitamin K. Liver biopsy showed moderate to severe lymphocytic and plasmacytic portal and lobula...

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ژورنال

عنوان ژورنال: Drug Metabolism Reviews

سال: 2014

ISSN: 0360-2532,1097-9883

DOI: 10.3109/03602532.2014.984070