Antituberculosis drug-induced hepatitis: risk factors, prevention and management.

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dc.contributor.authorHussain, Zen_US
dc.contributor.authorKar, Pen_US
dc.contributor.authorHusain, S Aen_US
dc.date.accessioned2009-05-28T14:46:46Z
dc.date.available2009-05-28T14:46:46Z
dc.date.issued2003-11-31en_US
dc.description67 references.en_US
dc.description.abstractApart from infectious or viral hepatitis, other most common non-infectious causes of hepatitis are alcohol, cholestatic, drugs and toxic materials. The most common mode that leads to liver injuries is antituberculosis drug-induced hepatitis. The severity of drug-induced liver injury varies from minor nonspecific changes in hepatic structure to fulminant hepatic failure, cirrhosis and liver cancer. Patients receiving antitubercular drug frequently develop acute or chronic hepatitis. The time required for the metabolites to reach hepatotoxic levels is much earlier with isoniazid plus rifampicin treatment than isoniazid alone and this has been shown to be synergistic rather than additive. Antituberculosis drug (ATT)-inducible cytochrome P-4502E1 (CYP2E1) is constitutively expressed in the liver. Recent studies show that polymorphism of the N-acetyltransferase 2 (NAT2) genes and glutathione-S-transferase (GST) are the major susceptibility risk factors for ATT-induced hepatitis. The hepatic NAT and GST are involved in the metabolism of several carcinogenic arylamines and drugs. The NAT2 enzyme has a genetic polymorphism in human. N-acetyltransferase 2 genes (NAT2) have been identified to be responsible for genetic polymorphism of slow and rapid acetylation in humans. Slow acetylators of NAT2 prove to develop more severe hepatotoxicity than rapid acetylators making it a significant risk factor. Deficiency of GST activity, because of homozygous null mutations at GSTM1 and GSTT1 loci, may modulate susceptibility to drug and xenobiotic-induced hepatotoxicity. Polymorphisms at GSTM1, GSTT1 and NAT2 loci had been linked to various forms of liver injury, including hepatocellular carcinoma.en_US
dc.description.affiliationDepartment of Medicine, Maulana Azad Medical College, New Delhi 110 002, India.en_US
dc.identifier.citationHussain Z, Kar P, Husain SA. Antituberculosis drug-induced hepatitis: risk factors, prevention and management. Indian Journal of Experimental Biology. 2003 Nov; 41(11): 1226-32en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/61146
dc.language.isoengen_US
dc.source.urihttps://www.niscair.res.in/ScienceCommunication/ResearchJournals/rejour/ijeb/ijeb0.aspen_US
dc.subject.meshAntitubercular Agents --adverse effectsen_US
dc.subject.meshArylamine N-Acetyltransferase --geneticsen_US
dc.subject.meshCytochrome P-450 CYP2E1 --antagonists & inhibitorsen_US
dc.subject.meshGenetic Predisposition to Disease --geneticsen_US
dc.subject.meshGlutathione Transferase --geneticsen_US
dc.subject.meshHepatitis, Toxic --blooden_US
dc.subject.meshHumansen_US
dc.subject.meshPolymorphism, Geneticen_US
dc.subject.meshRisk Factorsen_US
dc.subject.meshTuberculosis --drug therapyen_US
dc.titleAntituberculosis drug-induced hepatitis: risk factors, prevention and management.en_US
dc.typeJournal Articleen_US
dc.typeReviewen_US
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