Pharmacogenomics of anti-TB drugs-related hepatotoxicity

Papers of special note have been highlighted as considerable interest (•) to readers.

Bibliography

• 1  Farrell GC: Drug-induced acute hepatitis. In: Drug-induced liver disease Farrell GG (Ed.). Churchill Livingstone, Edinburgh, UK, 247–299 (1994).
  Google Scholar
• 2  Pessayre D, Larrey D: Drug-induced liver injury: In: Oxford Textbook of clinical Hepatology. Volume 2. McIntyre N, Benhamou JP, Bircher J, Rizetto M, Rodes J (Eds). Oxford University Press, Oxford, UK (1991).
  Google Scholar
• 3  Sim E, Payton M, Noble M, Minchin R: An update on genetic, structural and functional studies on arylamine N-acetyltransferases in eucaryotes and procaryotes. Hum. Mol. Genet.9,2435–2441 (2000).• Review on NAT enzymes and loci from bacteria and human.
  Medline CASGoogle Scholar
• 4  Nebert DW: Polymorphism in drug-metabolizing enzymes: what is their clinical relevance and why do they exist? Am. J. Hum. Genet.60,265–271 (1997).
  Medline CASGoogle Scholar
• 5  Mitchel JR, Thorgeirsson UP, Black M et al.: Increased incidence of isoniazid hepatitis in rapid acetylators: possible relation to hydrazine metabolites. Clin. Pharmacol. Ther.18,70–79 (1975).
  MedlineGoogle Scholar
• 6  Yamamoto T, Suou T, Hirayama C: Elevated serum aminotransferase induced by isoniazid in relation to isoniazid acetylator phenotype. Hepatology6,295–298 (1986).
  Medline CASGoogle Scholar
• 7  Mitchell JR, Zimmerman HJ, Ishak KG et al.: Isoniazid liver injury: clinical spectrum, pathology and probable pathogenesis. Ann. Intern. Med.84,181–192 (1976).
  Medline CASGoogle Scholar
• 8  Gurumurthy P, Krishnamurthy MS, Nazareth O et al.: Lack of relationship between hepatic toxicity and acetylator phenotype in three thousand south Indian patients during treatment with isoniazid for tuberculosis. Am. Rev. Respir. Dis.129,58–61 (1984).
  Medline CASGoogle Scholar
• 9  Singh J, Garg PK, Thakur VS, Tandon RK: Antituberculosis treatment induced hepatotoxicity: Does acetylation status matter? Indian J. Physiol. Pharmacol.39,43–46 (1995).
  Medline CASGoogle Scholar
• 10  Benichou C: Criteria of drug induced liver disorder: report of an International Consensus Meeting. J. Hepatol.11,272–276 (1990).
  Medline CASGoogle Scholar
• 11  Rapp RS, Campbell RW, Howell JC, Kendig ELJ: Isoniazid hepatotoxicity in children. Am. Rev. Respir. Dis.118,794–796 (1978).
  Medline CASGoogle Scholar
• 12  Pande JN, Singh SPN, Khilnani GC, Khilnani S, Tandon RK: Risk Factors for hepatotoxicity from antituberculous drugs: a case control study. Thorax51,132–136 (1996).
  Medline CASGoogle Scholar
• 13  Kopanoff DE, Snider D, Caras G: Isoniazid related hepatitis: a U.S. Public Health Service cooperative Surveillance study. Am. Rev. Respir. Dis.117,991–1001 (1979).
  Google Scholar
• 14  Wong WM, Wu PC, Yuen MF et al.: Antituberculosis drug-related liver dysfunction in chronic hepatitis B infection. Hepatology31,201–206 (2000).
  Medline CASGoogle Scholar
• 15  Ungo JR, Jones D, Ashkin D et al.: Antituberculosis drug induced hepatotoxicity. The role of hepatitis C virus and the human immunodeficiency virus. Am. J. Respir. Crit. Care Med.157,1871–1876 (1998).
  Medline CASGoogle Scholar
• 16  Girling DJ: The hepatic toxicity of antituberculosis regimens containing isoniazid, rifampicin and pyrazinamide. Tubercle59,13–32 (1978).
  Medline CASGoogle Scholar
• 17  Bachs L, Pares A, Elena M, Piera C, Rodes J: Effects of long-term rifampicin administration in primary biliary cirrhosis. Gastroenterology102,2077–2080 (1992).
  Medline CASGoogle Scholar
• 18  Pessayre D, Bentata M, Deggott C et al.: Isoniazid rifampicin fulminant hepatitis: a possible consequence of enhancement of isoniazid hepatotoxicity by enzyme induction. Gastroenterology72,284–289 (1977).
  Medline CASGoogle Scholar
• 19  Lees AW, Allen GW, Smith J, Tyrrell WF, Fallon RJ: Toxicity from rifampicin plus isoniazid and rifampicin plus ethambutol therapy. Tubercle52,182–190 (1971).
  Medline CASGoogle Scholar
• 20  Fountain FF, Tolley E, Chrisman CR, Self TH: Isoniazid hepatotoxicity associated with treatment of latent tuberculosis infection: a 7-year evaluation from a public health tuberculosis clinic. Chest128,116–123 (2005).
  Medline CASGoogle Scholar
• 21  Saukkonen JJ, Cohn DL, Jasmer RM et al.: An official ATS statement: hepatotoxicity of antituberculosis therapy. Am. J. Respir. Crit. Care Med.174,935–952 (2006).
  Medline CASGoogle Scholar
• 22  Garg PK, Tandon RK: Antituberculous Agents Induced Liver Injury. In: Drug-induced Liver Disease. Kaplowitz N, Deleve LD (Eds). Marcel Dekker, New York, USA. (2003).• Review on TB treatment, hepatotoxicity and management.
  Google Scholar
• 23  Thompson NP, Caplin ME, Hamilton MI et al.: Anti-tuberculosis medication and the liver: dangers and recommendations in management. Eur. Respir. J.8,1384–1388 (1995).
  Medline CASGoogle Scholar
• 24  Singh J, Garg PK, Tandon RK: Hepatotoxicity due to antituberculosis therapy: clinical profile and reintroduction of therapy. J. Clin. Gastroenterol.22,211–214 (1996).
  Medline CASGoogle Scholar
• 25  Nelson SD, Mitchell JR, Timbrell JA, Snodgrass WR, Corcoran GB: Isoniazid and iproniazid: activation of metabolites to toxic intermediates in man and rat. Science193,901–903 (1976).
  Medline CASGoogle Scholar
• 26  Lauterburg BH, Smith CV, Todd EL, Mitchel JR: Oxidation of hydrazine metabolites formed from isoniazid. Clin. Pharmacol. Ther.38,566–571 (1985).
  Medline CASGoogle Scholar
• 27  Sarma GR, Immanuel, C, Kailasam S, Narayana AS, Venkatesan P: Rifampicin-induced release of hydrazine from isoniazid. A possible cause of hepatitis during treatment of tuberculosis with regimens containing isoniazid and rifampicin. Am. Rev. Respir. Dis.133,1072–1075 (1986).
  Medline CASGoogle Scholar
• 28  Payton M, Auty R, Delgoda R, Everett M, Sim E: Cloning and characterization arylamine N-acetyltransferase genes from Mycobacterium smegmatis and Mycobacterium tuberculosis: Increased expression results in isoniazid resistance. J. Bacteriol.181,1343–1347 (1999).
  Medline CASGoogle Scholar
• 29  Upton AM, Mushtaq A, Victor TC et al.: Arylamine N-acetyltransferase of Mycobacterium tuberculosis is a polymorphic enzyme and a site of isoniazid metabolism. Mol. Microbiol.42,309–317 (2001).• Study on bacterial N-acetyl transferases.
  Medline CASGoogle Scholar
• 30  Majumder M, Sikdar N, Ghosh S, Roy B: Polymorphisms at XPD and XRCC1 DNA repair loci and increased risk of oral leukoplakia and cancer among NAT2 slow acetylators. Int. J. Cancer120,2148–2156 (2007).• Simple method to reconstruct haplotypes from genotype data.
  Medline CASGoogle Scholar
• 31  Golka K, Blaszkewicz M, Samimi M, Bolt HM, Selinski S: Reconstruction of N-acetyltransferase 2 haplotypes using PHASE. Arch. Toxicol. (2007) (Epub ahead of print).• Use of program to reconstruct haplotypes from genotype data.
  Google Scholar
• 32  Batra J, Sharma SK, Ghosh B: Arylamine N-acetyl transferase gene polymorphisms markers for atopic asthma serum IgE and blood eosinophil counts. Pharmacogenomics7,673–682 (2006).• Study of linkage disequilibrium between SNPs at NAT2.
  CASGoogle Scholar
• 33  Chen C, Ricks S, Doody DR, Fitzgibbons ED, Porter PL, Schwartz SM: N-acetyltranferase 2 polymorphisms, cigarette smoking and alcohol consumption, and oral squamous cell cancer risk. Carcinogenesis22,1993–1999 (2001).
  Medline CASGoogle Scholar
• 34  Morita S, Yano M, Tsujinaka T et al.: Genetic polymorphisms of drug-metabolizing enzymes and susceptibility to head-and-neck squamous carcinoma. Int. J. Cancer80,685–688 (1999).
  Medline CASGoogle Scholar
• 35  Ohno M, Yamaguchi I, Yamamoto I et al.: Slow N-acetyltransferase 2 genotype affects the incidence of isoniazid and rifampicin-induced hepatotoxicity. Int. J. Tuberc. Lung Dis.4,256–261 (2000).• Polymorphism at NAT2 increased the risk of anti-TB drug (ATD) hepatotoxicity in Japanese patients.
  Medline CASGoogle Scholar
• 36  Huang YS, Chern HD, Su WJ et al.: Polymorphisms of the N-acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug-induced hepatitis. Hepatology35,883–889 (2002).• Polymorphism at NAT2 increased the risk of ATD hepatotoxicity in Chinese patients.
  Medline CASGoogle Scholar
• 37  Cho HJ, Koh WJ, Ryu YJ et al.: Genetic polymorphisms of NAT2 and CYP2E1 associated with antituberculosis drug-induced hepatotoxicity in Korean patients with pulmonary tuberculosis. Tuberculosis (Edinb.)87(6),551–556 (2007).• Polymorphism at NAT2 increased the risk of ATD hepatotoxicity in Korean patients.
  Medline CASGoogle Scholar
• 38  Roy B, Chowdhury A, Kundu S et al.: Increased risk of antituberculosis drug-induced hepatotoxicity in individuals with glutathione S-transferase M1 ‘null’ mutation. J. Gastroenterol. Hepatol.16,1033–1037 (2001).• Polymorphism at GSTM1 increased the risk of ATD hepatotoxicity in Indian patients.
  Medline CASGoogle Scholar
• 39  Vuilleumier N, Rossier MF, Chiappe A et al.: CYP2E1 genotype and isoniazid-induced hepatotoxicity in patients treated for latent tuberculosis. Eur. J. Clin. Pharmacol.62,423–429 (2006).• Polymorphism at CYP2E1 increased the levels of liver enzymes.
  Medline CASGoogle Scholar
• 40  Watkins PB: The role of cytochrome P450s in drug-induced liver disease. In: Drug-induced liver disease Kaplowitz N, Deleve LD (Eds). Marcel Dekker, New York, USA 15–33, (2003).• Possible roles of CYP2E1 enzyme in hepatotoxicity.
  Google Scholar
• 41  Yue J, Peng RX, Yang J, Kong R, Liu J: CYP2E1 mediated isoniazid-induced hepatotoxicity in rats. Acta Pharmacol. Sin.25,699–704 (2004).• Regulation of CYP2E1 synthesis by isoniazid.
  Medline CASGoogle Scholar
• 42  Huang YS, Chern HD, Su WJ et al.: Cytochrome P450 2E1 genotype and the susceptibility to antituberculosis drug-induced hepatitis. Hepatology37,924–930 (2003).• Polymorphism at CYP2E1 increased the risk of ATD hepatotoxicity in Chinese patients.
  Medline CASGoogle Scholar
• 43  Watanabe J, Hayashi S, Kawajiri K et al.: Different regulation and expression of the human CYP2E1 gene due to the Rsa 1 polymorphism in the 5’ flanking region. J. Biochem116,321–326 (1994).
  Medline CASGoogle Scholar
• 44  Carriere V, Berthou F, Baird S, Belloc C, Beaune P, Waziers ID: Human cytochrome P4502E1 (CYP2E1): from genotype to phenotype. Pharmacogenetics6,203–211 (1996).
  Medline CASGoogle Scholar
• 45  Powell H, Kitteringham NR, Pirmohamed M, Smith DA, Park BK: Expression of cytochrome P4502E1 (CYP2E1) in human liver: assessment on mRNA genotype and phenotype. Pharmacogenetics8,411–421 (1998).
  Medline CASGoogle Scholar
• 46  Le Marchand L, Sivaraman L, Pierce L et al.: Association of CYP1A1, GSTM1 and CYP2E1 polymorphisms with lung cancer suggest cell type specificities to tobacco carcinogens. Cancer Res.58,4858–4863 (1998).
  Medline CASGoogle Scholar
• 47  Sikdar S, Mahmud SKA, Paul RR, Roy B: Polymorphism in CYP1A1 and CYP2E1 genes and susceptibility to leukoplakia in Indian tobacco users. Cancer Lett.195,33–42 (2003).
  Medline CASGoogle Scholar
• 48  Roy B, Ghosh SK, Sutradhar D, Sikdar N, Mazumder S, Barman S: Predisposition of antituberculosis drug induced hepatotoxicity by cytochrome P450 2E1 genotype and haplotype in pediatric patients. J. Gastroenterol. Hepatol.21,781–786 (2006).• Polymorphism at CYP2E1 increased the risk of ATD hepatotoxicity in Indian patients.
  MedlineGoogle Scholar
• 49  Strange RC, Jones PW, Fryer AA: Glutathione S-transferase: genetics and role in toxicology. Toxicol. Lett.112–113, 357–363 (2000).
  Google Scholar
• 50  Simon T, Becquemont L, Mary-Krause M et al.: Combined glutathione-S-transferase M1 and T1 genetic polymorphism and tacrine hepatotoxicity. Clin. Pharmacol. Ther.67(4),432–437 (2000).
  Medline CASGoogle Scholar
• 51  Huang YS, Su WJ, Huang YH et al.: Genetic polymorphisms of manganese superoxide dismutase, NAD(P)H: quinone oxidoreductase, glutathione S-transferase M1 and T1, and the susceptibility to drug-induced liver injury. J. Hepatol.47,128–134 (2007).• Polymorphism at GSTM1 increased the risk of ATD hepatotoxicity in Chinese patients.
  Medline CASGoogle Scholar
• 52  Pemble S, Schroeder KR, Spencer SR et al.: Human glutathione-S-transferase theta (GSTT1): cDNA cloning and the characterization of a genetic polymorphism. Biochem. J.300,271–276 (1994).
  Medline CASGoogle Scholar
• 53  Sikdar N, Paul RR, Roy B: Glutathione S transferase M3 (A/A) genotype as a risk factor for oral cancer and leukoplakia among Indian tobacco smokers. Int. J. Cancer:109,95–101 (2004).
  Medline CASGoogle Scholar
• 54  Rebbeck T, Walker A, Jaffe J, White DL, Wein AJ, Malkowicz SB: Glutathione-S-transferase µ (GSTM1) and theta (GSTT1) genotypes in the etiology of prostate cancer. Cancer Epidemiol. Biomarkers Prev.8,283–287 (1999).
  Medline CASGoogle Scholar
• 55  Cotton S, Sharp L, Little J, Brockton N: Glutathione-S-transferase polymorphisms and colorectal cancer: HuGE review. Am. J. Epidemiol.151,7–32 (2000).
  Medline CASGoogle Scholar
• 56  Geisler SA, Olshan AF: GSTM1, GSTT1 and risk of squamous cell carcinoma of head and neck: a mini-HuGE review, Am. J. Epidemiol.154,95–105 (2001).
  Medline CASGoogle Scholar
• 57  Roy B, Majumder PP, Dey B et al.: Ethnic differences in distributions of GSTM1 and GSTT1 homozygous “null” genotypes in India. Hum. Biol.73,443–450 (2001).
  Medline CASGoogle Scholar
• 58  Lee EJ, Wong JY, Yeoh PN, Gong NH: Glutathione S-transferase-theta (GSTT1) genetic polymorphism among Chinese, Malays and Indians in Singapore. Pharmacogenetics5,332–334 (1995).
  Medline CASGoogle Scholar
• 59  Sodhi CP, Rana SV, Mehta SK et al.: Study of oxidative stress in isoniazid induced hepatic injury in young rats with and without protein energy malnutrition. J. Biochem. Toxicol.11,139–146 (1996).
  Medline CASGoogle Scholar
• 60  Sodhi CP, Rana SV, Mehta S, Vaiphei K, Goel RC, Mehta SK: Study of oxidative stress in rifampicin induced hepatic injury in young rats with and without protein energy malnutrition. Hum. Exp.Toxicol.16,315–321 (1997).
  Medline CASGoogle Scholar
• 61  Chowdhury A, Santra A, Kundu S et al.: Induction of oxidative stress in antitubercular drug-induced hepatotoxicity. Indian J. Gastroenterol.20,97–100 (2001).
  Medline CASGoogle Scholar
• 62  Mehra NK, Taneja V, Chaudhuri TK et al.: Pulmonary tuberculosis In: HLA in Asia-Oceania-1986. Aizawa M (Ed.). Hokkaido University Press, Sapporo, Japan, 374–379 (1986).
  Google Scholar
• 63  Sharma SK, Balamurugan A, Saha PK, Pandey RM, Mehra NK: Evaluation of clinical and immunogenetic risk factors for the development of hepatotoxicity during antituberculosis treatment. Am. J. Respir. Crit. Care Med.166,916–919 (2002).• HLA alleles increased the risk of ATD hepatotoxicity in Indian patients.
  MedlineGoogle Scholar
• 64  Agundez JAG, Martinez C, Garcia-Martin E: Analyses of linkage disequilibrium of seven NAT2 SNPs in 2,068 genes form Caucasians: Three SNPs are enough to predict 99.4% of slow acetylation genes. Fourth International workshop on the Arylamine N-acetyltransferases, Alexandroupolis, Greece, 14–16 September (2007).
  Google Scholar
• 65  Brennan P: Gene–environment interaction and aetiology of cancer: what does it mean and how can we measure it? Carcinogenesis23,381–387 (2002).• A review for quantitative gene-environment interaction.
  Medline CASGoogle Scholar
• 66  Westwood IM, Bhakta S, Russell AJ et al.: Small molecule inhibitors of arylamine N-acetyltransferase (NAT) in Mycobacterium tuberculosis mimic deletion of the nat gene: support for a novel anti-tubercular target. Fourth International workshop on the Arylamine N-acetyltransferases, Alexandroupolis, Greece, 14–16 September (2007).
  Google Scholar
• 101  Description of different alleles at NAT2 and corresponding acetylating status www.louisville.edu/medschool/pharmacology/nat.html
  Google Scholar
• 102  A software to restructure the haplotypes from genotype data www.stat.washington.edu/stephens/
  Google Scholar
• 103  New nomenclature for CYP2E1 allele www.cypalleles.ki.se/cyp2e1.htm
  Google Scholar