Lack of association between genetic polymorphisms of CYP3A4, CYP2C9 and CYP2C19 and antituberculosis drug-induced liver injury in a community-based Chinese population

Clinical and Experimental Pharmacology and Physiology

Volumn 40, Issue 5, 2013, Pages 326-332

  Tang, Shao Wen ^a,b   Lv, Xiao Zhen ^a,c   Chen, Ru ^a   Wu, Shan Shan ^a   Yang, Zhi Rong ^a   Chen, Da Fang ^a   Zhan, Si Yan ^a  

^a PEKING UNIVERSITY HEALTH SCIENCE CENTER   (China)

^b NANJING MEDICAL UNIVERSITY   (China)

^c PEKING UNIVERSITY SIXTH HOSPITAL   (China)

Author keywords

Antituberculosis drug induced liver injury; CYP2C19; CYP2C9; CYP3A4; Tagging single nucleotide polymorphism

Indexed keywords

ALANINE AMINOTRANSFERASE; ASPARTATE AMINOTRANSFERASE; BILIRUBIN; CYTOCHROME P450 2C19; CYTOCHROME P450 2C9; CYTOCHROME P450 3A4; ETHAMBUTOL; ISONIAZID; PYRAZINAMIDE; RIFAMPICIN; STREPTOMYCIN; TUBERCULOSTATIC AGENT;

ADULT; AGED; ANTITUBERCULOSIS DRUG INDUCED LIVER INJURY; ARTICLE; CASE CONTROL STUDY; CHINESE; COHORT ANALYSIS; CONTROLLED STUDY; DISEASE SEVERITY; FEMALE; GENE FREQUENCY; GENETIC ASSOCIATION; GENETIC RISK; GENOTYPE; HAPLOTYPE; HUMAN; LIVER INJURY; MAJOR CLINICAL STUDY; MALE; MEDICAL HISTORY; SINGLE NUCLEOTIDE POLYMORPHISM; TUBERCULOSIS;

ADULT; AGED; AGED, 80 AND OVER; ANTITUBERCULAR AGENTS; ARYL HYDROCARBON HYDROXYLASES; ASIAN CONTINENTAL ANCESTRY GROUP; CASE-CONTROL STUDIES; CHINA; COHORT STUDIES; CYTOCHROME P-450 CYP3A; DRUG-INDUCED LIVER INJURY; FEMALE; GENE FREQUENCY; GENETIC ASSOCIATION STUDIES; HUMANS; MALE; MIDDLE AGED; POLYMORPHISM, SINGLE NUCLEOTIDE; PROSPECTIVE STUDIES; TUBERCULOSIS; YOUNG ADULT;

EID: 84876825439     PISSN: 03051870     EISSN: 14401681     Source Type: Journal    
DOI: 10.1111/1440-1681.12074     Document Type: Article

References (47)

1. World Health Organization. Global Tuberculosis Control. World Health Organization, Geneva, 2011.
2. Blumberg HM, Burman WJ, Chaisson RE et al. American Thoracic Society/Centers for Disease Control and Prevention/Infectious Diseases Society of America: Treatment of tuberculosis. Am. J. Respir. Crit. Care Med. 2003; 167: 603-62.
3. Burman WJ, Reves RR. Hepatotoxicity from rifampin plus pyrazinamide: Lessons for policymakers and messages for care providers. Am. J. Respir. Crit. Care Med. 2001; 164: 1112-13.
4. Yee D, Valiquette C, Pelletier M, Parisien I, Rocher I, Menzies D. Incidence of serious side effects from first-line antituberculosis drugs among patients treated for active tuberculosis. Am. J. Respir. Crit. Care Med. 2003; 167: 1472-7.
5. Saukkonen JJ, Cohn DL, Jasmer RM et al. An official ATS statement: Hepatotoxicity of antituberculosis therapy. Am. J. Respir. Crit. Care Med. 2006; 174: 935-52.
6. Tostmann A, Boeree MJ, Aarnoutse RE, de Lange WC, van der Ven AJ, Dekhuijzen R. Antituberculosis drug-induced hepatotoxicity: Concise up-to-date review. J. Gastroenterol. Hepatol. 2008; 23: 192-202.
7. Yew WW, Leung CC. Antituberculosis drugs and hepatotoxicity. Respirology 2006; 11: 699-707.
8. Knowles SR, Uetrecht J, Shear NH. Idiosyncratic drug reactions: The reactive metabolite syndromes. Lancet 2000; 356: 1587-91.
9. Naisbitt DJ, Williams DP, Pirmohamed M, Kitteringham NR, Park BK. Reactive metabolites and their role in drug reactions. Curr. Opin. Allergy Clin. Immunol. 2001; 1: 317-25.
10. 2 genetic polymorphisms and anti-tuberculosis drug-induced hepatotoxicity in Chinese community population. Ann. Hepatol. 2012; 11: 700-7.
11. Huang YS, Chern HD, Su WJ et al. Polymorphism of the N-acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug-induced hepatitis. Hepatology 2002; 35: 883-9.
12. 2 and CYP2E1 associated with antituberculosis drug-induced hepatotoxicity in Korean patients with pulmonary tuberculosis. Tuberculosis 2007; 87: 551-6.
13. 2 and CYP2E1 polymorphisms and susceptibility to first-line anti-tuberculosis drug-induced hepatitis. Int. J. Tuberc. Lung Dis. 2010; 14: 622-6.
14. 2 and CYP2E1 and isoniazid hepatotoxicity in a diverse population. Pharmacogenomics 2009; 10: 1433-45.
15. Bose PD, Sarma MP, Medhi S, Das BC, Husain SA, Kar P. Role of polymorphic N-acetyl transferase2 and cytochrome P4502E1 gene in antituberculosis treatment-induced hepatitis. J. Gastroenterol. Hepatol. 2011; 26: 312-18.
16. An HR, Wu UQ, Wang ZY, Zhang JX, Liang Y. NAT2 and CYP2E1 polymorphisms associated with antituberculosis drug-induced hepatotoxicity in Chinese patients. Clin. Exp. Pharmacol. Physiol. 2012; 39: 535-43.
17. Huang YS, Chern HD, Su WJ et al. Cytochrome P450 2E1 genotype and the susceptibility to antituberculosis drug-induced hepatitis. Hepatology 2003; 37: 924-30.
18. Chen Y, Guo M, Li SM et al. [Study of the relationship between polymorphisms of cytochrome P450 2E1 and antituberculosis drug induced hepatic injury.] Zhong Hua Chuan Ran Bing Za Zhi 2010; 28: 748-52 (in Chinese).
19. 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. 2006; 21: 784-6.
20. Wang T, Wang W, Wang ZY, Pan YY, Su QQ, He LX. [Association of P450-2E1 and GSTM1 genetic polymorphisms with susceptibility to antituberculosis drug-induced hepatotoxicity.] Zhong Hua Jie He Yu Hu Xi Za Zhi 2009; 32: 585-7 (in Chinese).
21. Wang T, Yu HT, Wang W, Pan YY, He LX, Wang ZY. Genetic polymorphisms of cytochrome P450 and glutathione S-transferase associated with antituberculosis drug-induced hepatotoxicity in Chinese tuberculosis patients. J. Int. Med. Res. 2010; 38: 977-86.
22. Tang SW, Lv XZ, Zhang Y et al. CYP2E1, GSTM1 and GSTT1 genetic polymorphisms and susceptibility to antituberculosis drug-induced hepatotoxicity: A nested case-control study. J. Clin. Pharm. Ther. 2012; 37: 588-93.
23. 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. 2001; 16: 1033-7.
24. 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. 2007; 47: 128-34.
25. Leiro V, Fernandez-Villar A, Valverde D et al. Influence of glutathione S-transferase M1 and T1 homozygous null mutations on the risk of antituberculosis drug-induced hepatotoxicity in a Caucasian population. Liver Int. 2008; 28: 835-9.
26. Tang W, Stearns RA. Heterotropic cooperativity of cytochrome P450 3A4 and potential drug-drug interactions. Curr. Drug Metab. 2001; 2: 185-98.
27. Liu ZW, Hu ZH, Cai YY. [The combined effect of isoniazid and rifampicin on the activities of CYP4501A2 and CYP4503A4 in primary hepatocytes from healthy human adults.] Zhonghua Jie He He Hu Xi Za Zhi 2005; 28: 785-8 (in Chinese).
28. Phillips KA, Veenstra DL, Oren E, Lee JK, Sadee W. Potential role of pharmacogenomics in reducing adverse drug reactions: A systematic review. JAMA 2001; 286: 2270-9.
29. Madan A, Graham RA, Carroll KM et al. Effects of prototypical microsomal enzyme inducers on cytochrome P450 expression in cultured human hepatocytes. Drug Metab. Dispos. 2003; 31: 421-31.
30. Kim SH, Bahn JW, Kim YK et al. Genetic polymorphisms of drug-metabolizing enzymes and anti-TB drug-induced hepatitis. Pharmacogenomics 2009; 10: 1767-79.
31. Xia YY, Hu DY, Liu FY et al. Design of the anti-tuberculosis drugs induced adverse reactions in China National Tuberculosis Prevention and Control Scheme Study (ADACS). BMC Public Health; 2010; 10: 267-76.
32. Shang P, Xia Y, Liu F et al. Incidence, clinical features and impact on anti-tuberculosis treatment of anti-tuberculosis drug induced liver injury (ATLI) in China. PLoS ONE 2011; 6: e21836.
33. Benichou C. Criteria of drug-induced liver disorders. Report of an international consensus meeting. J. Hepatol. 1990; 11: 272-6.
34. World Health Organization. The Use of the WHO-UMC System for Standardized Case Causality Assessment. The Uppsala Monitoring Centre, Uppsala. 2005.
35. Robins JM, Gail MH, Lubin JH. More on 'Biased selection of controls for case-control analyses of cohort studies'. Biometrics 1986; 42: 293-9.
36. National Tuberculosis Association of the USA. Diagnostic Standards and Classification of Tuberculosis. National Tuberculosis Association, New York. 1961.
37. Barrett JC, Fry B, Maller J, Daly MJ. Haploview. Analysis and visualization of LD and haplotype maps. Bioinformatics 2005; 21: 263-5.
38. Teuber M, Wenz MH, Schreiber S, Franke A. GMFilter and SXTestPlate: Software tools for improving the SNPlex genotyping system. BMC Bioinformatics 2009; 10: 81.
39. Kivisto KT, Kroemer HK, Eichelbaum M. The role of human cytochrome P450 enzymes in the metabolism of anticancer agents: Implications for drug interactions. Br. J. Clin. Pharmacol. 1995; 40: 523-30.
40. Haas DW, Bartlett JA, Andersen JW et al. Pharmacogenetics of nevirapine-associated hepatotoxicity: An Adult AIDS Clinical Trials Group collaboration. Clin. Infect. Dis. 2006; 43: 783-6.
41. Ciccacci C, Borgiani P, Ceffa S et al. Nevirapine-induced hepatotoxicity and pharmacogenetics: A retrospective study in a population from Mozambique. Pharmacogenomics 2010; 11: 23-31.
42. Miners JO, Birkett DJ. Cytochrome P4502C9: An enzyme of major importance in human drug metabolism. Br. J. Clin. Pharmacol. 1998; 45: 525-38.
43. Hirota T, Eguchi S, Ieiri I. Impact of genetic polymorphisms in CYP2C9 and CYP2C19 on the pharmacokinetics of clinically used drugs. Drug Metab. Pharmacokinet. 2013; 28: 28-37.
44. Roy PD, Majumder M, Roy B. Pharmacogenomics of anti-TB drugs-related hepatotoxicity. Pharmacogenomics 2008; 9: 311-21.
45. Mitchell JR, Zimmerman HJ, Ishak KG et al. Isoniazid liver injury: Clinical spectrum, pathology, and probable pathogenesis. Ann. Intern. Med. 1976; 84: 181-92.
46. Nelson SD, Mitchell JR, Timbrell JA, Snodgrass WR, Corcoran GB. Isoniazid and iproniazid activation of metabolites to toxic intermediates in man and rat. Science 1976; 193: 901-3.
47. Metushi IG, Cai P, Zhu X, Nakagawa T, Uetrecht JP. A fresh look at the mechanism of isoniazid-induced hepatotoxicity. Clin. Pharmacol. Ther. 2011; 89: 911-14.