Tuberculosis Drug-Induced Liver Injury
Downloads
Effective tuberculosis (TB) treatment requires a combination of bactericidal and/or bacteriostatic TB drugs. The combination of these regimens is the standard therapy recommended by World Health Organization (WHO). The standard therapy consists of 5 first-line anti-TB drugs (isoniazid, rifampicin, pyrazinamide, ethambutol, and streptomycin). TB drugs have mild to severe side effects. Side effects that arise not only cause mortality and morbidity but also cause the cessation of treatment with the effect of not achieving cure, even arising drug resistance. Drug-induced liver injury (DILI) is a form of side effect that causes the cessation of TB treatment or regimen changes due to treatment failure, relapse, and drug resistance. DILI increases the problem, covering more than 7% of all side effects. DILI is also one of the concerns in the treatment of TB.
Totstmann A, Boeree MJ, Aarnoutse RE, et al. Antituberculosis Drug-Induced Hepatotoxicity: Concise up-to-date Review. J Gastroenterol Hepatol 2008;23:192–202.
Baghaei P, Tabarsi P, Chitsaz E, et al. Incidence, Clinical and Epidemiological Risk Factors, and Outcome of Drug-Induced Hepatitis Due to Antituberculous Agents in New Tuberculosis Cases. Am J Ther 2010;17:17–22.
Soedarsono, Mandayani S, Prayuni K, Yuliwulandari R. The Risk Factors for Drug Induced Hepatitis in Pulmonary Tuberculosis in dr. Soetomo. IJTID. 2018;7(3):73–79.
World Health Organization. Treatment of Extrapulmonary Tuberculosis and Tuberculosis in Special Situation. Geneva WHO Press 2010;95–111.
Singh A, Balasubramanian V, Gupta N, et al. Prevalence of Adverse Drug Reaction With First Line Drug Among Patients Treated for Pulmonary Tuberculosis. CEGH. 2015;3(1) : 80-90.
Hasan MM, Akbar SMFZ, Mahtab MA. Textbook of Hepato-Gastroenterology. Health Science Publisher. 2015;52:2463–2471.
Chowdhury A, Santra A, Bhattacharjee K, et al. Mitochondrial Oxidative Stress and Permeability Transition in Isoniazid and Rifampicin Induced Liver Injury in Mice. J Hepatol. 2006; 45:117–126.
Kim J, Nam WS, Kim SJ, et al. Mechanism Investigation of Rifampicin-Induced Liver Injury Using Comparative Toxicoproteomics in Mice. Int J Mol Sci. 2017; 18(7) 1417
Marzuki OA, Fauzi ARM, Ayoub S, Imran MK. Prevalence and Risk Factors of Antituberculosis Drug-Induced Hepatitis in Malaysia. Singapore med J. 2008;49(9):698.
Vuppalanchi R, Chalasani N. Risk Factors for Drug-Induced Liver Disease. Chapter 16. 3rd Edition. Kaplowitz N, Leve LD. Elsevier Inc.; 2013. 265-274.
Chalasani N, Björnsson E. Risk Factors for Idiosyncratic Drug-Induced Liver Injury. AGA Journals. 2010;138(7):2246–2259.
Shapiro MA, Lewis JH. Causality Assessment of Drug-Induced Hepatotoxicity : Promises and Pitfalls. Elsevier Inc. 2007;11:477–505.
Lucena MI, Fernandez MC, Romero-gomez M, et al. Phenotypic Characterization of Idiosyncratic Drug- Induced Liver Injury: The Influence of Age and Sex. AASLD. 2009;2001–2009.
Anand AC, Seth AK, Paul M, Puri P. Risk Factors of Hepatotoxicity During Anti-Tuberculosis Treatment. MJAFI. 2006;62:45-49
Zimmerman HJ. Hepatotoxicity : the Adverse Effects of Drugs and Other Chemical on the Liver. 2nd ed. Lippincott Williams and Wilkins. 1999. 427-456.
Bleibel W, Kim S, Silva KD, Lemmer ER. Drug-Induced Liver Injury : Review Article. Springer Sci + Bus Media inc 2007;52:2463–2471.
Lee WM. Drug-induced hepatotoxicity (review). NEJM. 2003;349:474–485.
Lee WM, Senior J. Recognizing Drug-Induced Liver Injury: Current Problems, Possible Solutions. Toxical Patol 2005;33:155–164.
Cullen JM. Mechanistic Classification of Liver Injury. Toxicol Pathol 2005;33:6–8.
Mackay IR.. Immunological Perspectives on Chronic Hepatitis: Virus Infection, Autoimmunity and Xenobiotics. Hepato-gastroenterology 1999;33:3021–3033.
Rashid M, Goldin R, Wright M. Drug and the Liver. J Hosp Med 2004; 65 : 456–461.
Kaplowitz N. Biochemical and Cellular Mechanisms of Toxic Liver Injury. Semin Liver Dis 2002;2:137–144.
Holt MP, Ju C. Mechanism of Drug-Induced Liver Injury. AAPS J 2006; 8 : E48–E54.
Kaplowitz N. Drug-Induced Liver Injury. Clin Infect Dis 2004; 38 : 844–849.
Velayudham LS. Drug-Induced Cholestasis. Expert opin drug saf 2003; 2 : 287–304.
Park BK, Kitteringham NR, Maggs JL, Pirmohamed M, William D. The Role of Metabolic Activation in Drug-Induced Hepatotoxicity. Annu Rev Pharmacol Toxicol 2005;30:177–202.
Ju C. Immunological Mechanisms of Drug-Induced Liver Injury. Curr Opin Drug Discov Devel. 2005;(8):38–43.
Maddrey WC. Drug Induced Hepatotoxicity. J Clin Gastroenterol 2005; 39 (suppl 2) : 883–889.
Aithal GP. Diclofenac-Induced Liver Injury : a Paradigm of Idiosyncratic Drug Toxicity. Expert opin drug saf 2004; 3 : 519–523.
Gunawan B, Kaplowitz N. Clinical Perspectives on Xenobiotic-Induced Hepatotoxicity. Drug Metab Rev 2004;(36):301–312.
Russo MW, Watkins P. Are Patients With Elevated Liver Tests at Increased Risk of Drug-Induced Liver Injury? Gastroenterology 2004; 126(5) : 1477–1480.
Kaplowitz N. Drug-Induced Liver Disorder: Implications for Drug Development and Regulation. Drug Saf 2001;(24):483–490.
Kaplowitz N. Drug-Induced Liver Disorders : Introduction and Overview. 2002;1–13.
Hasan MM, Akbar SMF, Mahtab MA. Textbook of Hepato-Gastroenterology. The Health Science Publisher; 2015;346-358.
Ghabril M, Chalasani N, Bjornsson E. Drug-induced liver injury : a clinical update. Curr Opin Gastroenterol 2010;26(3):222–226.
Naven C, Ramakant D. Adjunctive Corticosteroid Theraphy in Tuberculosis Management : a Critical Appraisal. IJPSR 2(1):10–15.
Helmia H. Buku Ajar Ilmu Penyakit Paru. Departemen Ilmu Penyakit Paru FK Unair - RSUD dr. Soetomo; 2010;9-30.
Copyright (c) 2020 Soedarsono Soedarsono, Agustinus Rizki Wirawan Riadi
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
1. The journal allows the author to hold the copyright of the article without restrictions.
2. The journal allows the author(s) to retain publishing rights without restrictions.
3. The legal formal aspect of journal publication accessibility refers to Creative Commons Attribution Share-Alike (CC BY-SA).
4. The Creative Commons Attribution Share-Alike (CC BY-SA) license allows re-distribution and re-use of a licensed work on the conditions that the creator is appropriately credited and that any derivative work is made available under "the same, similar or a compatible license”. Other than the conditions mentioned above, the editorial board is not responsible for copyright violation.
JR (