Journals / Tüberküloz ve Toraks / 2002 / Cilt: 50 - Sayı: 4

The management of antituberculosis drug induced hepatotoxicity

Tüberküloz tedavisi sırasında gelişen hepatotoksisitede klinik yaklaşım

Pages
480–484
Publication Date
2022-11-05
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In conclusion, when hepatotoxicity occures, we think that it will be apropriate to stop all the drugs at the same time and also begin all of them at same time after clinical regression and reaching normal enzyme values.

📌 3 Key Takeaways

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Objective & Hypothesis:In this study, any relation was searched between hepatotoxicity -caused by antituberculous therapy- and sex, age, coexisting disease occurence of previous treatment or not.
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Key Findings & Data:In 1995 to 1999, 18 women and 17 men, totally 35 patients, suffer from hepatotoxicity while having antituberculous therapy were included the study.
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Conclusion & Impact:In conclusion, when hepatotoxicity occures, we think that it will be apropriate to stop all the drugs at the same time and also begin all of them at same time after clinical regression and reaching normal enzyme values.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

In this study, any relation was searched between hepatotoxicity -caused by antituberculous therapy- and sex, age, coexisting disease occurence of previous treatment or not. In this cases, it was also examined if there existed any difference of recurrence and clinical adherance for beginning the drugs step by step or all at same time after stopping the drugs. In 1995 to 1999, 18 women and 17 men, totally 35 patients, suffer from hepatotoxicity while having antituberculous therapy were included the study. The period between the beginning of the therapy and appearing of hepatotoxicity was 13.71 ± 10.9 (4-60) days. After stopping the therapy, normal enzyme values were seen in 12.25 ± 6.9 (5-30) days. These 2 periods did not reflect any statistically difference between 2 sex (p> 0.05). In all cases, all of the drugs were stopped at same time. They were begun all at same time in 22 (62.9%) cases, step by step in 13 (37.1 %) cases. There were no statistically difference for mean values of age between these 2 groups of cases (p= 0.265). Hepatotoxicity was recurred in 2 cases (5.7%). Regarding the recurrence of hepatotoxicity, there was not seen any difference between groups begun all at same time or step by step, between groups having treatment with streptomycin or ethambutol (p> 0.05). In conclusion, when hepatotoxicity occures, we think that it will be apropriate to stop all the drugs at the same time and also begin all of them at same time after clinical regression and reaching normal enzyme values.

Özet

Bu çalışmada, tüberküloz ilaçlarına bağlı gelişen hepatotoksisitenin cinsiyet, yaş, eşlik eden hastalık, daha önce tedavi alıp almama ile ilişkisi incelendi. Ayrıca, bu olgularda ilaçlar kesildikten sonra ilaçların hepsine birden ya da kademeli başlanmasının, nüks ve klinik uyum açısından fark yaratıp yaratmadığı araştırıldı. Çalışmaya 1995-1999 yılları arasında, tüberküloz tedavisi sırasında hepatotoksisite gelişen 18 kadın, 17 erkek toplam 35 olgu alındı. Tedavinin başlangıcı ile hepatotoksisite gelişmesi arasında geçen ortalama süre 13.71 ± 10.9 (4-60) gün idi. Tedavi kesildikten sonra normal enzim değerlerine ortalama 12.25 ± 6.9 (5-30) günde ulaşıldı. Hepatotoksisite gelişmesi için geçen süre ve düzelme süresi her iki cins arasında istatistiksel farklılık göstermedi (p> 0.05). Olguların tümünde ilaçların hepsi kesildi. Yirmiiki (%62.9) olguda kesilen ilaçların hepsine birden, 13 (%37.1) olguda kademeli olarak başlandı. Bu iki grubun yaş ortalamaları arasında istatistiksel farklılık yoktu (p= 0.265). iki (%5.7) olguda hepatotoksisite nüks etti. Hepatotoksisite düzeldikten sonra ilaçların tümünün tam doz ya da kademeli başlandığı olgular ve streptomisinli ve etambutollü rejim alan olgular arasında nüks açısından istatistiksel farklılık izlenmedi (p> 0.05). Sonuçta; hepatotoksisite geliştiğinde ilaçların tümünün kesilmesinin, klinik iyileşme ile birlikte enzim düzeylerinin normale döndükten sonra ilaçların tümüne tam doz başlanmasının uygun olacağını düşünüyoruz.

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Cite This Article

ERBAYCU, A. E., ÇAKAN, A., DERELİ, Ş., ÖZSÖZ, A. (2022). The management of antituberculosis drug induced hepatotoxicity. Tüberküloz ve Toraks, Cilt: 50 - Sayı: 4, 480–484. https://ajindex.com/articles/619341

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References (19)

  1. Tahaoğlu K. Tüberküloz Tedavisi Sırasında Gelişen Hepatotoksisitede Klinik Yaklaşım. ANKEM Dergisi 1998; 12: 378-83
  2. Steele MA, Burk RF, Desperez RM. Hepatitis with isonasid and rifampicin-a meta-analysis. Chest 1971; 99: 465-71
  3. Askgaard BS, Wilke T, Dossing M. Hepatotoxicity caused by the combined action of isoniazid and rifampicin. Thorax 1995; 50: 213-4
  4. Lee WM. Drug-induced hepatotoxicity. N Engl J Med 1995; 333: 1118-27
  5. Steele MA, Des Prez RM. The role of pyrazinamide in tuberculosis chemoterapy. Chest 1988; 94: 845-50
  6. Ohno M, Yamaguchi I, Yamamoto I, et al. Slow N-acetylt-ransferase 2 genotype affects the incidence of isoniazid and rifampicin-induced hepatotoxicity. Int J Tuberc Lung Dis 2000; 4: 256-61
  7. Chowdhury A, Santra A, Kundu S, et al. Induction of oxidatiue stress in antitubercular drug-induced hepatotoxicity. Indian J Gastroenterol 2001; 20: 97-100
  8. Omerod LP, Skinner C, Wales C. Hepatotoxicity of antituberculosis drugs. Thorax 1996; 51: 111-3
  9. Thampson NP Caplinnnn ME, Hamilton MI, et al. Antituberculosis medication and the liver: Dangers and recommendations İn management. Eur Respir J 1995; 8: 1384-8
  10. Steete MA, Burk RF, Des Prez RM. Toxic hepatitis with isoniazid and rifampin. Chest 1991; 99: 465-71
  11. Moulding TS, Redeker AG, Kanel GC. Twenty isoniazid-associated deaths in one state. Am Rev Respir Dis 1989; 140: 700-5
  12. Schossberg T. The dark side of antituberculosis therapy: Adverse events involving liver function. Eur Resp Rev 1995; 4: 1247
  13. Gilroy SA, Rogers MA, Blair DC. Treatment of latent tuberculosis infection in patients aged > or = 35 years. Clin Infect Dis 2000; 31: 826-9
  14. Kumar A, Misra PK, Mehotra R, et al. Hepatotoxicity of rifampin and isoniazid. Am Rev Resp Dis 1991; 143: 1350-2
  15. Mc Glynn KA, Lustbader ED, Sharrar RG, et al.İsoniazid prophylaxis In hepatitis B carriers. Am Rev Res Dis 1986; 134: 666-8
  16. Türktaş H, Ünsal M, Tülek N, Örüç O. Hepatotoxicity of antituberculosis therapy (rifampicin, isoniazid and pyrazinamide) or viral hepatitis. Tubercl Lung Dis 1994; 75: 58-60
  17. Wong WM, Wu PC, Yuen MF, et at. Antituberculosis drugrelated liver dysfunction In chronic hepatitis B infection. Hepatology 2000; 3): 201-6
  18. Grönhagen RC, Hellstrom PE, Fröseth B.Predisposing factors in hepatitis induced by isoniazid-rifampin treatment of tuberculosis. Am Rev Resp Dis 1978; 118: 461-6
  19. Dossing M, Wilcke JT, Askgaard DS, Nybo B. liver injury during antituberculosis treatm