ACUTE SUB FULMINANT HEPATITISINDUCED BY ANTI-TUBERCULOSIS DRUGS

Introduction :Hepatotoxicity is a prominent adverse effect of anti-tuberculosis drugs, with a frequency of up to 20%, but it is often reversible on cessation of treatment, and fatal outcome is exceptional. We report an observation of acute subfulminant hepatitis induced by antituberculosis treatment. Observation : A 60-year-old patient with a three-year history of insulin-dependent diabetes was started on anti-tuberculosis treatment for smear-positive pulmonary tuberculosis. After two months of treatment, the patient complained of asthenia, epigastric pain, and conjunctival jaundice. Physical examination revealed only jaundice, with no signs of chronic liver disease. Laboratory tests showed hepatic cytolysis (transaminases 10 times the upper limit of normal), associated with cholestasis (alkaline phosphatase 2 times the upper limit of normal, total bilirubin 98 μmol/L), and hepatic insufficiency (prothrombin time = 53%). Despite adjustment of anti-tuberculous drug doses based on serum concentrations, the decision was made to discontinue anti-tuberculosis treatment and admit the patient to the hospital. During the etiological work-up, viral serologies (hepatitis B, C, and HIV) were all negative, as was the autoimmune screening. There was no inflammatory syndrome or hyper eosinophilia. The patient denied alcohol consumption, and no potentially hepatotoxic medications were identified on medication review. Abdominal ultrasound and CT showed normal hepatic and biliary structures with the presence of ascites. Paracentesis revealed transudative fluid, attributed to hypoalbuminemia of 12 mg/L. Liver biopsy was deferred due to clinical and biochemical deterioration (total bilirubin elevated to 288 μmol/L) and worsening hepatic failure (prothrombin time at 7%, unresponsive to vitamin K supplementation). The patient died from grade III hepatic encephalopathy 35 days after discontinuation of treatment. Discussion et Conclusion: In the light of this observation, we emphasise the role of screening and early diagnosis of toxic hepatitis, and we reiterate the importance of monitoring patients on anti-tuberculosis drugs to avoid a severe and fatal course due to adverse liver reactions.

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Publication Details

Journal
International Journal of Advanced Research
Published
2024-11-30
DOI
https://doi.org/10.21474/ijar01/19931
Primary Topic
Drug-Induced Hepatotoxicity and Protection
Type
article
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article

ACUTE SUB FULMINANT HEPATITISINDUCED BY ANTI-TUBERCULOSIS DRUGS

Boucaid Abdelhalim, R. Ben Ismaïl, Rafik Anis
International Journal of Advanced Research
Drug-Induced Hepatotoxicity and Protection
article

ACUTE SUB FULMINANT HEPATITISINDUCED BY ANTI-TUBERCULOSIS DRUGS

Boucaid Abdelhalim, R. Ben Ismaïl, Rafik Anis
article en

Abstract

Introduction :Hepatotoxicity is a prominent adverse effect of anti-tuberculosis drugs, with a frequency of up to 20%, but it is often reversible on cessation of treatment, and fatal outcome is exceptional. We report an observation of acute subfulminant hepatitis induced by antituberculosis treatment. Observation : A 60-year-old patient with a three-year history of insulin-dependent diabetes was started on anti-tuberculosis treatment for smear-positive pulmonary tuberculosis. After two months of treatment, the patient complained of asthenia, epigastric pain, and conjunctival jaundice. Physical examination revealed only jaundice, with no signs of chronic liver disease. Laboratory tests showed hepatic cytolysis (transaminases 10 times the upper limit of normal), associated with cholestasis (alkaline phosphatase 2 times the upper limit of normal, total bilirubin 98 μmol/L), and hepatic insufficiency (prothrombin time = 53%). Despite adjustment of anti-tuberculous drug doses based on serum concentrations, the decision was made to discontinue anti-tuberculosis treatment and admit the patient to the hospital. During the etiological work-up, viral serologies (hepatitis B, C, and HIV) were all negative, as was the autoimmune screening. There was no inflammatory syndrome or hyper eosinophilia. The patient denied alcohol consumption, and no potentially hepatotoxic medications were identified on medication review. Abdominal ultrasound and CT showed normal hepatic and biliary structures with the presence of ascites. Paracentesis revealed transudative fluid, attributed to hypoalbuminemia of 12 mg/L. Liver biopsy was deferred due to clinical and biochemical deterioration (total bilirubin elevated to 288 μmol/L) and worsening hepatic failure (prothrombin time at 7%, unresponsive to vitamin K supplementation). The patient died from grade III hepatic encephalopathy 35 days after discontinuation of treatment. Discussion et Conclusion: In the light of this observation, we emphasise the role of screening and early diagnosis of toxic hepatitis, and we reiterate the importance of monitoring patients on anti-tuberculosis drugs to avoid a severe and fatal course due to adverse liver reactions.

International Journal of Advanced ResearchVol. 12(11)
Good health and well-being
Openalex Percentile: Top 69%
Drug-Induced Hepatotoxicity and Protection
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ACUTE SUB FULMINANT HEPATITISINDUCED BY ANTI-TUBERCULOSIS DRUGS — Boucaid Abdelhalim, R. Ben Ismaïl, et al. · International Journal of Advanced Research (2024) | TGRS Research Map | TGRS