DECIPHERING DRUG-INDUCED LIVER INJURY POST ANTI-TUBERCULAR TREATMENT: CASE REPORT AND DIAGNOSTIC INSIGHTS

Abstract

First-line anti-tubercular medications are viable in treating tuberculosis brought about by susceptible strains of Mycobacterium tuberculosis. Most antibacterial medications are known to cause hepatotoxicity, which might keep the microscopic organisms from sticking to the medicine and subsequently cause drug resistance in mycobacteria. Anything from mild, nonspecific alterations to fulminant hepatic failure, cirrhosis, and liver cancer can be caused by drug-induced liver injury. It has been reported that isoniazid plus Rifampicin treatment results in metabolites reaching hepatotoxic levels much faster than isoniazid alone. This is because the two treatments work synergistically rather than requiring further medication. Inducible CYP2E1 by ATT is constitutively expressed in the liver. A female patient, aged 25 years, was brought to the Emergency Room in an unconscious state and reported seven days of bilious non-projectile vomiting, yellowish sclera, anorexia, and pain and discomfort in the abdomen especially on the right side. She was diagnosed with tuberculosis one month ago, and she has been on the first category of anti-tubercular medication ever since. Furthermore, she was additionally recommended corticosteroids 10 days prior. On the CT scan of the chest, areas of decreased density were observed in the posterior segments of the Left Upper lobe. The results of her liver function test indicated that she had hepatitis. After stopping the present hepatotoxic drug and switching to a different regimen, her symptoms were relieved and her laboratory values started to recover to normal. When treating ATT-induced liver injury, second-line anti-tuberculosis medications should be recommended while taking cirrhosis and hepatitis B into account as well as the hepatic resilience of hepatotoxic treatments.