Biochemical Investigation of Drug-Induced Liver Injury in Tuberculosis Patients on First-Line Antitubercular Therapy in Borno State

First-line antitubercular drugs including isoniazid, rifampicin, and pyrazinamide are hepatotoxic in a clinically significant proportion of treated patients, and the biochemical characterization of drug-induced liver injury in tuberculosis patients in Borno State, where tuberculosis burden is high, is important for improving treatment safety monitoring. This study investigates the biochemical profile of drug-induced liver injury in patients receiving first-line antitubercular therapy at the University of Maiduguri Teaching Hospital, Borno State. A prospective cohort of one hundred and twenty newly diagnosed pulmonary tuberculosis patients was enrolled at treatment initiation. Liver function tests including ALT, AST, ALP, GGT, total and direct bilirubin, albumin, and prothrombin time were measured at baseline and at weeks two, four, eight, and sixteen of therapy. Drug-induced liver injury was defined as ALT elevation above five times the upper limit of normal with symptoms, or above ten times without symptoms. Genetic risk was assessed by NAT2 acetylator status genotyping for slow-acetylator alleles associated with isoniazid hepatotoxicity. Results show that clinically significant drug-induced liver injury occurred in 14.2 percent of patients. Peak hepatotoxicity frequency occurred at week four. Slow NAT2 acetylator genotype was present in 47 percent of patients and was significantly associated with drug-induced liver injury risk. Baseline ALT elevation, malnutrition as indicated by serum albumin below 35 g/L, and coexisting HIV infection were independent biochemical predictors of hepatotoxicity. ALT elevation preceded clinical jaundice by a mean of eleven days in affected patients. The study recommends biweekly liver function monitoring in high-risk patients. Keywords: drug-induced liver injury, tuberculosis, antitubercular therapy, NAT2 genotype, Borno State.