LIVER INJURY

Methimazole (MMI) is a widely used antithyroid drug for hyperthyroidism.However its clinical use is associated with many deleterious effects including hepatotoxicity.MMI induced liver injury is dependent upon bio-activation to toxic intermediates revealing theimportant role of drug metabolizing enzymes in generation of this adverse reaction. Studydesign: Randomized controlled laboratory trial. Period: 04 months from March 2015 to June2015. Settings: Department of Pharmacology and Therapeutics, Army Medical College,Rawalpindi. Aim of the study: The effect of isoniazid (INH) on MMI induced hepatotoxicity wasevaluated in mice. Materials and Method: Thirty male BALB/c mice were randomly dividedinto five groups. Group I served as control group (C-I). Group II (C-II) served as control forINH treated group and received plain drinking water for ten consecutive days. Hepatotoxicitywas induced by single intraperitoneal injection of MMI at a dose of 1000mg/kg in Group III(MMI).Group IV (INH) received isoniazid (0.1%w/v) in drinking water for ten consecutive days.A separate group V (INH +MMI) of isoniazid pretreated mice was given MMI at eleventh day fordetermination of combined effect of both drugs. The extent of hepatic damage was determinedby estimation of serum ALT and ALP along with histopathological analysis of liver samples.Results: MMI resulted in markedly elevated ALT and ALP with hepatic inflammation. INHadministration produced no significant change in both serum biomarkers and histopathologyappearance. Pretreatment of INH with MMI produced insignificant escalation of liver enzymesand microscopic parameters. However, biochemical and histological comparison of this groupwith MMI group revealed statistically consequential differences. Conclusion: INH has beneficialrole in preventing MMI induced hepatic injury.