Zunera Hakim, Akbar Waheed, Bareera Hakim, Najam-ul Hassan.
Liver injury; protective effect of isoniazid on thionamide induced in mice.
Professional Med J Jan ;23(10):1269-75.

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 the important role of drug metabolizing enzymes in generation of this adverse reaction. Study design: Randomized controlled laboratory trial. Period: 04 months from March 2015 to June 2015. Settings: Department of Pharmacology and Therapeutics, Army Medical College, Rawalpindi. Aim of the study: The effect of isoniazid (INH) on MMI induced hepatotoxicity was evaluated in mice. Materials and Method: Thirty male BALB/c mice were randomly divided into five groups. Group I served as control group (C-I). Group II (C-II) served as control for INH treated group and received plain drinking water for ten consecutive days. Hepatotoxicity was 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 for determination of combined effect of both drugs. The extent of hepatic damage was determined by 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. INH administration produced no significant change in both serum biomarkers and histopathology appearance. Pretreatment of INH with MMI produced insignificant escalation of liver enzymes and microscopic parameters. However, biochemical and histological comparison of this group with MMI group revealed statistically consequential differences. Conclusion: INH has beneficial role in preventing MMI induced hepatic injury.

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