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.

Diabetes Mellitus has become a global health concern due to its continued rise in prevalence. According to International Diabetic Federation (IDF), Type II diabetes mellitus (T2DM) currently affects 462 million people worldwide and is expected to grow from this figure to 642 million by 2040. Objective: The study was conducted to evaluate the glycemic response to metformin in Type-II diabetes and assess its association with age and gender. Methods: A cross sectional study was conducted at the Pharmacology Department of Riphah International University from Jan 2020 to Dec 2021.Type-II diabetic patients (n=200) on metformin monotherapy fulfilling the inclusion criteria were enrolled and followed up till three months. Baseline parameters were documented and reduction in HbA1c was determined. Numerical and categorical data was analyzed by chi-square and t-test using SPPS 23. Results: Our study demonstrates that 52% (104) of the patients were metformin responders while 48% (96) were non-responders. The reduction in HbA1c was significantly greater in responders than non- responders (- 1.58±1.07 % VS -0.32±0.35 %).  Out of 85 males, 46 (54%) responded to metformin optimally while only half (50%) of the female subjects produced desirable response. However, there was no effect of gender on metformin response status with p=0.60 and changes in HbA1c levels over time were not significantly different in either sex. The mean age of responders and non-responders was found to be 48.23±9.64 years and 44.13±7.82 respectively. The effect of age on response of metformin and mean change in HbA1c among different age groups was found to be statistically significant with p=0.03 and p=0.04 respectively. Conclusion: There exists variability in response to metformin in type-II diabetes which is associated with age of the patient but remains un-influenced by gender of the patient.