Objective:The objective was to assess the role of homocysteine in the development of atherosclerosis in common carotid artery in the carbamazepine treated epileptic patients.Methods:This study was conducted in the Department of Biochemistry, Basic Medical Sciences Institute (BMSI), Jinnah Postgraduate Medical Center (JPMC), Karachi. Three hundred individuals, aged 34 ± 9.5 years were selected and divided into three groups. Each group comprised of 100 subjects labeled as Group-A (control group had healthy individuals), Group-B (newly diagnosed epileptic patients without antiepileptic therapy), Group-C (epileptic patients on Carbamazepine therapy, which was further subdivided into C-I having epileptic patients on Carbamazepine therapy less than 1 year n=33, C-II had epileptic patients on Carbamazepine therapy 1-2 years n = 33 and C-III comprised of epileptic patients on Carbamazepine therapy more than 2 years n = 34). Blood concentration of homocysteine was measured and ultrasound of Common Carotid Artery for intima-media thickness was performed.Results:Significantly elevated level of homocysteine was observed in epileptic patients on CBZ therapy. Common Carotid Artery Intima-media thickness (CCA IMT) was observed significantly high throughout group C but it was more profound in Group-C-III. Homocysteine was found positively correlated with right CCA IMT, left CCA IMT and mean CCA IMT.Conclusion:Hyperhomocysteinemia was linked with increased risk of atherosclerosis in CBZ treated epileptic patients.

Objectives: To observe the association between dyslipidemia and homocysteine level in epileptic patients; especially on carbamazepine monotherapy. Study Design: Cross sectional study. Setting: Neurology Department and Epilepsy Centre of Jinnah Post Graduate Medical Centre, Karachi. Period: From January 2015 – January 2016. Material & Methods: Total 300 subjects, aged more than 15 years were included and divided into three groups.  Group A (100 healthy individuals) was control group, Group B (100 newly diagnosed epileptic patients without antiepileptic therapy), Group C (100 epileptic patients on Carbamazepine therapy, which was further subdivided into C-I (n=33) had epileptic patients on Carbamazepine therapy less than 1 year, C-II (n=33) comprised of epileptic patients on Carbamazepine therapy 1-2 years and C-III (n=33) had epileptic patients on Carbamazepine therapy more than 2 years. Serum lipid profile and homocysteine levels were measured. Results: In patients with different durations of carbamazepine monotherapy; a noteworthy incremental trend in the levels of homocysteine, total cholesterol, triglyceride, low density lipoprotein cholesterol, very low density lipoprotein cholesterol was observed. Homocysteine was found positively correlated with total cholesterol, triglyceride, low density lipoprotein cholesterol, very low density lipoprotein cholesterol. Conclusion: In our study dyslipidemia was associated with hyperhomocysteinemia, which in turn was correlated with atherosclerosis in CBZ treated epileptic patients.

Objectives: The aim of this study was to evaluate the major determinants of diabetic retinopathy. Study Design: Cross sectional, case control study. Setting: Department of Biochemistry, Basic Medical Sciences Institute, Jinnah Post Graduate Medical Centre, Karachi. Period: March 2015 to April 2016. Material & Methods: Ethical approval was taken from the Institutional Review Board of JPMC. A total of 208 people including type 2 diabetic patients and healthy control subjects; of male gender, aged between ≥30 years and ≤ 60 years were recruited and assigned to four study groups. Each group comprise of 52 individuals, depending on the ophthalmoscopy findings, i.e. healthy controls, diabetic without retinopathy (NDR), diabetic with non-proliferative diabetic retinopathy (NPDR) and diabetic with proliferative diabetic retinopathy (PDR). Fasting blood sugar was estimated using GOD-PAP method, while HbA1c was estimated by HPLC method. Data was analyzed on SPSS software version 16. Results: Diabetics with Diabetic Retinopathy had a poor glycemic control as compare to Diabetics without Diabetic Retinopathy (FBS; 109.12 ± 13.81 vs. 184.29 ± 40.07 vs. 188.6 ± 47.68 vs. 217.06 ± 62.33; p-value = 0.001) (HbA1c; 6.73 ± 0.56 vs. 8.40 ± 1.77 vs. 9.71 ± 1.85 vs. 14.91 ± 3.87; p-value = 0.001). For Diabetic Retinopathy the odds ratio of glycemic control i.e. FBS was observed as 1.019 & HbA1c was recorded as 1.561; which was statistically significant. Conclusion: Glycemic indicators; including FBS and HbA1c, are found to be the major determinants of Diabetic Retinopathy in our study.

Objective: This study was planned over the hypothesis that pomegranate extract rich in ellagic acid used with minocycline could decrease its adverse effect and prolong its therapeutic use and efficacy. Study design and Setting: This experimental study was done in the department of anatomy, Basic Medical Sciences Institute, Jinnah Postgraduate Medical Center, Karachi, Methodology: We acquired 40 guinea pigs (male, adult, 450 – 550 gm), randomly divided them into 4 groups.Group B received 0.0003mg/g bodyweight of minocycline only, group C was given 0.0003mg/g bodyweight of minocycline with 0.4mg/g bodyweight of pomegranate, group D was given 0.4mg/g bodyweight pomegranate only; with keeping group A with no intervention at laboratory diet for 8 weeks. After the experimental period, the animals were sacrificed, H & E and DOPA-OXIDASE staining was done on harvested skin tissues for morphometric observations under light microscopy. Results: The results showed that minocycline induced reduction in mean thickness of epidermis and increased melanin pigment deposition. Mean number of melanocytes decreased with pomegranate use though the difference was insignificant (P-value > 0.05) but consistent and measurable. Conclusions: It was proven that by including pomegranate in our daily diet, the process of hyperpigmentation of skin induced by the broad spectrum tetracycline particularly minocycline, can be slow down by decreasing the activity of tyrosinase enzyme, thus it provides a novel pathway to fight against any other drug induced hyperpigmentation occurring due to increase activity of tyrosinase enzyme

Objectives: To observe the association between dyslipidemia and homocysteine level in epileptic patients; especially on carbamazepine monotherapy. Study Design: Cross sectional study. Setting: Neurology Department and Epilepsy Centre of Jinnah Post Graduate Medical Centre, Karachi. Period: From January 2015 – January 2016. Material & Methods: Total 300 subjects, aged more than 15 years were included and divided into three groups.  Group A (100 healthy individuals) was control group, Group B (100 newly diagnosed epileptic patients without antiepileptic therapy), Group C (100 epileptic patients on Carbamazepine therapy, which was further subdivided into C-I (n=33) had epileptic patients on Carbamazepine therapy less than 1 year, C-II (n=33) comprised of epileptic patients on Carbamazepine therapy 1-2 years and C-III (n=33) had epileptic patients on Carbamazepine therapy more than 2 years. Serum lipid profile and homocysteine levels were measured. Results: In patients with different durations of carbamazepine monotherapy; a noteworthy incremental trend in the levels of homocysteine, total cholesterol, triglyceride, low density lipoprotein cholesterol, very low density lipoprotein cholesterol was observed. Homocysteine was found positively correlated with total cholesterol, triglyceride, low density lipoprotein cholesterol, very low density lipoprotein cholesterol. Conclusion: In our study dyslipidemia was associated with hyperhomocysteinemia, which in turn was correlated with atherosclerosis in CBZ treated epileptic patients.