Abstract
Background: Type-2 diabetes mellitus, is associated with low-grade chronic inflammation, which could contribute to its pathogenesis. The objective of this study is to evaluate the role of the nonsteroidal antinflammatory drug (diclofenac sodium) in type 2 diabetic patients who are not achieving target HbA1c. Patients and Methods: Fifty four, type-2 diabetic patients consulting Al-Faiha Diabetes, Endocrine and Metabolism Center (FDEMC) in Basrah were included in this study after meeting a set of inclusion criteria. Their HbA1c was more than 7% (53 mmol/mol) despite the optimal use of oral antihyperglycemic drugs. They were overweight with a BMI of 25 or more. They served as the study group and treated with diclofenac sodium. Diclofenac sodium was administered to each patient as 100 mg sustained-release capsule, given once daily for one month (with omeprazole 20 mg daily). Another fifty patients of similar inclusion criteria were also followed for 3 months, but without treatment with diclofenac sodium and served as a control group. Results: Treatment with diclofenac sodium 100 mg sustained-release capsules (in presence of Original Research Article Abdullah et al.; BJMMR, 9(11): 1-9, 2015; Article no.BJMMR.19458 2 omeprazole 20 mg daily), resulted in a significant improvement in the glycemic control and inflammation parameters in the form of a reduction in the HbA1c, fasting plasma glucose and postprandial plasma glucose. The mean ± SEM of HbA1c before the start of treatment with diclofenac sodium is 9.26±0.269 percentage which was reduced significantly to 8.25 ± 0.255 percentages after one month of diclofenac treatment (a reduction by 10.9%, p˂0. 001). HbA1c levels continued to decrease even after stopping diclofenac treatment reaching a level of 7.41% (a reduction of 19.9% compared to pre-treatment level, p ˂0. 001). Fasting plasma glucose decreased significantly from a mean ± SEM of 153.87±4.65 mg/dl to 129.98±3.41 mg/dl (a decrease of 16%, p˂0. 001). High-sensitivity C-reactive protein also decreased by 19% one month after diclofenac treatment. Two months after stopping treatment, high-sensitivity C-reactive protein continued to decrease reaching a value of 0.379±0.291 mg/L (a reduction by 45%, p˂0. 001). There was no significant change in insulin level after diclofenac treatment. Insulin resistance, measured by the Homeostasis Model of Assessment Insulin Resistance (HOMA-IR) equation, decreased two months after diclofenac treatment from 83.3% to 68.5%. Conclusion: If the results of this study are confirmed by other studies in the future,type-2 diabetic patients who are not achieving target HbA1c after treatment with two oral antihyperglycemic drugs, showed a significantly reduced HbA1c levels compared with pre-treatment levels when treated with diclofenac sodium 100 mg SR capsule for one month, with no side effects. This reduction, increased further even after cessation of diclofenac treatment with reduction in the markers of insulin resistance and inflammation.
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