Causality analysis of myopathy secondary to dapagliflozin therapy in type II Diabetes – A case study

Abstract

Diabetes mellitus is a chronic metabolic condition that is becoming more prevalent globally. Diabetic patients must maintain adequate glycemic control in order to avoid or postpone diabetic complications. Diabetes care has evolved since the introduction of sodium-glucose co-transporter 2 inhibitors (SGLT2i). Postmarketing surveillance has shown cases of diabetic ketoacidosis and increased bone fracture risk associated with the use of SGLT2 inhibitors. We present a case of a 55-year-old female with a 6-year history of diabetes who exhibited weakness, muscular pains, and a burning feeling in her left thigh as a result of Dapagliflozin. Before initiating dapagliflozin treatment, the patient's fasting blood sugar (FBS) was 314 mg/dl and postprandial blood sugar (PPBS) was 343 mg/dl. After adding dapagliflozin as part of the therapy, the FBS improved to 179.24 mg/dl, and the PPBS decreased to 214.39 mg/dl, indicating a significant reduction in blood glucose levels. The introduction of Dapagliflozin in the treatment reduces the therapeutic gap compared to earlier treatment schedule, but retain the same side effect and became rechallenge. The instance of myopathy linked to dapagliflozin was confirmed following the causality evaluation by WHO Schales. It exemplifies the need for detecting drug-induced myopathy. Recently, minimal evidence has emerged showing a link between prolonged SGLT2 inhibitor use and accelerated myopathy. Myopathy is the generalised loss of skeletal muscle mass and function that occurs with ageing. Its existence is linked to negative health outcomes such as physical impairment, low quality of life, and death. Clinically, no other cause of myopathy was detected, and biochemical analysis indicated that dapagliflozin was the cause of her myopathy.