Empagliflozin Improves Muscle Weakness in a Patient with Suspected Glycogen Storage Myopathy: A Case Report

Objective To describe the clinical course of a patient with chronic progressive muscle weakness and intramyocellular glycogen deposition who received empagliflozin. Methods We present a case of a young male patient with chronic progressive proximal limb weakness, exercise intolerance, and supine dyspnea. Muscle biopsy revealed massive glycogen deposition in skeletal myocytes. Genetic testing for glycogen storage diseases identified no pathogenic variants. After conventional therapies failed, the patient received empagliflozin 10 mg once daily for 3 months. Clinical symptoms, laboratory parameters, and safety outcomes were assessed. Results Before treatment, the patient had proximal muscle strength of grade 3/5 on manual muscle testing, elevated creatine kinase (856 U/L), and abnormal liver function tests. After 3 months of empagliflozin treatment, muscle strength normalized to grade 5/5, creatine kinase decreased to 142 U/L, liver function tests returned to the normal range, and exercise intolerance resolved. Fasting blood glucose remained stable at 4.2–5.6 mmol/L, with no hypoglycemia or adverse events reported. Conclusion In this patient, empagliflozin was temporally associated with improved muscle weakness and metabolic parameters. However, because this is a single case report, these findings are hypothesis-generating and cannot establish causality. Further studies with