Steroid-Induced Diabetic Ketoacidosis Following High-Dose Intravenous Methylprednisolone Pulse Therapy in a Patient with Dermatomyositis: A Case Report
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Background: Diabetic ketoacidosis (DKA) is a life-threatening acute metabolic complication of diabetes mellitus characterized by hyperglycemia, metabolic acidosis, and ketosis. Although glucocorticoid therapy is a well-recognized cause of steroid-induced hyperglycemia, the development of DKA in patients without previously diagnosed diabetes is uncommon. High-dose intravenous methylprednisolone pulse therapy may significantly increase insulin resistance and precipitate severe metabolic decompensation, particularly in patients with underlying inflammatory disorders.
Case Presentation: We report the case of a 62-year-old patient with active dermatomyositis who developed severe diabetic ketoacidosis shortly after receiving high-dose intravenous methylprednisolone pulse therapy. Before hospitalization, the patient had no history of diabetes mellitus, and self-monitored blood glucose levels had remained within the normal range. Following pulse therapy, the patient presented with profound hyperglycemia (545 mg/dL), positive ketonuria, metabolic acidosis (pH 7.20, bicarbonate 14.8 mmol/L), and an elevated anion gap, fulfilling the diagnostic criteria for DKA. Intensive management, including aggressive intravenous fluid resuscitation, continuous intravenous insulin infusion, electrolyte replacement, and close metabolic monitoring, resulted in gradual correction of hyperglycemia and metabolic acidosis. Despite metabolic stabilization, the patient experienced progressive muscle weakness, dysphagia, and respiratory deterioration related to active dermatomyositis.
Conclusion: This case highlights high-dose glucocorticoid pulse therapy as a potential precipitating factor for diabetic ketoacidosis, even in individuals without previously diagnosed diabetes mellitus. Clinicians should closely monitor blood glucose levels before, during, and after corticosteroid pulse therapy, particularly in patients with autoimmune inflammatory diseases receiving prolonged glucocorticoid treatment. Early recognition and prompt management of steroid-induced DKA are essential to reduce morbidity and improve clinical outcomes.
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