Abstract
<h2>ABSTRACT</h2> <b>Objective:</b> To report an episode of diabetic ketoacidosis (DKA) in a patient with type 1 diabetes mellitus treated with low doses of neutral protamine Hagedorn insulin. The patient had recently initiated treatment with a sodium-glucose cotransporter-2 inhibitor as well. <b>Methods:</b> We describe the clinical presentation, laboratory data, and management of a diabetic patient with DKA. <b>Results:</b> A 50-year-old diabetic male presented with weight loss, fatigue, nausea, recurrent vomiting, muscle pain, malaise, and shortness of breath 2 weeks after initiation of empagliflozin and reduction in insulin dose. On admission to the emergency department, the glucose concentration was 541 mg/dL, pH 7.087, bicarbonate 4.5 mmol/L, blood urea nitrogen 50 mg/dL, creatinine 2.0 mg/dL, and beta-hydroxybutirate 4.1 mmol/L. The estimated osmolality was 319.9 mOsm/L and the anion gap was 25.6 mEq/L. Empagliflozin was discontinued; the patient was treated with balanced electrolyte solutions and continuous insulin infusion with resolution of acute kidney injury and metabolic acidosis. C-peptide level was <0.1 ng/mL and anti-glutamic acid decarboxylase-65 was 6 IU/mL (reference range is <5 IU/mL). <b>Conclusion:</b> In this patient, who was misdiagnosed with type 2 diabetes mellitus, the insulin dose reduction provoked DKA. When selecting sodium-glucose cotrans-porter-2 inhibitors in diabetics, physicians must assure adequate insulin provision as well as strict monitoring of blood glucose and urine ketones. <b>Abbreviations: DKA</b> = diabetic ketoacidosis; <b>NPH</b> = neutral protamine Hagedorn; <b>SGLT2</b> = sodium-glucose cotransporter-2; <b>T1DM</b> = type 1 diabetes mellitus; <b>T2DM</b> = type 2 diabetes mellitus
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