MON-548 - Latent Autoimmune Diabetes in Adults Unmasked by SGLT2 Inhibitor-Associated Euglycemic Diabetic Ketoacidosis

Latent Autoimmune Diabetes in Adults (LADA) is an autoimmune form of diabetes typically presenting after age 30-35 years, frequently misclassified as type 2 diabetes mellitus due to its gradual onset in adulthood. Maturity-Onset Diabetes of the Young (MODY) is a monogenic form of diabetes characterized by hyperglycemia typically presenting before age 25 years, frequently misdiagnosed as type 1 or type 2 diabetes mellitus. Misclassification of diabetes subtypes can delay therapy and expose patients to inappropriate pharmacologic agents. Sodium-glucose cotransporter-2 (SGLT2) inhibitors are contraindicated in insulin-deficient states and are associated with an increased risk of euglycemic diabetic ketoacidosis (euDKA), particularly in patients with insulin deficiency.

We report the case of a 30 year old male with a 5 year history of presumed MODY who presented with 24 hours of malaise, persistent nausea, and one episode of vomiting. He denied recent infection, fasting, or alcohol use. His history was notable for progressively worsening glycemic control despite escalating oral therapy, including empagliflozin/metformin, glipizide, pioglitazone, and alogliptin, with a glycosylated hemoglobin (HbA1c) of 11.3%. Physical examination revealed severe volume depletion, heart rate 97 bpm, blood pressure 139/84 mmHg, and mild diffuse abdominal tenderness. Laboratory evaluation demonstrated serum glucose 181 mg/dL, arterial pH 7.047, bicarbonate 6.2 mmol/L, an anion gap of 33, β-hydroxybutyrate >8.0 mmol/L, glycosuria and ketonuria, confirming euDKA, likely precipitated by SGLT2 inhibitor therapy. The patient was treated with intravenous isotonic fluids, continuous intravenous insulin infusion, electrolyte replacement, and dextrose supplementation. Further evaluation revealed a low C-peptide at 0.31 ng/mL (0.10 nmol/L), indicating severe insulin deficiency. Autoimmune testing revealed glutamic acid decarboxylase (GAD) autoantibodies >250 IU/mL, confirming LADA. He was discharged on a basal-bolus insulin regimen, with subsequent improvement in glycemic control and a follow-up HbA1c of 6.6%.

This case illustrates multiple diagnostic pitfalls: initial MODY misclassification in a young, non-obese patient; progressive glycemic failure despite multiple oral agents; and the serious complication of SGLT2 inhibitor use in unrecognized autoimmune diabetes. It highlights the importance of accurate diabetes classification to guide appropriate therapy. The combination of young age, non-obesity, and treatment failure on multiple oral agents should prompt autoantibody and C-peptide testing. SGLT2 inhibitors are not approved for type 1 diabetes and should not be used in patients with insulin-deficient states or prior diabetic ketoacidosis.

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