MON-622 - Refractory Diabetic Ketoacidosis: A Rare Case of Exogenous Insulin Antibody Syndrome

Exogenous insulin antibody syndrome (EIAS) should be considered in patients with severe insulin resistance as early recognition is critical for appropriate management. We present a case of refractory diabetic ketoacidosis (DKA) caused by EIAS.

A 64-year-old man with end stage renal disease on hemodialysis (HD) and type 2 diabetes presented with 1 week of abdominal pain, nausea, and diarrhea. His diabetes was well-controlled (A1c 6.6%) on liraglutide and 70/30 insulin 10 units twice a day. He denied steroid use and did not appear Cushingoid or acromegalic. Initial labs showed glucose 1274 mg/dL, bicarbonate 17 mmol/L, anion gap 29, beta-hydroxybutyrate 6.5 mmol/L, and pH of 7.28 consistent with DKA. Infectious workup yielded Clostridioides difficile PCR positivity with negative toxin, for which he was treated empirically.

He remained in severe DKA despite receiving regular insulin infusion at 30 units/hour and NPH insulin 30 units daily and needed emergent HD on day 1 and 3. His insulin requirement temporarily improved with correction of his acidosis, however, DKA recurred when he started eating and insulin requirement escalated to >800 units per day. Switching to Lantus and Novolog did not improve glycemic control. He was able to avoid DKA with glucose 150-500 mg/dL on insulin infusion at 30 units/hour, subcutaneous insulin 250-300 units per day, plus daily HD.

Insulin autoantibodies returned elevated at >50 U/mL on day 8 confirming EIAS. Plasma exchange (PLEX) was initiated on day 9 with minimal improvement in insulin requirements after 2/5 sessions. Methylprednisolone 1 mg/kg was initiated on day 11 and reduced insulin requirement to 250-300 units within 24 hours. Adding liraglutide on day 14 slightly reduced insulin requirement. Mycophenolate mofetil (MMF) was started on day 15, and methylprednisolone dose was decreased to 0.6 mg/kg to reduce steroid-induced hyperglycemia. Since he still required around 200 units of insulin daily, intravenous immunoglobulin (IVIG) 500 mg/kg was administered on day 20 with plans for rituximab while inpatient.

Early detection of EIAS is crucial for diagnosis and prompt treatment of this rare condition. Insulin autoantibodies should be obtained early to prevent delays in management. In other cases of EIAS, immunosuppression was initiated once the antibodies were detected; however, in this case, PLEX was initiated first due to his concurrent infection. Management of EIAS can be challenging as there is no established treatment algorithm for this condition. Utilization of multiple treatment modalities targeting antibody clearance and immunosuppression may be required as exemplified by this case.

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