SUN-182 When Insulin Is Not Enough...

Introduction: Multiple factors contribute to hyperglycemia in hospitalized patients, such as underlying medical conditions, pathophysiological stress, and medications. The development of transient insulin resistance is a known cause of hyperglycemia in both diabetic and non-diabetic patients. Rarely, patients can develop extreme insulin resistance, defined as having an insulin requirement of more than 3 units/kg/day. We report a case of extreme insulin resistance in a patient admitted with diabetic ketoacidosis (DKA) mediated by anti-insulin receptor antibodies. Case: 91 y/o F with history of CLL and IDDM (diagnosed three months prior, Last Hemoglobin A1C 14.2%) that was brought to the ED by EMS after being found covered in urine, lethargic and confused. On admission, she was found to be tachycardic, afebrile, normotensive, BMI 28.71. On physical exam she was diaphoretic and altered, but moving all extremities. She showed no findings consistent with acromegaly, hirsutism, red striae, moon-like facies, buffalo hump, or acanthosis nigricans. Initial labs included pronounced leukocytosis of 29.24, potassium of 5.9, glucose of 655, Anion Gap 25, HCO3 4, Beta Hydroxybutyrate 91.55, Lactic Acid 4.1, BUN 33, and a serum Cr of 1.49. UA showed: +30 protein, +80 ketones, Glucose >500, (-) nitrite and leukocyte esterase, & 2+ WBCs. The urine was positive for Bence Jones Protein Lambda Type. Her Kappa/Lambda Ratio was WNLs at 1.42 mg/L. UCx & BCx were negative. Patient was admitted to the ICU with an insulin drip following our hospital’s DKA protocol. After admission, she became hypotensive with increase work of breathing, for which she was intubated and started on vasopressin. On the second day of admission, Endocrinology was consulted due to inability to control blood glucose levels despite maximizing the rate of IV insulin infusion and persistent acidosis. Additional labs revealed a normal TSH, FT4, AM cortisol, IGF-1 27 ng/mL, AM Glucagon, Troponin, CEA and CA-125. Hemoglobin A1C was 8.9%. On the third day of admission, patient’s blood glucose levels persisted in the 400s-500s despite increasing her insulin infusion to 21 units/h and adding 15 units of HumuLIN R/per hour plus Insulin Glargine 40 units twice daily. She received over 900,000 U of insulin in the first 72 hours of hospitalization. In the setting of critical condition without a clear path to recovery, the family decided to pursue palliative care with comfort measures. Patient expired two hours after palliative extubation. Four days after patient expired, the blood work for the antibodies was received. The results were consistent with Negative Islet Cell Antibody, Negative GAD-65 Ab, & Positive Insulin Autoantibody (more than 50 U/ML). Conclusion: This case highlights the importance of considering immune-mediated IR along with other more common causes of IR in hospitalized patients with marked insulin demands.