SUN-123 An Unusual Case of How Statin-Induced Diabetes Revealed Underlying Latent Autoimmune Diabetes of Adulthood

Introduction: Over the last two decades, multiple landmark trials have established the significant reduction in cardiovascular events with the use of statins for primary prevention. The JUPITER trial in 2008 first drew attention to statin-induced new-onset diabetes (NOD). We present an unusual case of a patient initially diagnosed with statin-induced diabetes that later was established as latent autoimmune diabetes of adulthood (LADA). Case: A 34-year-old Serbian woman with a past history only significant for hypothyroidism due to subtotal thyroidectomy for Graves’ disease was found to have an LDL of 260 mg/dL. Her family history was unremarkable. She occasionally drank alcohol and smoked half of a pack of cigarettes per day. Her BMI was 20. She was started on Atorvastatin 40 mg daily which decreased her LDL to 129 mg/dL. However, a year later, she was diagnosed with diabetes mellitus (DM) based on a hemoglobin A1c (HbA1C) of 7.5% and a glucose of 363 mg/dL after a 2-hour glucose tolerance test. Atorvastatin was thought to be the culprit and was therefore discontinued. She was monitored regularly with HbA1c testing without initiation of any medications and her HbA1C decreased to 5.9% within six months. Two years later, she became pregnant and was able to maintain a HbA1c less than 6.2% throughout her pregnancy with only dietary changes. Over a 6-year period, she had been able to maintain her blood sugar readings at goal and HbA1C between 5.6% and 6.2%. However, at age 40, her HbA1c suddenly increased to 7.3%, fasting blood sugar (FBS) readings increased to 180-220 mg/dL, and she had an unintentional 6-pound weight loss over a 12-month period. She was assessed for LADA and found to have glutamic acid decarboxylase antibody titer greater than 250 IU/mL (normal 0 - 5.0 IU/mL) and a low fasting C-peptide of 0.8 ng/mL (normal 0.8-3.5 ng/mL) with a FBS of 161 mg/dL. Based on those results, she was diagnosed with LADA and initiated on insulin therapy. Within 3 months her HbA1c decreased to 5.9%. Discussion: The association between statins and NOD has been well-established. The proposed mechanisms include both impaired insulin secretion and diminished insulin sensitivity. Patients at risk have a predisposition to diabetes including two or more of the following: metabolic syndrome, impaired fasting glucose, BMI of 30 or greater, and HbA1c 6.0% or greater. In a patient with a normal BMI and no apparent risk factors for statin-induced diabetes, LADA should be considered as another potential underlying risk factor for statin-induced NOD. Establishing the correct nature of DM has long term implications regarding the prognosis, treatment and complications associated with the disease. References: Gandpa OP. Statin-induced diabetes: incidence, mechanisms and implications. F1000Res. 2016 Jun 24; 5. Aiman U, Najmi A, Khan RA. Statin induced diabetes and its clinical implications. J Pharmacol Pharmacother 2014;5:181-5