MON-603 - From Granuloma Annulare to Diabetic Ketoacidosis: A Case of Rapid Diabetes Progression Post Steroid Treatment

Introduction: Granuloma annulare (GA) is a rare skin manifestation that has been associated with diabetes mellitus. We present a case in which GA appeared to precede the diagnosis of diabetes and was followed by rapid progression to type 2 diabetes mellitus (T2DM) and diabetic ketoacidosis (DKA) after brief steroid exposure.

Case: A 68-year-old woman with prediabetes, hypertension (on lisinopril) and hyperlipidemia was instructed to come to the emergency department for severe hyperglycemia noted on outpatient labs. She reported two weeks of polyuria, polydipsia, odynophagia, and a 20-pound unintentional weight loss. Three weeks prior, she developed an erythematous rash on her face, extremities, and trunk. This was initially attributed to a lisinopril-related allergic reaction and was treated with a two-week course of prednisone 20 mg. She had no history of hepatitis C, HIV, autoimmune disorders, recent skin injury, or antibiotic or allopurinol use. A subsequent skin biopsy confirmed granuloma annulare. Her hemoglobin A1c three months prior was 6.4%.

Laboratory studies revealed glucose 695 mg/dL, anion gap of 13, bicarbonate 17 mmol/L, moderate serum and urine ketones, pseudohyponatremia of 127 mmol/L (corrected 137 mmol/L), and acute kidney injury (BUN 38, Cr 1.51). Arterial blood gas showed a pH of 7.34, CO₂ of 30 mmHg, and bicarbonate of 16 mmol/L. She received insulin regular and potassium supplementation.

She was admitted to the ICU for management of metabolic acidosis for presumed starvation ketosis and uncontrolled hyperglycemia. An A1c of 13.4 confirmed T2DM and DKA. She was treated with intravenous fluids, insulin infusion, and electrolyte replacement, and then transitioned to basal-bolus insulin. She was discharged on insulin and metformin. Outpatient evaluation demonstrated negative islet cell and glutamic acid decarboxylase (GAD) antibodies with C-peptide levels of 2.2 with glucose of 96. Insulin was eventually discontinued, with sustained glycemic control on metformin and no recurrence of ketoacidosis.

Discussion: This case demonstrates a convergence of two rare processes in a single patient: GA as the initial manifestation of diabetes and rapid steroid-induced progression from prediabetes to T2DM with DKA. Although GA is usually associated with established diabetes, in our case, GA preceded her diagnosis, suggesting GA may be an early marker of glucose dysregulation.

Glucocorticoids are known to cause hyperglycemia, however progression from prediabetes to T2DM with DKA following a short course of oral prednisone is rare. The absence of diabetes-associated autoantibodies and preserved beta cell function supports a diagnosis of ketosis-prone T2DM. Together, these findings suggest increased caution with glucocorticoid use even in patients with prediabetes and also raises awareness of GA as a possible indicator of underlying glucose dysregulation.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*