ODP183 Diabetic Ketoacidosis Precipitated by Ketogenic Diet and SGLT-2 Inhibitor Use in an Individual with T2DM

Abstract

Abstract Background SGLT-2 inhibitors have been associated with increased risk of ketoacidosis even with normal blood glucose levels. A ketogenic diet is a low-carb, high-fat diet which has recently gained popularity for weight loss by producing a state of ketosis. We present this case to emphasize the risk of ketoacidosis in patients on SGLT-2 inhibitors and a ketogenic diet. Clinical Case A 48-year-old woman with a 16-year history of T2DM presented to the ER with a 3-day history of upper abdominal cramping and headaches, decreased urine output, and progressively worsening nausea and vomiting. Her glycated hemoglobin level was 9.4% (n: 4-6%) and her blood glucose readings were not elevated during this time. Other medical issues include dyslipidemia, transaminitis and hypertension. She does not smoke or drink alcohol. She takes glimepiride 0.5 mg daily and canagliflozin was added approximately 1.5 weeks prior to presentation. She was on a ketogenic diet. A few days prior to these symptoms she was in the process of moving out of her home, spending long days physically exerting herself. On exam she was in mild distress with dry mucous membranes. Vitals showed tachycardia (119BPM) but otherwise were stable. Labs revealed that she was severely acidotic with an anion gap of >27 and pH < 6.9 (n: 7.34-7.43), with urinalysis positive for ketones (2+, n: negative), protein (3+, n: negative), and glucose (3+, n: negative). Complete blood count showed leukocytosis (WBC: 18,000, n: 4. 00-12. 00*10 3 /mcL). Complete metabolic panel showed hyponatremia (130, n: 136-145mmol/L), elevated glucose (305, n: 70-99,g/dL), and low bicarbonate (<5, n: 22-30mmol/L). A chest X-ray, lumbar puncture and CT of head and abdomen were unrevealing. She was admitted to the ICU for treatment of suspected DKA with severe acidosis and hypovolemia. She was hydrated with IV fluids and was started on an insulin drip according to DKA protocol. Her anion gap closed in 22 hours. The patient spent 3 days in the ICU and 1 day on general floor before discharge on home medications and was advised to follow up with endocrinology. At follow up 2 months later her C-peptide was 2.14 (0.78-5.19 ng/mL) and GAD65 antibody assay was 0. 00 (<0. 02 nmol/L), the SGLT-2 inhibitor was discontinued, and she was instead started on a GLP-1 agonist. Conclusion The mechanism behind DKA with SGLT-2 inhibitor use involves glycosuria and volume depletion, lowering the insulin-to-glucagon ratio, while stimulating lipolysis. The addition of a low carbohydrate or ketogenic diet produces a state of ketosis as fat is utilized for energy and ketones are produced, further promoting DKA. With increased use of SGLT-2 inhibitors in patients with and without diabetes mellitus extreme caution should be exercised in prescribing SGLT-2 inhibiters in a patient on a low carbohydrate diet. Presentation: No date and time listed