MON-LB125 Dka From a Ketogenic Diet and Intermittent Fasting or Ketosis-Prone Diabetes?

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Background: Ketogenic diets and intermittent fasting (IF) are popularly used for weight loss. Generation of ketone bodies for fuel from fatty acid oxidation underlies both diets, combined or separately. We present a case of a prediabetic patient admitted for DKA after starting a combination keto/IF diet. Clinical Case: A 63-year-old man with hypertension, prediabetes, and alcohol use was admitted from clinic after receiving lab test results consistent with diabetic ketoacidosis (DKA). Two months ago, he had started a keto diet with IF (5 days/week, 18 hour fast/day) and achieved weight loss of 20 pounds. He reported polyuria and polydipsia, which was attributed to the recent initiation of chlorthalidone. Laboratory testing revealed glucose 519 (</= 199 mg/dL), bicarbonate 12 (20-30 mmol/L), creatinine 1.6 (0.5-1.5 mg/dL), anion gap of 23 (6-16 mEq/L), HbA1c 12.2% (4-5.6%), c-peptide 1.37 (0.80-3.85 ng/mL) with glucose 294, GAD65 Ab <5 (<5 IU/mL), IA2 Ab <5.4 (<5.4 U/mL), Insulin Ab <0.4 (<0.4 U/mL), triglyceride 546 (0-199 mg/dL), LDL-d 176 (0-129 mg/dL), cholesterol 310 (0-199 mg/dL) and HDL 39 (>/= 40 mg/dL). Workup for precipitating causes of DKA was negative including normal lactate, lipase and troponin. The patient was managed with an insulin drip and discharged on subcutaneous insulin (Lantus 45 units/day, Aspart 13 units with meals) and metformin. The patient re-introduced carbohydrates into his diet after meeting with the nutritionist. Eight weeks later, the HbA1c decreased to 6.6% and insulin was significantly reduced to Lantus 25 units/day. Sixteen weeks after discharge, the HbA1c further declined to 5.1% and Lantus was reduced to 10 units/day. Beta cell function at that time was preserved as evidenced by c-peptide 1.82 ng/mL. Insulin therapy was discontinued and the patient was closely monitored for urinary ketones and recurrence of hyperglycemia, neither which have developed. Conclusion: This is a unique case of DKA precipitated by a keto/intermittent fasting diet, without the use of SGLT2 inhibitor. Interestingly, previous metabolic studies show that nutritional ketosis typically generates low levels of serum ketones without a clinically significant anion gap metabolic acidosis. With negative beta cell autoantibodies and preserved beta cell function, this presentation is also consistent with ketosis-prone diabetes type 2B. It is possible that nutritional ketosis triggered the onset of KPD, although the mechanism remains unclear particularly since it is known that lipotoxicity is not pathogenic in the development of KPD.