Abstract Background Little is known about the impact of over-the-counter ketone supplementation, used by patients to promote weight loss, on ketosis and serum ketone values. Recent literature suggests that acute ingestion of exogenous ketones leads to increased blood beta-hydroxybutyrate and decreased blood glucose1. Clinical Case A 61-year-old man with a history of type 2 diabetes mellitus, atrial fibrillation, hypertension, and hyperlipidemia presented as a transfer to the neurocritical care ICU from an outside hospital for subarachnoid hemorrhage secondary to intracranial saccular aneurysm. His admission hemoglobin A1c was 9.9% (ref 4.4-5.6), blood glucose was 205 mg/dL (ref 70-99), beta-hydroxybutyrate was markedly elevated at 26.2 mg/dL (ref 0-3), and urinalysis showed 80mg/dL ketones (ref 0). Serum toxicology screen was notable for detectable acetone 8mg/dL (ref: none detected). His lactate was 2 mmol/L (ref 0.5-1.9), Cr 0.99mg/dL (0.67-1.17), and HCO3 22 mmol/L (ref 22-27). Arterial blood gas showed pH of 7.37 (ref 7.38-7.47), and an anion gap metabolic acidosis (AGMA) of 15 mmol/L (ref <12). Given the patient's profound ketosis, hyperglycemia, and mild AGMA, the patient was started on an insulin drip for presumed diabetic ketoacidosis (DKA). After 4 hours, the patient's anion gap had decreased to 12mmcol/L. The following day, he was transitioned to basal/bolus insulin, and underwent embolization of his cerebral aneurysm. After further recovery, Endocrinology was consulted for insulin recommendations. The patient denied any prior history of DKA or use of any SGLT2-inhibitors, and denied decreased oral intake or vomiting prior to admission. He did report taking ketone supplements, "Keto Strong: Ketogenic Weight Management – Advanced Formulation," two tabs (700mg "proprietary keto blend") BID for 2-3 years with ingredients listed as: sodium beta-hydroxybutyrate, calcium beta-hydroxybutyrate, magnesium beta-hydroxybutyrate, medium chain triglyceride oil, L-arginine, alpha-ketoglutaric acid, and 7-keto-dehydroepiandrosterone. Given a lack of acidosis, mild hyperglycemia, and mild lactic acidosis without risk factors for euglycemic DKA, it was suspected his profound ketosis out of proportion to clinical picture was secondary to ketone supplementation with a misdiagnosis of DKA. Conclusion This is one of the first cases to report profound ketosis in a hospitalized patient likely secondary to exogenous ketone supplementation. Ketosis secondary to nutritional supplementation should be considered once more common etiologies are ruled out. Additional research is needed to determine the role of exogenous ketone use on metabolism and glycemic control. References: Falkenhain, Kaja et al. "Effects of Exogenous Ketone Supplementation on Blood Glucose: A Systematic Review and Meta-Analysis." Advances in nutrition (Bethesda, Md.), nmac036. 5 Apr. 2022 Presentation: No date and time listed