SAT-268 Beta-Shift Phenomenon Following Resolution of Diabetic Ketoacidosis: A Case Report

Abstract Disclosure: M.J. Barnett: None. C. Casipit: None. J.R. Lam: None. C. Polycarpe: None. K. Gadalla: None. P. Lekprasert: None. Background: Lipoprotein lipase (LPL) is integral for hydrolyzation of triglyceride-rich lipoproteins. In healthy subjects, hyperglycemia leads to insulin release, up-regulation of LPL transcription, and hydrolysis of circulating lipoproteins. During prolonged fasting or states of diabetic ketoacidosis (DKA) where insulin levels fall, LPL activity decreases. Clinical Case: A 58-year-old female with hyperlipidemia and type 2 diabetes mellitus (non-adherence with metformin and basal-bolus insulin) is admitted to the medical intensive care unit for DKA. An insulin infusion was immediately commenced, and she is transitioned back to her basal-bolus regimen two days later. Her HbA1c this admission was > 14%, with a prior measurement of around 7.3% nearly two years prior at an outside hospital. Following transitioning, a lipid panel was ordered three days into her admission, returning with an LDL of 234 mg/dL (reference: < 70 mg/dL), triglyceride 141 mg/dL (reference: 0 - 150 mg/dL), total cholesterol 391 mg/dL (reference: 0 - 200 mg/dL), HDL 39 mg/dL (reference: > 40 mg/dL) and VLDL 28 mg/dL (reference: 10 - 40 mg/dL). Upon review of her outside records, it appeared that her LDL had previously been as high as 175 mg/dL, however, after initiating Atorvastatin 80 mg, her last measured LDL was 100 mg/dL around two years prior. Endocrinology was consulted due to concern for familial hypercholesterolemia with such an elevation in LDL. Endocrinology had recommended repeating a lipid panel in one month to assess for persistent hyperlipidemia (in which case genetic testing could be pursued), or, if resolution, likely suggestive of a retrospective diagnosis of the ‘beta-shift’ phenomenon. A repeat LDL measured two weeks later was 98 mg/dL, and one month after admission was 62 mg/dL. Genetic testing was therefore not pursued, and the elevated LDL was attributed to the beta-shift phenomenon. Clinical Lessons: States of insulin resistance/deficiency are associated with elevated triglyceride levels, with subsequent impaired conversion of VLDL to LDL. The introduction of insulin (with up-regulation of LPL), leads to an excess conversion to LDL. Due to a longer half-life of LDL, it may persist even when triglycerides and VLDL have normalized. In our case, we did not have a triglyceride level before her DKA presentation, however, it was presumed to be significantly elevated in the setting of her severe insulin resistance and non-compliance. This phenomenon of temporary elevated LDL is known as the beta-shift and is diagnosed retrospectively once laboratory testing after discharge demonstrates resolution of the hypercholesterolemia; with persistence, the differential diagnosis of familial hypercholesterolemia can be investigated. Reference: Gardner, D. G., Shoback, D. M., & Greenspan, F. S. (2018). Greenspan’s Basic & Clinical Endocrinology (8th ed.). McGraw-Hill Education LLC. Presentation: Saturday, July 12, 2025