SAT-552 Non-Insulin Mediated Postprandial Hypoglycemia following Roux-en-Y Gastric Bypass in a Patient with Panhypopituitarism

Abstract Disclosure: B.A. Weisbrot: None. B. Singh: None. F. Meah: None. Worldwide adult obesity has more than doubled since 1990. Bariatric surgery (BS) is highly effective in remission of metabolic and cardiovascular disease with weight loss projections of 20-50% reported in the literature. It is also associated with serious side effects such as post-BS hypoglycemia (PBH). Our case is unique due to the delayed diagnosis of PBH in an individual with panhypopituitarism. A 54-year-old female presented for evaluation of post-prandial syncope 30 months post Roux-en-Y gastric bypass (RYGB) surgery. Her medical history was significant for well controlled diabetes managed with lifestyle changes and panhypopituitarism secondary to partially empty sella. Secondary adrenal insufficiency (AI) was diagnosed at age 21 and the patient was maintained on hydrocortisone. In regards to the chief complaint of syncope, extensive evaluation by neurology was unremarkable. Glucometer readings during episodes resulted in blood glucose 30-50 mg/dL, with improvement of neuroglycopenic symptoms with carbohydrate intake meeting Whipple’s triad. She had lost 80lb (∼27% of original weight) since BS. Initial recommendations for treatment of her hypoglycemia included consumption of small mixed meals and snacks multiple times daily. She was also prescribed acarbose with meals and snacks. Following no response to these interventions, her hydrocortisone frequency was increased from twice a day to four times a day with daily dose remaining at the same total of 20 mg. Four months later, the patient endorsed persistent fasting and post-prandial hypoglycemia confirmed by continuous glucose monitor and fingerstick. A 72 hour fast revealed the following results: glucose 60 (RR 70-90 mg/dL), insulin 2.2 (RR 3-25 mIU/L), proinsulin <4.0 (RR <18.8 pmol/L), C-peptide 0.75 (RR 0.81-3.85 ng/mL), beta-hydroxybutyrate 2.20 (RR 0.02-0.27 mmol/L) consistent with a non-insulin mediated process. IGF-1, insulin autoantibodies, celiac screen, and hypoglycemia panel were unremarkable. The total dosage of hydrocortisone was increased to 25 mg/day with doses divided into 4 times per day. This led to a decrease of hypoglycemia episodes and resolution of nocturnal hypoglycemia. This case illustrates the challenge of diagnosing and treating PBH in a patient with secondary adrenal insufficiency. While there is literature describing the association between new onset hyperinsulinemic hypoglycemia post RYGB and transient adrenal insufficiency, there are few cases reported of managing PBH in patients with history of AI. Moreover, this patient presented with new onset hypoinsulinemic hypoglycemia, suggesting possible blunted counter-regulatory response to hypoglycemia exacerbated by malabsorption of hydrocortisone. This case highlights that further research is required to determine diagnostic criteria and treatment algorithms for patients with AI who are at risk for PHB. Presentation: Saturday, July 12, 2025