SUN-703 Post Bariatric Hypoglycemia Successfully Treated With GLP-1 Receptor Agonist

Abstract Disclosure: S. Khan: None. A. Lampe Dominguez: None. Background: Post-bariatric hypoglycemia (PBH) is a serious complication of bariatric surgery that is challenging to treat. While the precise mechanism remains unclear, PBH is thought to result, in part, from accelerated nutrient transit to the small intestine, leading to an exaggerated release of insulin and incretins, such as GLP-1. Interestingly, although GLP-1 is implicated in the pathogenesis of PBH, a few case reports have documented improvement of PBH with GLP-1 receptor agonists. Here we present the case of a patient with PBH successfully treated using a GLP-1 receptor agonist. Case: A 54-year-old female with a history of Roux-en-Y gastric bypass six years prior presented to the clinic following a hypoglycemic seizure. She had been following a ketogenic diet but had been nonadherent in the week leading up to the event. Two hours after consuming a high carbohydrate meal, she experienced a seizure with a recorded blood sugar of <20 mg/dL. Home glucose log revealed multiple episodes of postprandial hypoglycemia (50-60 mg/dL) within two hours of eating, without fasting hypoglycemia. Labs included: AM cortisol 11.9 ug/dL, Insulin 7.0 uIU/mL, C-peptide 2.0 ng/mL, TSH 4.180. Alternative causes of hypoglycemia, including medication-induced, insulinoma, and adrenal insufficiency, were ruled out. PBH was diagnosed based on her postprandial hypoglycemia pattern. After unsuccessful trials or contraindications to acarbose, octreotide, nifedipine, and diazoxide, the patient was started on liraglutide (0.6 mg subcutaneously daily). Two months later, hypoglycemia episodes had nearly resolved. Dexcom data revealed that time spent with blood glucose <70 mg/dL and <55 mg/dL was both 1%. Liraglutide was titrated to 1.8 mg daily, maintaining good control. The patient was later switched to Semaglutide for weekly dosing, with the dose titrated to 1 mg weekly, and continued to experience resolution of hypoglycemia. Discussion: This case highlights the potential utility of GLP-1 receptor agonists in treating PBH. Although the exact mechanism is unclear, it is hypothesized that exogenous GLP-1 at consistent concentrations may attenuate the exaggerated GLP-1 release following rapid nutrient delivery after bariatric surgery. However, given the limited data available, further high-quality studies are needed to validate this theory and evaluate the overall efficacy of GLP-1 receptor agonists in managing PBH. Presentation: Sunday, July 13, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.210
Citations
1
Primary Topic
Pharmacology and Obesity Treatment
Type
article
Field-Weighted Citation Impact
1.39
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article

SUN-703 Post Bariatric Hypoglycemia Successfully Treated With GLP-1 Receptor Agonist

A Domínguez, Samiya Khan
1 citations
Journal of the Endocrine Society
Pharmacology and Obesity Treatment
1.39
article

SUN-703 Post Bariatric Hypoglycemia Successfully Treated With GLP-1 Receptor Agonist

A Domínguez, Samiya Khan
article en
1 citations

Abstract

Abstract Disclosure: S. Khan: None. A. Lampe Dominguez: None. Background: Post-bariatric hypoglycemia (PBH) is a serious complication of bariatric surgery that is challenging to treat. While the precise mechanism remains unclear, PBH is thought to result, in part, from accelerated nutrient transit to the small intestine, leading to an exaggerated release of insulin and incretins, such as GLP-1. Interestingly, although GLP-1 is implicated in the pathogenesis of PBH, a few case reports have documented improvement of PBH with GLP-1 receptor agonists. Here we present the case of a patient with PBH successfully treated using a GLP-1 receptor agonist. Case: A 54-year-old female with a history of Roux-en-Y gastric bypass six years prior presented to the clinic following a hypoglycemic seizure. She had been following a ketogenic diet but had been nonadherent in the week leading up to the event. Two hours after consuming a high carbohydrate meal, she experienced a seizure with a recorded blood sugar of <20 mg/dL. Home glucose log revealed multiple episodes of postprandial hypoglycemia (50-60 mg/dL) within two hours of eating, without fasting hypoglycemia. Labs included: AM cortisol 11.9 ug/dL, Insulin 7.0 uIU/mL, C-peptide 2.0 ng/mL, TSH 4.180. Alternative causes of hypoglycemia, including medication-induced, insulinoma, and adrenal insufficiency, were ruled out. PBH was diagnosed based on her postprandial hypoglycemia pattern. After unsuccessful trials or contraindications to acarbose, octreotide, nifedipine, and diazoxide, the patient was started on liraglutide (0.6 mg subcutaneously daily). Two months later, hypoglycemia episodes had nearly resolved. Dexcom data revealed that time spent with blood glucose <70 mg/dL and <55 mg/dL was both 1%. Liraglutide was titrated to 1.8 mg daily, maintaining good control. The patient was later switched to Semaglutide for weekly dosing, with the dose titrated to 1 mg weekly, and continued to experience resolution of hypoglycemia. Discussion: This case highlights the potential utility of GLP-1 receptor agonists in treating PBH. Although the exact mechanism is unclear, it is hypothesized that exogenous GLP-1 at consistent concentrations may attenuate the exaggerated GLP-1 release following rapid nutrient delivery after bariatric surgery. However, given the limited data available, further high-quality studies are needed to validate this theory and evaluate the overall efficacy of GLP-1 receptor agonists in managing PBH. Presentation: Sunday, July 13, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
University of Southern California (US)
Openalex Percentile: Top 15%
Pharmacology and Obesity Treatment
1.39
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