OR08-05 Nesidioblastosis in Patients With Severe Post-bariatric Hypoglycemia: A Monocentric Case Series

Abstract Disclosure: D.K. Dawes: None. H.M. Lawler: Helen Lawler received compensation from Vogenx for clinical research and from Amylyx for advisory board participation. P. Trivedi: Financial disclosures are: Consulting fees from Boston Scientific and Cook Medical Advisory Board for Pneumonix Grant funding from NHLBI, NCI and American Heart Association unrelated to current work. K. Devaraj: None. Purpose: The role of nesidioblastosis in the pathophysiology of post-bariatric hypoglycemia (PBH) is controversial. Partial pancreatectomy, once explored as a treatment option for persistent PBH, has fallen out of favor due to frequent hypoglycemia recurrence. At our institution, from 2010-2024, 7 patients with severe PBH experiencing daily neuroglycopenia resistant to dietary modification and pharmacotherapy underwent selective arterial calcium stimulation tests (SACSTs) to assess for nesidioblastosis and 5 subsequently opted for pancreatic surgery. SACSTs and pathology results are presented. Additionally, long-term follow-up with a comprehensive chart review assessing recurrence of hypoglycemia was performed on the 4 patients who opted for partial pancreatectomy and the 1 patient who chose a complete pancreatectomy. Methods: SACST results were reviewed for all 7 patients to assess the presence of nesidioblastosis and pathology results were reviewed for the 5 patients who underwent pancreatic surgery. Clinical outcomes, including recurrence of hypoglycemia and post-surgical complications were documented. Results: All 7 patients (100%) had SACST results consistent with nesidioblastosis. Of the 4 patients who underwent partial pancreatectomy, hypoglycemia initially resolved in 3 but subsequently recurred at 1, 3, and 7 years. One patient experienced incomplete improvement with return of hypoglycemia to baseline 9 months after partial pancreatectomy. The patient who underwent complete pancreatectomy achieved sustained hypoglycemia resolution but developed insulin-dependent diabetes post-surgically. Upon pathology review, 2 of the 5 patients had islet cell changes consistent with nesidioblastosis. Conclusion: Nesidioblastosis likely contributes to PBH pathophysiology, as suggested by both the SACST findings and the temporary resolution of hypoglycemia following partial pancreatectomy. However, hypoglycemia recurrence after partial pancreatectomy suggests that nesidioblastosis may redevelop over time, especially if the underlying Roux-en-Y gastric bypass (RYGB) anatomy remains intact, which may perpetuate pathological insulin secretion. Hypoglycemia recurrence indicates that other mechanisms, likely triggered by altered gastrointestinal anatomy and accelerated nutrient absorption, significantly contribute to the ongoing pathology of PBH. Histologic features of nesidioblastosis, confirmatory in the appropriate clinical context, are nonspecific and not pathognomonic for diagnosis. SACST is a more reliable diagnostic tool for identifying nesidioblastosis. Long-term monitoring demonstrated hypoglycemia recurrence in 100% of our patients with PBH who underwent partial pancreatectomy. Overall, these cases highlight the need for better treatment options for PBH. Presentation: Saturday, July 12, 2025