SUN-861 - Recurrent Hypoglycemia after Roux-En-Y Gastric Bypass in A Patient with SLE and Multiple Sclerosis

Background:
Post-bariatric hypoglycemia is an increasingly recognized late complication of bariatric surgery, typically manifesting more than one year post operatively and affecting 32% of patients with Roux-en-Y gastric bypass. In patients with SLE, multiple sclerosis (MS), and atrial fibrillation (AFib), overlapping symptoms can obscure diagnosis, underscoring the need for systematic evaluation and the critical role of continuous glucose monitoring (CGM) in management.

Case Presentation:
A 45-year-old woman with RYGB (13 years prior), SLE, relapsing and remitting MS, AFib and generalized anxiety disorder presented to the clinic with recurrent symptomatic hypoglycemia occurring 2–3 times weekly over the preceding year. Home capillary glucose nadirs ranged 30–50 mg/dL meeting criteria for level 2 hypoglycemia. Neuroglycopenic symptoms consisted of fatigue, weakness, and lower-extremity tingling/numbness and reliably improved with oral glucose; she used glucose tablets frequently. With no history of diabetes and normal HbA1c levels, endocrinology evaluation revealed appropriately suppressed insulin and C-peptide levels and negative insulin autoantibodies. A prior CGM trial showed average glucose readings in the 100s mg/dL with lowest reading in the 40s. Dietary counseling for small, frequent, high-protein, low-carbohydrate meals was provided but adherence was limited due to poor baseline appetite. Given recurrent hypoglycemia, CGM reauthorization was pursued, dietary counseling reinforced, and nutrition referral recommended.

Discussion:
This case underscores the diagnostic difficulty of post-bariatric hypoglycemia (PBH) in patients with overlapping neurologic and autoimmune disease. The pathophysiology of PBH involves altered gastric emptying, rapid intestinal glucose absorption, and excessive postprandial glucagon-like peptide-1 secretion, resulting in exaggerated insulin responses typically 1–3 hours postprandially. Symptom overlap with MS/SLE manifestations and blunted adrenergic warning signs (from AF and anxiolytic use) increased the risk of severe neuroglycopenia. Limited CGM access remains a major barrier, despite evidence that real-time CGM reduces hypoglycemia exposure and enables earlier intervention, highlighting the need for improved recognition and monitoring to prevent morbidity and preserve quality of life.

Conclusion:
Post-bariatric hypoglycemia should be considered in patients with recurrent neuroglycopenic symptoms, particularly in individuals with autoimmune or neurological comorbidities. Improved clinician awareness, systematic workup, and CGM access are essential for effective management of this potentially debilitating condition.

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