Management of Late Dumping Syndrome Induced Hypoglycemia With GLP-1R Agonist

Background: Late dumping syndrome is a prominent post-bariatric surgery side effect. Glucose-dependenthyperinsulinemia, induced by elevated gastric inhibitory polypeptide (GIP) and glucagon-likepeptide-1 (GLP-1) levels, leading to 2–3 hours post-prandial hypoglycemia. In literature, several managements are available: dietary changes, glucosidase inhibitor, andsomatostatin analogues. In case of failure of those strategies, partial or total pancreatectomy isindicated. Recently, management using GLP-1R agonists showed promising effect inmanagement of late dumping syndrome induced post-prandial hypoglycemia. (1)AimThe aim of this study was to investigate the effect of using GLP-1R agonists w/o low glycemicindex diet for treating dumping syndromes induced post-prandial hypoglycemia in post bariatricsurgery patients. Methods: A sample of 27 cases (25 females, 2 males) mean age 44.64, SD 10.2 of post-bariatric surgerywere managed using GLP-1R w/o low-glycemic index diet after being diagnosed with the latedumping syndrome induced post-prandial hypoglycemia for duration 1–3 years post-surgery. The27 were sent a survey of 13 questions related to their experience pre-and post-management plan. Results: Out of the 27 patients, 15 responded to the survey. The results showed 100% of the participantsdeveloped episodes of severe symptomatic late dumping syndrome with hypoglycemiasymptoms diagnosed after one and half years of their symptoms. 87% of them experiencedhypoglycemia post meals 2–3 hours.70 % of the participants got hypoglycemia more than 5episodes per week (less than 4.0 mmol/l) which was confirmed by blood glucose monitoring. After starting treatment with GLP-1R agonists with or without low-glycemic index diet, 87% ofthe participants reported that the hypoglycemia episodes were reduced. Out of those 87%participants 46% did not get any hypoglycemia episode and 54% of them experienced 1–2 timeshypoglycemia episodes. Conclusion: The results of the survey showed the successful reduction or prevention of late dumpinghypoglycemia episodes frequency post-bariatric surgery by GLP 1R agonist with or without lowglycemicindex diet. References: Non, A.N.H.W.H. and Black, H., 2012. Scope of the Problem. Am J Prev Med, 42, pp.563–70.Chiappetta, S. and Stier, C., 2017. A case report: Liraglutide as a novel treatment option in late dumping syndrome. Medicine, 96(12).

Continuous glucose monitoring to diagnose hypoglycemia due to late dumping syndrome in children after gastric surgeries

Gastrostomy tubes (G-tubes) and Nissen fundoplication are common surgical treatments for feeding difficulties and gastroesophageal reflux disease in children. A common, yet often missed, complication is dumping syndrome. We present three pediatric patients with post-prandial hypoglycemia due to late dumping syndrome after gastric surgeries. All patients received gastrostomy tubes for feeding intolerance, two had Nissen fundoplication for gastroesophageal reflux disease, and one had tracheoesophageal repair. All patients underwent multiple imaging studies to attempt to diagnose dumping syndrome. Continuous glucose monitoring (CGM) was essential for detecting asymptomatic hypoglycemia and glycemic excursions occurring with feeds that would have gone undetected with point-of-care (POC) blood glucose checks. CGM was also used to monitor the effectiveness of treatment strategies and drove treatment plans. These cases highlight the utility of CGM in diagnosing post-prandial hypoglycemia due to late dumping syndrome, which is infrequently diagnosed by imaging studies and intermittent POC blood glucose measurements.

MON-599 Post-Bariatric Hypoglycemia: A Clinical Vignette on an Increasingly Recognized Disease

Introduction: Previously referred to as late dumping syndrome, post-bariatric hypoglycemia (PBH) is thought to represent at least 1% of all hospitalizations for hypoglycemia and 10% of all clinically recognized hypoglycemia cases. However, through the advent of CGM and more strict criteria over the last decade these numbers are likely an underestimate. As obesity continues to remain prevalent and with rising bariatric centers to help deal with this epidemic, endocrinologists will play an increasing role in managing PBH patients. Clinical Case: A 39-year female with a PMH of hypothyroidism and bariatric surgery (BS) in 2009 presented to our ER for a seizure. She has been having seizures nearly every 2 weeks for one year. Neurology started her on Keppra; however, no etiology was identified. EMS had documented a blood glucose of 40 mg/dL; the patient was given an amp of D50 with resolution of neuroglycopenic symptoms. TSH and cortisol levels were within normal range. A sulfonylurea panel in the ED was negative. The patient states the symptoms can occur while fasting but also mainly post-prandial. A 72-hr fast was conducted with the patient nadir POC glucose of 77. Subsequently, the patient had a mixed meal tolerance performed and after 2 hours had a seizure and was found to have a BG of 50 mg/dL with an insulin level of 49 uIU/mL and a c-peptide of 18.8 ng/mL. The patient was diagnosed with PBH, and was discharged with a CGM, started on acarbose and was seen by nutrition to discuss dietary modifications. She is now seen in our clinic with control of her symptoms with the addition of diazoxide. Conclusion: Altered anatomy after bariatric surgery, particularly after gastric bypass and sleeve gastrectomy is thought to play a major role in developing PBH. By bypassing normal anatomy, gastric emptying is increased 2–3 x, which leads to a higher and more rapid appearance of glucose in the distal foregut. This subsequently leads to an amplified incretin response leading to a hyperinsulinemic response in patients who have had bariatric surgery; however, for unclear reasons some patients develop an even more amplified hyperinsulinemic response that leads to subsequent hypoglycemia. History of neuroglycopenic symptoms 1–3 hours after eating in a patient who had a gastric bypass > 6–12 months and with relief of symptoms with carbohydrates should raise an endocrinologist’s suspicion of PBH. Fasting hypoglycemia is an atypical feature that should raise one’s suspicion of a broader differential. Altered nutrition habits is the cornerstone of therapy with which the primary aim is to reduce post-prandial glucose spikes in these patients after they eat carbohydrates. These spikes in turn lead to hyperinsulinism leading to subsequent hypoglycemia. Primary diet modifications include controlled carbohydrate consumption of less than 30g per meal, avoiding high glycemic carbs, and always taking in ample fat and proteins with every meal.