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      Hyperinsulinemic Hypoglycemia after Bariatric Surgery: Diagnosis and Management Experience from a Spanish Multicenter Registry

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          Background: Severe postprandial hypoglycemia after bariatric surgery is a rare but invalidating complication. Our aim was to describe the different tests performed for its diagnosis and their outcomes as well as the response to the prescribed pharmacological and surgical treatments. Methods: Multicenter, retrospective systematic review of cases with recurrent severe postprandial hypoglycemia. Results: Over 11 years of follow-up, 22 patients were identified. The test most used to provoke hypoglycemia was the oral glucose load test followed by the mixed meal test which was the least standardized test. With pharmacological treatment, 3 patients were symptom-free (with octreotide) and in 12 patients hypoglycemic episodes were attenuated. Seven patients had persistent hypoglycemic episodes and underwent surgery. Partial pancreatectomy was performed in 3 patients who had positive selective arterial calcium stimulation, and nesidioblastosis was confirmed in 2 patients. Reconversion to normal anatomy was performed in 3 patients, and 1 patient underwent a resection of the ‘candy cane' roux limb, with resolution of hypoglycemia in all cases. Conclusions: There is high heterogeneity in the evaluation and treatment options for postoperative hypoglycemia. In patients that do not respond to pharmacological treatment, reconstruction of gastrojejunal continuity may be the safest and most successful procedure.

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          Most cited references 31

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          Hyperinsulinemic hypoglycemia after gastric bypass surgery is not accompanied by islet hyperplasia or increased beta-cell turnover.

          The purpose of this study was to establish whether hypoglycemia after gastric bypass surgery (GBS) for morbid obesity is due to increased fractional beta-cell area or inappropriately increased insulin secretion. We examined pancreata obtained at partial pancreatectomy from 6 patients with post-GBS hypoglycemia and compared these with 31 pancreata from obese subjects and 16 pancreata from lean control subjects obtained at autopsy. We addressed the following questions. In patients with post-GBS hypoglycemia, is beta-cell area increased and is beta-cell formation increased or beta-cell apoptosis decreased? We report that in patients with post-GBS hypoglycemia, beta-cell area was not increased compared with that in obese or even lean control subjects. Consistent with this finding, there was no evidence of increased beta-cell formation (islet neogenesis and beta-cell replication) or decreased beta-cell loss in patients with post-GBS hypoglycemia. In control subjects, mean beta-cell nuclear diameter correlated with BMI (r(2) = 0.79, P < 0.001). In patients with post-GBS hypoglycemia, beta-cell nuclear diameter was increased (P < 0.001) compared with that for BMI in matched control subjects but was appropriate for BMI before surgery. We conclude that post-GBS hypoglycemia is not due to increases in beta-cell mass or formation. Rather, postprandial hypoglycemia after GBS is due to a combination of gastric dumping and inappropriately increased insulin secretion, either as a failure to adaptively decrease insulin secretion after GBS or as an acquired phenomenon.
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            Reversible hyperinsulinemic hypoglycemia after gastric bypass: a consequence of altered nutrient delivery.

            Severe hypoglycemia after Roux-en-Y gastric bypass surgery (RYGB) is an increasingly recognized condition, characterized by neuroglycopenia and inappropriately elevated insulin concentrations that occur primarily in the postprandial state. Both pathophysiology and treatment of this disorder remain elusive, but it has been postulated that hyperplasia and/or hypertrophy of beta-cells due to morbid obesity and/or postsurgical nesidioblastosis may contribute. The objective of this study was to elucidate the pathophysiology of this condition; specifically, we hypothesized that metabolic abnormalities were a function of altered nutrient transit through the gastrointestinal tract rather than anatomical changes to pancreatic beta-cells that would lead to consistently high insulin secretion irrespective of nutrient transit route. DESIGN/SETTING/SUBJECT/OUTCOME MEASURES: We describe a unique case wherein gastrostomy tube (GT) insertion into the remnant stomach reversed neuroglycopenic symptoms. This subject was admitted to a university hospital research center for standardized measurement of glucose, insulin, and incretin hormones including glucagon-like peptide-1, gastric-inhibitory peptide, and glucagon. Standardized liquid meal administration via GT vs. oral route demonstrated complete reversal of severe metabolic abnormalities that included hypersecretion of insulin and GLP-1. Post-RYGB hyperinsulinemia and hypoglycemia result entirely from altered nutrient delivery rather than generalized hyperfunction of beta-cells due to presurgical hypertrophy/hyperfunction or postsurgical nesidioblastosis. These findings support the use of GT for treatment of severe cases and have implications for surgical manipulations that may reverse/prevent this condition.
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              Post-prandial hypoglycemia after bariatric surgery: pharmacological treatment with verapamil and acarbose.

              Postprandial hypoglycemia is a common complication of bariatric surgery. It is usually caused by late dumping syndrome, but a few other causes have already been described, including insulinoma and noninsulinoma pancreatogenous hypoglycemic syndrome (NIPHS). Considering that NIPHS is a recently described syndrome and is also very rare, therapeutic approaches are still not consensual. We report the case of a 26-year-old woman who was submitted to bariatric surgery and presented episodic postprandial hypoglycemic episodes after 16 months. Fasting C-peptide, insulin, and glucose were normal. Because of the possibility of NIPHS, clinical treatment was initiated with verapamil and acarbose, leading to a significant reduction of hypoglycemic episodes and also their severity. Surgery is the most common approach to NIPHS. However, in cases of mild or moderate symptoms, it is important to consider the possibility of pharmacological treatment. This approach may result, at least for some time, in an amelioration of symptoms without the need of an aggressive procedure.

                Author and article information

                Obes Facts
                Obesity Facts
                S. Karger AG
                March 2016
                23 February 2016
                : 9
                : 1
                : 41-51
                aDepartment of Endocrinology and Nutrition, Hospital Universitario de Bellvitge-IDIBELL, L´Hospitalet de Llobregat, Barcelona, Spain; bCIBERDEM-CIBER de Diabetes y Enfermedades Metabólicas Asociadas. Instituto de Salud Carlos III, Madrid, Spain.; cEndocrinology and Nutrition Unit, Hospital del Mar, Barcelona, IMIM, Institut Mar dʼInvestigacions, Barcelona, Spain; dDepartment of Medicine, Universitat Autònoma de Barcelona, CIBERobn (Centros de Investigación Biomédica en Red - CIBER, Physiopathology of Obesity and Nutrition), Instituto de Salud Carlos III, Madrid, Spain; eDepartment of Endocrinology &amp; Nutrition, Hospital Clínico San Carlos. IDISSC, Madrid, Spain; fEndocrinology and Nutrition Department, Sabadell University Hospital (UAB), Corporació Sanitària Parc Taulí, Sabadell, Spain; gEndocrinology and Nutrition Department, IMPPC, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain; hCIBERDEM-CIBER de Diabetes y Enfermedades Metabólicas Asociadas. Instituto de Salud Carlos III, Madrid, Spain; iEndocrinology and Nutrition Department. Morbid Obesity Unit, Hospital Vall d´Hebron, Barcelona, Spain; jEndocrinology and Nutrition Department, Hospital Universitario Reina Sofía, Córdoba, Spain; jEndocrinology and Nutrition Department, Hospital Universitario Ramón y Cajal, IRyCIS y CIBERobn, Madrid, Spain; kEndocrinology and Nutrition Department, Hospital Universitario Gregorio Marañón, Madrid, Spain; lHospital del Meixoeiro, Vigo, Spain; mDepartment of Endocrinology and Nutrition, Hospital Valle del Nalon., Riaño, Spain; nU. Nutricion. U.G. Endocrinologia y Nutricion, Hospital Universitario Virgen del Rocío, Sevilla, Spain; oEndocrinology and Nutrition Department, Hospital Universitari Arnau de Vilanova, Lleida, Spain
                Author notes
                *Nuria Vilarrasa, Hospital Universitario de Bellvitge - IDIBELL, C/ Feixa Llarga s/n, L´Hospitalet de Llobregat, 08907 Barcelona, Spain,
                442764 Obes Facts 2016;9:41-51
                © 2016 S. Karger GmbH, Freiburg

                Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) (, applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, Tables: 3, References: 38, Pages: 11
                Original Article


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