Laparoscopic Spleen-Preserving Distal Pancreatectomy as Treatment for Nesidioblastosis after Gastric Bypass Surgery

Alvarez, Glauco C.; Faria, Everton Neubauer; Beck, Maristela de Oliveira; Girardon, Dener T.; Machado, Ana Cristina

doi:10.1007/s11695-007-9096-0

Cited by 55 publications

(34 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A link between GLP1 hypersecretion causing pancreatic b-cell growth, hyperfunction and nesidioblastosis was suggested. Subsequently, more cases of nesidioblastosis following GBS have been reported and all received pancreatectomy to control their symptoms (17,18,19).…”

Section: Discussionmentioning

confidence: 99%

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

Myint

Greenfield²,

Farooqi³

et al. 2012

European Journal of Endocrinology

View full text Add to dashboard Cite

Background: Spontaneous hyperinsulinaemic hypoglycaemia following gastric bypass surgery (GBS) is increasingly recognised. However, its pathophysiology remains unclear. Some patients require pancreatectomy. Medical therapy with calcium channel blockers, acarbose and diazoxide has been reported to be beneficial but has variable adherence and response. Method: We demonstrate the role of GLP1, counter-regulatory hormones and the subsequent response of GLP1 to somatostatin analogue therapy in a 42-year-old woman with persistent neuroglycopaenia 6 years after GBS. Plasma GLP1, insulin and glucose were measured for 5 h on three settings: i) a 75 g oral glucose tolerance test (OGTT); ii) a standard liquid test meal (LTM); and iii) an OGTT 30 min after a s.c. injection of 100 mg octreotide. Results: In comparison with obese non-diabetic controls, the patient had an elevated fasting and a markedly enhanced GLP1 response during the OGTT, followed by an exaggerated insulin response and a subsequent low glucose level. The GLP1 response to a LTM was similar but greater. Octreotide given prior to the OGTT attenuated both the GLP1 and insulin responses and abolished hypoglycaemia. Octreotide therapy significantly improved the patient's neuroglycopaenic symptoms. The hormone profile was reassessed after 6 months following the LTM preceded by octreotide injection. Peak GLP1 and insulin responses were less pronounced than pretreatment responses and without hypoglycaemia. The patient was treated with lanreotide and had remained symptom-free and euglycaemic for 4 years. Conclusion: An exaggerated incretin response following altered gastrointestinal anatomy was the likely cause of hypoglycaemia in our GBS patient. Somatostatin successfully suppressed this response acutely and in the long term, thereby avoiding pancreatectomy and its sequelae.

show abstract

Section: Discussionmentioning

confidence: 99%

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

Myint

Greenfield²,

Farooqi³

et al. 2012

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…All of the nine patients had resolution of their symptoms after the surgery initially; however, 77% developed recurrence in their symptoms (47). The study by Alvarez et al described a laparoscopic spleenpreserving distal pancreatectomy in a patient with post-RYGB hypoglycemia who remained free of symptoms at 10 months (48). The extent of pancreatic resection differs in the literature with Mathavan describing pancreatic resection of 80% of the parenchyma in eight of nine patients (47), the study by Thompson et al described pancreatic resection of 80% (49) and the study by Harness et al described pancreatic resection of up to 50-100% (50).…”

Section: Post Bariatric Hypoglycemiamentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Pathogenesis and management of hypoglycemia

Kittah

Vella

2017

European Journal of Endocrinology

View full text Add to dashboard Cite

Glucose is the main substrate utilized by the brain and as such multiple regulatory mechanisms exist to maintain glucose concentrations. When these mechanisms fail or are defective, hypoglycemia ensues. Due to these robust mechanisms, hypoglycemia is uncommon and usually occurs in the setting of the treatment of diabetes using glucose-lowering agents such as sulfonylureas or insulin. The symptoms of hypoglycemia are non-specific and as such it is important to confirm hypoglycemia by establishing the presence of Whipple's triad before embarking on an evaluation for hypoglycemia. When possible, evaluation of hypoglycemia should be carried out at the time of spontaneous occurrence of symptoms. If this is not possible then one would want to create the circumstances under which symptoms occur. In cases where symptoms occur in the post absorptive state, a 72-h fast should be performed. Likewise, if symptoms occur after a meal then a mixed meal study may be the test of choice. The causes of endogenous hyperinsulinemic hypoglycemia include insulinoma, post-bariatric hypoglycemia and noninsulinoma pancreatogenous hypoglycemia syndrome. Autoimmune hypoglycemia syndrome is clinically and biochemically similar to insulinoma but associated with high levels of insulin antibodies and plasma insulin. Other important causes of hypoglycemia include medications, non-islet cell tumors, hormonal deficiencies, critical illness and factitious hypoglycemia. We provide an overview of the pathogenesis and management of hypoglycemia in these situations.

show abstract

“…Potential risks include hyperinsulinaemic hypoglycaemia as well as nausea and vomiting, which are the most common side effects observed with high doses of GLP-1 analogues. 32,33 The underlying mechanisms causing pancreatic nesidioblastosis after gastric bypass [34][35][36] are currently unknown and only very few cases have been reported during the last 5 years, 34 suggesting that it is a rare complication of gastric bypass. However, cases of hyperinsulinaemic hypoglycaemia suggest a possible risk resulting from long-term stimulation of GLP-1 signalling, which must be considered before using high doses of GLP-1 in the long-term.…”

Section: Time [H] Food Intake [G]mentioning

confidence: 99%

Exogenous peptide YY3-36 and Exendin-4 further decrease food intake, whereas octreotide increases food intake in rats after Roux-en-Y gastric bypass

et al. 2011

View full text Add to dashboard Cite

Background: Patients show an elevated postprandial satiety gut hormone release after Roux-en-Y Gastric bypass (gastric bypass). The altered gut hormone response appears to have a prominent role in the reduction of appetite and body weight (BW) after gastric bypass. Patients with insufficient BW loss after gastric bypass have an attenuated postprandial gut hormone response in comparison with patients who lost an adequate amount of BW. The effects of additional gut hormone administration after gastric bypass are unknown. Methods: The effects of peripheral administration of peptide YY3-36 (PYY3-36; 300 nmol kg À1 ), glucagon-like peptide-1 (GLP-1) analogue Exendin-4 (20 nmol kg À1 ) and somatostatin analogue octreotide (10 mg kg À1 ) on feeding and BW were evaluated in rats after gastric bypass. Results: Gastric bypass rats weighed (Po0.01) and ate less on postoperative day 5 (Po0.001) and thereafter, whereas postprandial plasma PYY and GLP-1 levels were higher compared with sham-operated controls (Po0.001). Administration of both PYY3-36 and Exendin-4 led to a further decrease in food intake in bypass rats compared with saline treatment (P ¼ 0.02 and Po0.0001, respectively). Similar reduction in food intake was observed in sham rats (P ¼ 0.02 and Po0.001, respectively). Exendin-4 treatment resulted in a significant BW loss in bypass (P ¼ 0.03) and sham rats (P ¼ 0.04). Subsequent treatment with octreotide led to an increase in food intake in bypass (P ¼ 0.007), but not in sham rats (P ¼ 0.87). Conclusion: Peripheral administration of PYY3-36 and Exendin-4 reduces short-term food intake, whereas octreotide increases short-term food intake in rats after gastric bypass. The endogenous gut hormone response after gastric bypass can thus potentially be further enhanced by additional exogenous therapy with pharmacological doses of gut hormones in patients with insufficient weight loss or weight regain after surgery.

show abstract

Laparoscopic Spleen-Preserving Distal Pancreatectomy as Treatment for Nesidioblastosis after Gastric Bypass Surgery

Cited by 55 publications

References 12 publications

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

Prolonged successful therapy for hyperinsulinaemic hypoglycaemia after gastric bypass: the pathophysiological role of GLP1 and its response to a somatostatin analogue

MANAGEMENT OF ENDOCRINE DISEASE: Pathogenesis and management of hypoglycemia

Exogenous peptide YY3-36 and Exendin-4 further decrease food intake, whereas octreotide increases food intake in rats after Roux-en-Y gastric bypass

Contact Info

Product

Resources

About