Treatment of the Dumping Syndrome with the Somatostatin Analogue SMS 201–995

Hopman, W. P. M.; Wolberink, R. G. J.; Lamers, C. B. H. W.; Tongeren, J. H. M. Van

doi:10.1097/00000658-198802000-00007

Cited by 75 publications

(38 citation statements)

References 20 publications

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“…Somatostatin analogs such as octreotide have been used successfully in the treatment of early dumping syndrome [12][13][14][15], although octreotide does have problems, including being expensive and having adverse events, such as gallstone formation, prolonged QT and such as postprandial hyperglycemia. The data shown here suggest that increased secretion of GLP-1 and GIP might be an alternative mechanism leading to the occurrence of early dumping syndrome.…”

Section: Discussionmentioning

confidence: 99%

Octreotide improves early dumping syndrome potentially through incretins: a case report

et al. 2013

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Dumping synDrome, or rapid gastric emptying, is a serious complication that may occur after gastric surgery in approximately 5-10% of patients, although it may occur in approximately 20% after vagotomy with pyloroplasty and up to 50% after esophagectomy [1][2][3]. In spite of this level of occurrence, the pathophysiologic mechanisms underlying the symptoms of dumping syndrome are poorly understood. Here, we report a patient with dumping syndrome following distal gastrectomy with Billroth I reconstruction for early-stage gastric cancer. In this case, we have measured the levels of several hormones during a 75g oral glucose tolerance test (75g-OGTT), and found that glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were both inhibited by octreotide treatment. Abstract. Dumping syndrome, or rapid gastric emptying, is a frequent complication after gastric surgery. In this case, the patient was a 47-year-old woman who 10 years previously had undergone distal gastrectomy with Billroth I reconstruction for early-stage gastric cancer. She presented with symptoms of weakness, headache, palpitation, sweating, dizziness and significant fatigue between one and two hours after a meal. Because a 75g oral glucose tolerance test (75g-OGTT) induced both acute postprandial tachycardia (within 1 hour) and postprandial hypoglycemia, we diagnosed this patient with early and late dumping syndrome. Dietary measures and acarbose improved symptoms of late dumping syndrome but did not prevent the symptoms of early dumping syndrome such as postprandial tachycardia, weakness, headache, palpitation, and dizziness. We therefore used the somatostatin analogue octreotide, which has been reported as an effective therapy for early dumping syndrome. Octreotide prevented the symptoms of early dumping syndrome, especially postprandial tachycardia, but caused postprandial hyperglycemia. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were completely suppressed during the 75g-OGTT following subcutaneous injection of octreotide. No change was observed in vasoactive intestinal polypeptide (VIP), which is the gastrointestinal peptide hormone generally responsible for early dumping syndrome, suggesting possible contribution of incretins in early dumping syndrome of this patient.Key words: Dumping syndrome, GLP-1, Octreotide material and methods Laboratory analysesBlood samples were taken after an overnight fast. Plasma glucose concentrations were measured with the hexokinase G6PD UV method. Serum insulin concentrations were measured with a chemiluminescent enzyme immunoassay. Serum triglyceride concentrations were determined by Enzymatic method. Serum total cholesterol concentrations were measured by a cholesterol dehydrogenase ultraviolet method. Serum HDL cholesterol concentrations were determined by a direct method (Cholestest ® N HDL, Sekisui Medical, Japan). Hemoglobin A1c (NGSP) levels were measured by high performance liquid chromatographic assay (HPLC). Serum total GIP and...

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Section: Discussionmentioning

confidence: 99%

Octreotide improves early dumping syndrome potentially through incretins: a case report

et al. 2013

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“…These encouraging reports with somatostatin were soon followed by several studies with the analogue, octreotide (table 1). Although the total number of patients studied remains relatively small, the results show unani mously that octreotide 50-100 pg can almost completely relieve the symptoms of dumping induced by a standard glucose load or a meal [2,[5][6][7], Objective evidence of dumping, namely rise in pulse rate, occurred in all studies and this was also inhibited by octreotide. In three of the studies octreotide also prevented the rise in PCV [2,6,7], Two studies have examined the effect of octreotide long-term in dumping syndrome (table 2).…”

Section: Clinical Studiesmentioning

confidence: 77%

“…Evi dence, that inhibition of motility is contributory is pro vided by the study of Geer et al [2] which showed that octreotide substantially delays gastric emptying in pa tients with dumping syndrome (578 ± 244 min) com pared to controls treated with placebo (76 ± 23 min). Pre liminary evidence suggests that octreotide increases small bowel transit time in some patients with dumping syn drome [5].…”

Section: Mechanism O F Actionmentioning

confidence: 99%

Octreotide in Dumping and Short Bowel Syndromes

Farthing¹

1993

Digestion

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Octreotide inhibits intestinal motility and reduces gastrointestinal secretions. These actions have led to its evaluation in two postsurgical conditions: dumping syndrome and short bowel syndrome. Octreotide substantially reduces symptoms of early and late dumping and prevents the associated phenomena including the increase in packed cell volume considered to be indicative of reduced plasma volume. Its therapeutic benefit probably relates both to slowing of gastric emptying and small bowel transit and inhibition of the release of putative mediators (peptide hormones) of the vasomotor symptoms. Octreotide also reduces intestinal efflux in some patients with the short bowel syndrome. This can lead to a reduction in the volume of intravenous fluid requirements but does not allow an intravenous fluid-dependent patient to change back to an oral regimen. The major mechanism of octreotide’s therapeutic effect in this situation may be its ability to reduce endogenous gastric acid secretion.

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“…Similar increases have been reported previously in gastrectomized patients with symptoms of dumping [4,5], High doses of neurotensin cause vasodilatation; however, current evidence suggests that it is unlikely that this peptide plays a role in the pathophysiology of dumping [37], On the contrary, since both neurotensin and PYY have inhibitory effects on upper gastrointestinal motility and secretion, these in creased responses appear to be adaptive changes which tend to slow transit and improve absorption [ Long et al [43] reported that somatostatin infusion reduced the symptoms of the dumping syndrome with a corresponding decrease in secretion of peptides such as neurotensin and vasoactive intestinal polypeptide. More recent reports suggest that long-acting somatostatin ana logues offer promise in treating the condition [44,45], It is interesting that somatostatin not only slows bowel transit but also stimulates esophageal motor activity [46]. Total gastrectomy patients have more severe symptoms of re flux esophagitis and a lower nutritional state than those after distal partial gastrectomy.…”

Section: Discussionmentioning

confidence: 99%

Adaptive Gastrointestinal Hormone Changes after Gastric Resection

et al. 1997

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Circulating alimentary hormones were measured following a standardized meal in 10 patients after partial distal gastrectomy and 12 patients after total gastrectomy, both groups reconstructed by Billroth-II anastomosis, and in 9 age-matched healthy controls. Patients underwent resection for gastric cancer and were studied 45 ± 10 months after surgery. At the time of study, the patients had adapted well to surgery and no longer exhibited the symptoms of dumping seen immediately postoperatively. In contrast, the total gastrectomy patients exhibited severe symptoms of reflux esophagitis. The nutritional states of the patients, evaluated by measurement of rapid turnover proteins in serum, was impaired in proportion to the degree of gastric resection. Basal gastrin levels were reduced by partial (p < 0.05) and total gastrectomy (p < 0.01). Postprandial responses of both gastrin and pancreatic polypeptide were abolished following either partial gastrectomy or total gastrectomy (all p < 0.001). Glucose-dependent insulinotropic peptide and motilin were relatively normal after both procedures. In contrast, early cholecystokinin responses were increased 2-fold after partial gastrectomy (p < 0.05) and 3-fold after total gastrectomy (p < 0.001). Postprandially, a large increase in neurotensin levels and a moderate increase in peptide YY were seen after both partial and total gastrectomy (all p < 0.01). Fasting peptide YY levels were also increased after total gastrectomy (p < 0.01). The late adaptive changes in alimentary hormone secretion may help to compensate for loss of gastric motor function which accompanies gastric resection. On the other hand these hormonal changes may exacerbate the esophageal reflux seen following gastrectomy.

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Treatment of the Dumping Syndrome with the Somatostatin Analogue SMS 201–995

Cited by 75 publications

References 20 publications

Octreotide improves early dumping syndrome potentially through incretins: a case report

Octreotide improves early dumping syndrome potentially through incretins: a case report

Octreotide in Dumping and Short Bowel Syndromes

Adaptive Gastrointestinal Hormone Changes after Gastric Resection

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