View clinical trials related to Dumping Syndrome.
Filter by:Bariatric surgery is an effective anti-obesity treatment providing durable weight loss and profound beneficial effects on glucose metabolism. However, bariatric surgery also comes with an increased risk for a late metabolic complication known as postbariatric hypoglycaemia (PBH). The condition presents with hypoglycaemic episodes 1-3 hours after meals and develops one to several years after bariatric surgery, mainly gastric bypass. PBH affects approximately 30% of patients without preexisting diabetes. For a subset of patients, hypoglycaemia-associated impairment of daily living and social functioning are commonly observed. The underlying mechanisms of PBH are multifactorial. It is considered that inadequately high insulin secretion caused by both accelerated glucose absorption from the gut and increased insulinotropic hormones such as GLP-1 are important pathophysiologic mechanisms. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor reduces glucose exposure by increasing urinary glucose excretion. In a pilot study, a single dose of 10mg of empagliflozin taken before a mixed meal reduced the risk of PBH by 74%. Both, postprandial glucose and insulin exposure were significantly lower with empagliflozin vs. placebo, which makes Empagliflozin a potential treatment for PBH. In this study, treatment naïve patients will be randomized to receive either oral empagliflozin 25 mg daily in the morning for 20 days, followed by 2-6 weeks wash out and 20 days placebo once daily in the morning, or the reverse sequence. Urine and blood analysis will be performed as detailed in the protocol.
There is no consensus on what type of function-preserving gastrectomy can provide the best patient quality of life (QOL). This study aims to evaluate the incidence of dumping syndrome after vagus nerve-preserving distal gastrectomy (VPNDG).
The incidence of oesophagogastric cancer has increased by 400% since the 1970s in Ireland and the United Kingdom. In addition, refinement of perioperative management and the now widespread use of multimodal protocols for patients with locally advanced disease have significantly improved outcomes for patients with oesophagogastric cancer treatable with curative intent. Despite significant advances in chemoradiotherapy, surgical resection remains the primary curative option. Unintentional weight loss and nutritional complications represent serious concerns for patients after radical resection, even among those who remain free from recurrent disease in the long-term. A study from the Swedish Esophageal and Cardia Cancer Registry reported a mean three year weight loss of 10.8% among disease-free patients, with 33.8% of this cohort demonstrating malnutrition at three years post-oesophagectomy. Mechanisms contributing to weight loss for disease-free patients after upper gastrointestinal surgery are poorly understood, however an association between increasing magnitude of weight loss and the presence of increased satiety is described. Our recent studies at SJH have demonstrated four fold elevated postprandial satiety gut hormone concentrations after oesophagectomy, compared with baseline preoperative values. Postprandial gut hormone levels correlate significantly with postprandial symptoms and altered appetite at 3 months postoperatively, and with body weight loss at 2 years postoperatively. However, the mechanism leading to exaggerated postprandial gut hormone production after upper gastrointestinal surgery is poorly understood, limiting targeted therapeutic options. In this study, we aim to characterise the role of altered nutrient transit and enteroendocrine cell function in the pathophysiology of excessive post-prandial gut hormone responses after upper gastrointestinal surgery. To do this, we will measure the gut hormone response to a standardised 400 kcal meal, as per previous studies, while concurrently assessing gastrointestinal transit time, and enteroendocrine cell morphology and function. In this way, we will determine whether the magnitude of the postprandial gut hormone response correlates with the rate of nutrient transit into the enteroendocrine L-cell rich small intestine, and whether enteroendocrine cell adaptation occurs after oesophagectomy. Furthermore, we have previously observed that gut hormone suppression using octreotide is associated with increased ad libitum among subjects after upper gastrointestinal cancer surgery (Elliott JA et al, Annals of Surgery, 2015). The mechanism of action of octreotide may relate to SSTR-5-mediated negative feedback to the enteroendocrine L-cell, but this medication may additionally reduce enteroendocrine L-cell responses through its inhibitory effect on gastrointestinal motility - reducing the rapidity with which nutrients are delivered to the small intestine - and small intestinal nutrient sensing via inhibition of the Na+-dependent glucose transporter SGLT-18-10. Through conduction of this double-blind, randomised, placebo-controlled crossover study, we aim to establish the mechanism of action of octreotide-mediated increased food intake in patients after gastrointestinal surgery. This may inform the design of future targeted interventions for this patient group.
The purpose of the study is to investigate whether hypoglycaemia observed after food intake in bariatric patients can be either influenced by an SGLT2 inhibitor, empagliflozin, or via inhibition of inflammation with an human interleukin-1 receptor antagonist (IL1-RA, anakinra).
Patients who have undergone gastrectomy (removal of the stomach) to treat or prevent cancer are known to have a significantly reduced quality of life. To date, there is very little information on the physiological causes of this. The investigators suspect that overproduction of a hormone (chemical) called glucagon like peptide-1 (GLP-1) released by the lining of the gut may play a role in the reduced appetite, weight loss and low blood sugar symptoms seen in this group. To investigate this, the investigators will study the response of 16 patients who have previously had a gastrectomy to a glucose drink, and a meal, while receiving an infusion of a specific blocker of GLP-1 or placebo. The investigators will examine the levels of sugar and associated hormones in the blood, food consumption and food reward behaviour using standard tools. Participants will be invited to attend the Clinical Research Facility at Addenbrooke's Hospital for a screening visit, and two whole day study visits. The study has been designed to assess the role of overproduction of GLP-1 by completely blocking its actions, rather than assess the use of the blocking compound as a medication, and is therefore regarded as a physiological study, not a clinical trial. The goal of this study is to demonstrate the magnitude of effect of GLP-1 on blood sugar and appetite derangement in patients who have had a gastrectomy. This will guide future work on the development of novel treatment paradigms for the post-gastrectomy patient group.
The postprandial dumping syndrome is a frequent consequence of Roux-en-Y Gastric ByPass due to the rapid emptying of the stomach remnant in to the intestinal lumen. Dumping-related symptoms occur very early after eating (within 30 minutes), are not associated with concurrent hypoglycemia, and are most prominent in the early postoperative period. This syndrome very debilitating for the patient can be improved by dietary and nutritional recommendations. We hypothesize that a personalized approach based on dietary and nutritional recommendations conducted by a nurse would likely to decrease the frequency of dumping syndrome and improve the postoperative quality of life of patients in the early postoperative period.
The purpose of this study is to evaluate the prevalence at 3.5 months of age of dumping syndrome in children operated at birth for oesophageal atresia type III et IV.
The purpose of this study is to assess if Somatuline autogel 90 mg is effective in the treatment of dumping syndrome.
Dumping Syndrome consists of (1) a too rapid gastric emptying, (2) an inappropriate release of GI hormones (as a reaction to the hyperosmolar contents in the duodenum) and (3) an hyperinsulinemic response to a too rapid absorption of glucose. Because it is not well known which somatostatin receptor(s) (sst1-5) influence(s) Dumping Syndrome most, the goal of this trial is to evaluate : - the effect of pasireotide (sst1, 2, 3, 5 agonist) on the control of gastric emptying. - the effect of pasireotide (sst1, 2, 3, 5 agonist) on the release of GI hormones (during OGTT). - the effect of pasireotide (sst1, 2, 3, 5 agonist) on the hyperinsulimic response (during OGTT). - the efficacy of pasireotide (sst1, 2, 3, 5 agonist) for control of objective parameters of Dumping Syndrome (hematocrit (Hct), pulse rate and occurrence of hypoglycemia after an Oral Glucose Tolerance Test (OGTT) with 75g of glucose) - the efficacy of pasireotide (sst1, 2, 3, 5 agonist) for control of overall symptoms as measured by the combined Dumping Syndrome score - the efficacy of pasireotide (sst1, 2, 3, 5 agonist) for control of symptoms as measured by (a) early and (b) late phase dumping symptom score separately - the efficacy of pasireotide (sst1, 2, 3, 5 agonist) for control of quality of life (QoL SF-36)
multi-center, phase II study evaluating efficacy, safety and pharmacokinetics of pasireotide in patients with dumping syndrome