Dumping syndrome is a frequent complication of esophageal, gastric or bariatric surgery. Rapid gastric emptying, with the delivery to the small intestine of a significant proportion of solid food as large particles that are difficult to digest, is a key event in the pathogenesis of this syndrome. This occurrence causes a shift of fluid from the intravascular component to the intestinal lumen, which results in cardiovascular symptoms, release of several gastrointestinal and pancreatic hormones and late postprandial hypoglycemia. Early dumping symptoms comprise both gastrointestinal and vasomotor symptoms. Late dumping symptoms are the result of reactive hypoglycemia. Besides the assessment of clinical alertness and endoscopic or radiological imaging, a modified oral glucose tolerance test might help to establish a diagnosis. The first step in treating dumping syndrome is the introduction of dietary measures. Acarbose can be added to these measures for patients with hypoglycemia, whereas several studies advocate guar gum or pectin to slow gastric emptying. Somatostatin analogs are the most effective medical therapy for dumping syndrome, and a slow-release preparation is the treatment of choice. In patients with treatment-refractory dumping syndrome, surgical reintervention or continuous enteral feeding can be considered, but the outcomes of such approaches are variable.

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Dumping syndrome is a frequent complication of cancer and non-cancer oesophageal and gastric surgery, as well as bariatric surgery (also known as metabolic surgery). These interventions change gastric anatomy and innervation, which can enable a considerable amount of undigested food to reach the small intestine too rapidly 1-4. Dumping syndrome comprises a constellation of symptoms that can be subdivided into early and late dumping syndrome symptoms, which can occur jointly or separately 1-8. Typically, symptoms of early dumping syndrome occur within the first hour after a meal and include gastrointestinal symptoms (abdominal pain, bloating, borborygmi, nausea and diarrhoea) and vasomotor symptoms (flushing, palpitations, perspiration, tachycardia, hypotension, fatigue, desire to lie down and, rarely, syncope) 1,2. The underlying mechanisms might involve osmotic effects, peptide hormone release and autonomic neural responses 1. Symptoms of late dumping syndrome usually occur between 1 and 3 h after a meal and are primarily the manifestations of hypoglycaemia, which mainly results from an incretin-driven hyperinsulinaemic response after carbohydrate ingestion. Hypoglycaemia-related symptoms are attributable to neuroglycopenia (which is indicated by fatigue, weakness, confusion, hunger and syncope) and to vagal and sympathetic activation (indicated by perspiration, palpitations, tremor and irritability) 1,2. The literature has referred to late dumping syndrome as 'reactive hypoglycaemia' or, after bariatric surgery, as 'postbariatric hypoglycaemia'. However, on the basis of a common pathophysiology of rapid exposure of the small intestine to nutrients, which is also seen in early dumping syndrome (see subsequent discussion), we refer to this phenomenon as 'late dumping syndrome'. The prevalence of dumping syndrome depends on the type and extent of surgery, and on the criteria used to diagnose dumping syndrome. Dumping syndrome occurs in approximately 20% of patients undergoing

SUMMARY BackgroundUncontrolled studies suggest benefit of intrapyloric injection of botulinum toxin (botox) for the treatment of gastroparesis, but controlled data are lacking.

ObjectiveTo investigate the efficacy and safety of two different budesonide formulations (effervescent tablet for orodispersible use (BET) and viscous suspension (BVS)) with different daily dosages for short-term treatment of eosinophilic oesophagitis (EoE).DesignAdults with active EoE (n=76) randomly received 14 days’ treatment with either BET 2×1 mg/day (BET1, n=19) or BET 2×2 mg/day (BET2, n=19), or BVS 2×5 mL (0.4 mg/mL)/day (BVS, n=19) or placebo (n=19) in a double-blind, double-dummy fashion, with a 2-week follow-up. Primary end point was histological remission (mean of <16 eosinophils/mm2 hpf). Secondary end points included endoscopy score, dysphagia score, drug safety and patient's preference for drug formulation.ResultsHistological remission occurred in 100%, 94.7% and 94.7% of budesonide (BET1, BET2, BVS, respectively) and in 0% of placebo recipients (p<0.0001). The improvement in total endoscopic intensity score was significantly higher in the three budesonide groups compared with placebo. Dysphagia improved in all groups at the end of treatment; however, improvement of dysphagia persisted only in those treated with BET1 (p=0.0196 vs placebo). There were no serious adverse events. Local fungal infection (stained fungi) occurred in two patients of each budesonide group (10.5%). The effervescent tablet was preferred by 80% of patients.ConclusionsBET or BVS was highly effective and safe for short-term treatment of EoE. The 1 mg (twice daily) dosage was equally effective as the 2 mg twice daily dosage. The majority of patients preferred the effervescent tablet formulation.ClinicalTrials.gov numberNCT02280616; EudraCT number, 2009-016692-29.