Dumping Syndrome: Pragmatic Treatment Options and Experimental Approaches for Improving Clinical Outcomes

Abstract

Dumping syndrome is a common complication after esophageal, gastric and bariatric surgery and has a significant negative impact on the quality of life of patients. This narrative review describes the clinical syndrome, pathophysiology, diagnosis and reports on standard and pragmatic therapeutical treatment options in order to improve the clinical outcome of patients with dumping syndrome. Dumping syndrome consists of early and late dumping symptoms and can be diagnosed using clinical parameters with the help of the Sigstad's score, questionnaires or by provocative testing. The prevalence of dumping syndrome varies depending on the employed definition of dumping syndrome. Overall, dumping syndrome is more frequent nowadays due to increasing numbers of upper gastrointestinal and bariatric surgeries being performed. First treatment step includes dietary adjustment and dietary supplements, which are often sufficient to manage symptoms for the majority of patients. Next step of therapy includes acarbose, which is effective for late dumping symptoms, but the use is limited due to side effects. Somatostatin analogues are indicated after these two steps have failed. Somatostatin analogues are very effective for controlling early and late dumping, also in the long term. Glucagon like peptide-1 receptor agonists, endoscopic and surgical (re)interventions are reported as treatment options for refractory dumping syndrome; however, their use is not recommended in clinical practice due to the limited evidence on and uncertainty of outcomes. These alternatives should be considered only as last resort options in patients with otherwise refractory and invalidating dumping syndrome.

Physiological Appetite Regulation and Bariatric Surgery

“…Postprandial hyperinsulinemic hypoglycaemia is a complication of RYGB and GS [ 209 ]. Hypoglycaemia may accompany dumping syndrome [ 210 ], though dumping syndrome can often be missed [ 211 ]. Studies further suggest that postprandial hypoglycaemia is not exclusively postprandial [ 212 ].…”