Tu1845 In Functional Dyspepsia, Are Meal-Related Symptoms Linked to Less Drinking Capacity?

Abstract

Background: Serotonin (5-HT) signaling in the small intestine is involved in motor, sensory and secretory pathways. Studies of neuroendocrine cell mapping in functional dyspepsia (FD), characterized by upper gastrointestinal motor and sensory disturbances, are scarce although it has been previously noted that there is no significant difference in numbers of 5HT cells in duodenum in post infectious FD vs. controls1. In patients with irritable bowel syndrome, another functional bowel disorder, a low density of duodenal neuroendocrine cells is also described2. Aim: To examine the content of neuroendocrine cells in the duodenum of subjects with FD, specifically the relative content of serotonin (5-HT) containing cells and to investigate a possible relationship between neuroendocrine cell numbers and FD subtypes. Methods: A random sample of an adult Swedish population (n = 1000) (the Kalixanda study) underwent upper endoscopy and biopsies taken from the duodenal bulb (D1) and the second part of duodenum (D2). From this study 23 subjects with FD were identified, 13 with postprandial distress syndrome (PDS), 10 with epigastric pain syndrome (EPS) and 12 healthy controls. Immunocytochemistry was performed for Chromogranin A (CGA) and 5-HT. Positive cells were quantified per mm2. Results: Cases and controls showed similar demographics. The number of CGA stained cells was significantly lower in FD patients both in D1 (p = 0.01) and D2 (p = 0.04) whereas there was no significant difference in 5-HT content. See figure. When EPS and PDS were studied separately, the number of CGA stained cells was significantly decreased in D1 in patients with EPS (p = 0.03). Conclusions: The number of duodenal neuroendocrine cells is decreased in FD compared with control subjects, but this is not due to a reduction in the number of 5-HT containing cells. It is possible that this reduction reflects reduced cellular densities of other hormones (e.g. somatostatin) which could result in a high secretion of gastric acid, with a change in motility or visceral sensitivity leading to dyspeptic symptoms in these cases. 1. Futagami S et al. Am J Gastroenterol. 2010 ;105:1835-42. 2. El-Salhy M et al. Scand J Gastroenterol. 2010 ;45:1435-9.