THE RELATIONSHIP BETWEEN DYSPEPSIA SUBTYPE AND MUCOSAL INFLAMMATION

Abstract

Purpose: The current study was undertaken to determine if dyspepsia subtype or individual dyspeptic symptoms are predictive of the presence of mucosal inflammation. Methods: Sixty-five patients (ages 8-17, mean 12.3 years; 50 F) undergoing endoscopy for evaluation of dyspepsia were enrolled. By Rome II criteria, there were 48 patients with ulcer-like dyspepsia (ULD) and 17 with dysmotility-like dyspepsia (DLD). Additionally, the presence of specific symptoms including epigastric pain, post-prandial pain, early satiety, nausea, bloating, and fullness was determined by patient report. All patients had biopsies obtained from each of the esophagus, antrum, and duodenum. The presence of histologic esophagitis, gastritis, and duodenitis, respectively, were determined in a standard fashion. Additionally, mucosal cell densities were determined for eosinophils and mast cells, respectively, for both the antrum and duodenum. Results: ULD was not associated with an increase in esophagitis, gastritis, or duodenitis, respectively, as compared to DLD. ULD was associated with an increase in both mean (24.1 + 12.9 vs. 18.3 + 8.1, P = 0.04) and peak (35.4 + 19.8 vs. 27.3 + 8.9, P = 0.03) duodenal eosinophil counts as compared to DLD. With regard to individual symptoms, epigastric pain was associated with a lower prevalence of both gastritis (20% vs. 52%, P =.015) and duodenitis (16% vs. 48%, P = 0.013) and lower mean antral mast cells (12.8 + 4.1 vs. 15.3 + 4.8, P = 0.048). Post-prandial pain was associated with an increased prevalence of gastritis (48% vs. 9%, P = 0.03) but no difference in eosinophil or mast cell density. There were no other significant associations. Conclusions: Other than a mild increase in duodenal eosinophils, ULD is not associated with an increase in mucosal inflammation as compared to DLD. Post-prandial pain is associated with an increased prevalence of gastritis while epigastric pain appears to be a negative predictor of mucosal inflammation.