Esophageal mucosal eicosanoids in gastroesophageal reflux disease and Barrett's esophagus
Triadafilopoulos, G.; Kaczynska, M.; Iwane, M.
American Journal of Gastroenterology 91(1): 65-74
1996
ISSN/ISBN: 0002-9270 PMID: 8561146 Document Number: 462762
Objective: Eicosanoids (prostaglandins and leukotrienes) may contribute to the clinical manifestations of gastroesophageal reflux disease (GERD). In this cross-sectional study, our purpose was to assess the role of leukotriene B-4 (LTB-4) and prostaglandin E-2 (PGE-2) in the clinical, endoscopic, and histological manifestations of GERD. Methods: Using RIA, we measured ex vivo LTB-4 and PGE-2 content in esophageal mucosal biopsies from 141 patients with or without gastroesophageal reflux disease who underwent upper endoscopy. Patients were classified as normal symptomatic controls (n = 70), esophagitis stages 1-4 (n = 60), and Barrett's esophagus (n = 11), using clinical, endoscopic, histological, manometric, and esophageal 24-h ambulatory pH criteria. Results: Mean LTB-2 levels were significantly higher in both endoscopically and histologically identified erosive esophagitis and Barrett's esophagus patients, compared with normal controls. In contrast, PGE-2 levels did not differ significantly among endoscopic or histological groups. When eicosanoid levels and composite symptom score (frequency score x severity score summed over rive symptoms) were analyzed, no significant associations were found between LTB-4 or PGE-2 levels and the composite symptom score. There was no correlation between tissue eicosanoid levels and either the degree of esophageal acid exposure by ambulatory pH monitoring or the lower esophageal sphincter resting pressure as assessed by esophageal motility. Treatment with omeprazole 20 mg by mouth daily for 6 wk significantly reduced both LTB-4 and PGE-2 levels (p lt 0.05) and was associated with significant improvement of symptoms and the endoscopic and histological appearance of the esophagus in 25 patients. Conclusions: These results suggest that LTB-4, a prominent product of arachidonic acid metabolism in neutrophils, mediates the inflammatory phenomena of reflux esophagitis. The role of LTB-4 and PGE-2 in the induction of symptoms in patients with GERD and Barrett's esophagus remains unclear.