The potential role of the esophageal pre-epithelial barrier components in the maintenance of integrity of the esophageal mucosa in patients with endoscopically negative gastroesophageal reflux disease

Abstract

OBJECTIVE: Patients with gastroesophageal reflux disease (GERD) accompanied by erosive reflux esophagitis (RE) exhibit an impairment within the esophageal pre-epithelial barrier protective components that may facilitate the development and/or progression of the mucosal injury. Little is known, however, whether such impairment is a general phenomenon affecting all patients with GERD or whether this is a characteristic feature only of patients with erosive RE. We therefore studied the rate of secretion of esophageal inorganic and organic protective factors in patients with endoscopically negative [E (−)] GERD and compared these results with the corresponding values in asymptomatic volunteers (CTRL). METHODS: The study was conducted on 33 white asymptomatic volunteers and 10 white patients with a long history of GERD confirmed by 24-h pH monitoring and a grossly negative upper endoscopy. Esophageal secretion was collected during mucosal exposure to NaCl, HCl, HC/pepsin and NaCl using the esophageal perfusion catheter. In collected samples all investigated parameters were measured. RESULTS: The pH of esophageal secretion and its content of bicarbonate, EGF, and PGE 2 in patients with E (−) GERD and asymptomatic volunteers were similar. Unexpectedly, the rate of esophageal glycoconjugate (predominantly mucin) secretion was significantly higher in patients with E (−) GERD than in controls during perfusion with HCl ( p < 0.05). Furthermore, secretion of protein in patients with E (−) GERD was significantly higher than in the control group during the mucosal exposure to HCl/Pepsin ( p < 0.05). The nonbicarbonate buffer secretion during perfusion with HCl and HCl/Pepsin as well as the rate of esophageal TGFα output during infusion of final saline in patients with E (−) GERD were significantly lower than in CTRL group ( p < 0.05). CONCLUSIONS: Our data indicate that patients with E (−) GERD have an esophageal secretory potential, in terms of glycoconjugate and protein, higher than that in asymptomatic controls. This phenomenon in patients with E (−) GERD may, by enhancing the quantity of the esophageal pre-epithelial barrier, help to prevent the development of erosive esophagitis. A significantly lower esophageal secretory response in patients with E (−) GERD in terms of nonbicarbonate buffers and TGFα may facilitate the development of GERD symptoms and histological changes of GERD, respectively.