Monophasic luminal release of prostaglandin E2 in patients with reflux esophagitis under the impact of acid and acid/pepsin solutions. Its potential pathogenetic significance.

Normal human esophageal mucosa exhibits biphasic secretory responses to intraluminal stimuli in terms of PGE 2 release with a decline under the impact of HCl and an increase in PGE 2 release during mucosal exposure to HCl/Pepsin. PGE 2 secretory patterns in patients with reflux esophagitis (RE) remain unknown. We have studied, therefore, luminal release of PGE 2 in 28 patients with nonhealed and healed RE, and compared the obtained results with corresponding values recorded in controls. The rate of luminal release of PGE 2 in nonhealed RE exhibited a monophasic patterns, i.e., significantly decreased both during mucosal exposure to HCl (2,273 ± 444, vs. 3,655 ± 600 pg/min, p = 0.025) and HCl/pepsin (1,271 ± 244, vs. 3,655 ± 600 pg/min. p = 0.003) as compared to its basal value. However, the rate of luminal PGE 2 release in patients with nonhealed RE in basal conditions and during mucosal exposure to HCl was significantly higher than corresponding values in controls. Luminal release of PGE 2 in patients with healed endoscopic esophagitis was significantly lower as compared to corresponding values recorded in patients with nonhealed endoscopic changes and in controls. In conclusion, (a) monophasic inhibitory responses of the esophageal mucosa to intraluminal HCl and HCl/pepsin solutions in patients with RE indicate a different pattern of mucosal secretory response to intraluminal stimuli; (b) inhibition of the rate of luminal release of PGE 2 under the impact of HCl/pepsin may play a role in the development and/or progression of mucosal damage ; and (c) the decline in the rate of luminal PGE 2 release in healed RE indicates that its elevated value in active esophageal disease should be considered as an implication of mucosal damage induced by HCl/pepsin.