MONOPHASIC LUMINAL RELEASE OF PROSTAGLANDIN E(2) 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 t o 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 ex posure to HCl/Pepsin. PGE(2) secretory patterns in patients with reflu x esophagitis (RE) remain unknown. We have studied, therefore, luminal release of PGE(2) in 28 patients with nonhealed and healed RE, and co mpared the obtained results with corresponding values recorded in cont rols. The rate of luminal release of PGE(2) in nonhealed RE exhibited a monophasic patterns, i.e., significantly decreased both during mucos al 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) a s compared to its basal value. However, the rate of luminal PGE(2) rel ease in patients with nonhealed RE in basal conditions and during muco sal exposure to HCl was significantly higher than corresponding values in controls. Luminal release of PGE(2) in patients with healed endosc opic esophagitis was significantly lower as compared to corresponding values recorded in patients with nonhealed endoscopic changes and in c ontrols. In conclusion, (a) monophasic inhibitory responses of the eso phageal mucosa to intraluminal HCl and HCl/pepsin solutions in patient s with RE indicate a different pattern of mucosal secretory response t o 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 develo pment and/or progression of mucosal damage; and (c) the decline in the rate of luminal PGE(2) release in healed RE indicates that its elevat ed value in active esophageal disease should be considered as an impli cation of mucosal damage induced by HCl/pepsin.