PROSTAGLANDIN-E(2) IN GASTRIC-MUCOSA OF CHILDREN WITH HELICOBACTER-PYLORI GASTRITIS - RELATION TO THICKNESS OF MUCUS GEL LAYER

Aims-To evaluate the changes in mucus gel layer thickness and prostagl andin E2 (PGE2) content caused by Helicobacter pylori infection in the antral mucosa of children: to assess whether decreased mucus gel thic kness is related to PGE2 production. Methods-Antral biopsy specimens w ere taken at endoscopy from 153 children. H pylori gastritis was evide nt in 45 and normal mucosa in 59. The other 49 children were studied o ne month after antibiotic treatment that eradicated the infection in 3 7 of them had been stopped. One antral specimen was immersed in ice-co ld saline, put under an inverse microscope with an eyepiece graticule. Mucus gel thickness was measured and then the processed for histologi cal examination; another specimen was weighed and processed for in vit ro prostanoid generation. Results-Mucus gel layer thickness was signif icantly decreased in children with H pylori gastritis (90 (SD) 29) mum v 120 (58) mum in controls, p < 0.01) but returned to control values after H pylori had been eradicated. PGE2 generation was significantly increased in children with H pylori gastritis (1022 (811) ng/g v 641 ( 473) ng/g in controls, p < 0.01). One month after treatment PGE2 gener ation significantly decreased in children without infection (880 (534) , p < 0.01), but was still high where infection persisted. A significa nt inverse correlation was found between PGE2 generation and mucus gel layer thickness (p < 0.05). Conclusions-These data suggest that H pyl ori damages the mucus gel layer, and that the gastric mucosa increases generation of PGE2 in response to back diffusion of acid and pepsin.