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The Th2 cytokine IL-4 might limit H. pylori associated gastric inflammation and favour H. pylori clearance. The aim of the study was to verify whether IL-4 -588CT SNP, or two SNPs of the gene coding the alpha chain of IL-4 receptor (IL-4RA Ex5+14AG, IL-4RA Ex11+828AG) considered singly or as haplotypes, are correlated with H. pylori virulence genes or H. pylori associated diseases.We studied 144 patients with non-cardia gastric cancer (NCGC)(41/50 with present or past H. pylori infection), 75 with duodenal ulcer (DU)(66 H. pylori infected) and 171 with gastritis (CG)(107 H. pylori infected). cagA gene was present in 24/28 NCGC, 45/59 DU and 56/107 CG.All SNPs were in Hardy-Weinberg equilibrium. IL-4RA haplotypes frequencies were estimated using Arlequin software. Neither the SNPs nor the IL-4RA haplotype correlated with disease diagnosis, H. pylori infection, degree of mucosal inflammation or intestinal metaplasia. IL-4 -588T allele (OR=3.69, 95% CI:1.34-10.16) and IL-4RA GA haplotype (p0.05) enhanced the risk for cagA positive infections. IL-4RA GA haplotype correlated with IL-4 protein levels in H. pylori infected gastric mucosa.IL-4 and IL-4RA gene polymorphisms concur in selecting the H. pylori infecting strain, probably influencing the IL-4 signalling pathway.

Aim. GastroPanel combines the evaluation of pepsinogens A and C PGA, PGC), anti-H. pylori antibodies (Ab) and gastrin-17 (G17) to identify astric mucosal inflammation and atrophy. We analysed GastroPanel in H. ylori infected (Hp+) and coeliac disease (CD) children. Methods. Five hundred and forty-five children subjected to EGDS. In asting sera: PGA, PGC, G17, Ab (ELISAs) and total gastrin (tG) (RIA). In astric juice: pH. Histology for inflammation, Hp and CD diagnosis. Results. Eighty-nine Hp+, 45 CD and 411 Hp and CD negative (conrol children). PGC and Ab were higher in Hp+ than in controls (F= 12.2, < 0.001; F= 35.6, p< 0.001). PGA/PGC was reduced in Hp+ (6.8± 0.44, ean±S.E.M.) and in CD (6.7± 0.67) with respect to controls (10.1± 0.52) F= 6.25, p< 0.005). tG and G17 were higher in Hp+ (67.6± 3.2 ng/l and .0± 1.7 pmol/l) and CD (103.4± 23.6 and 8.6± 2.3) than in controls 61.2± 2.4 and 3.2± 0.4) (F= 9.23, p< 0.001; F= 9.48, p< 0.001). PGC, b and G17 correlated withHp density grade (F= 6.44, p< 0.005;F= 20.79, < 0.001; F= 7.43, p< 0.005). PGC correlated also with the degree of antral nflammation (F= 6.18, p< 0.005) and activity (F= 9.89, p< 0.001). In Hp+ direct correlation between PGA and tG was found (r= 0.396, p< 0.001); in D this association was opposite (r=−0.388, p< 0.05). In Hp+ intragastric H correlated directly with tG (r= 0.264, p< 0.05); in CD intragastric pH nversely correlated with PGA (r=−0.336, p= 0.06) and directly with tG r= 0.787, p< 0.001) and with G17 (r= 0.609, p< 0.01). In CD histology ailed to demonstrate frank gastric mucosal atrophy. Summary.Hp associated gastritis enhanced serum PGC, Ab and G17. In D the reduced levels of PGA/PGC suggest that atrophy might involve gasric body mucosa, probably with a patchy pattern escaping routine histology; he consequent reduced gastric acid secretion enhanced gastrin release. Conclusion. Hp associated gastritis enhances serum PGC and G17. In D, gastric mucosal atrophy, suggested by the combined PGA/PGC reduced nd G17 increased levels might be extended outside the duodenum affecting he stomach.