Helicobacter pylori non-cytotoxic genotype enhances mucosal gastrin and mast cell tryptase

Aims - To determine the association, if any, between H pylori genotype and the gastric mucosal variations in the levels of gastrin, somatostatin, tryp tase, and histamine. Methods - 49 patients affected by duodenal ulcer and 48 by non-ulcer dyspep sia were studied. To identify the H pylori genotype, the presence of the ca gA gene and vacA alleles m1, m2, s1, and s2 were analysed by polymerase cha in reaction. Gastrin, somatostatin, tryptase, and histamine were measured i n antral mucosal biopsies. Results - 57 patients were infected with H pylori (30 with duodenal ulcer a nd 27 with non-ulcer dyspepsia). Gastrin and tryptase were increased in pat ients with H pylori infection, although the variations were statistically s ignificant only for gastrin; somatostatin and histamine were not influenced by H pylori infection. In patients with non-ulcer dyspepsia the absence of the cagA gene and the presence of vacA alleles s2 and m2 were associated w ith higher values of tryptase and to a lesser extent of gastrin. These asso ciations were not found in patients with duodenal ulcer. Conclusions - The cagA negative s2m2 strain of H pylori may be less dangero us for the gastric mucosa than other H pylori strains since it enhances try ptase production by gastric mucosal mast cells; this enzyme is thought to s timulate tissue turnover and favour wound healing.