Abstract
Non-atrophic active chronic gastritis (ACG) is characterized by the presence of H. pylori in the gastric epithelium, known to be one of the first steps that precede progression to gastric adenocarcinoma. Inactive chronic gastritis (ICG) suggests that the patient has H. pylori gastritis, but this diagnosis is rarely made in routine histopathology. Clinical manifestations associated with H. pylori infection are potentially due to differences in virulence between strains; however, it is unclear if the progression of ACG to ICG depends on the H. pylori strain. The aim of this study was to compare the prevalence of the virulence factors of H. pylori found in patients with ACG and ICG, and its influence on the development of ICG. A significant association was observed between H. pylori detection by histological examination and the activity of gastritis (p 1 year) was reported by 28.6% of the ACG group and 42.5% of the ICG, while no evidence of association between long-term use of PPI and decreased inflammation was found in the patients studied. The genes cagA, cagE and virB11 were statistically associated with ACG (p = 0.01, p vacAs1 allele groups, ACG was associated with the most virulent group (p = 0.0015), while ICG was associated with the less virulent group (p H. pylori in the non-resolution of gastritis.
Highlights
The presence of Helicobacter pylori in the gastric epithelium typically leads to an antral-predominant nonatrophic active chronic gastritis (ACG) lesion, known to be one of the first pathologic markers of H. pylori infection and one of the steps preceding progression to gastric adenocarcinoma [1]
Long-term use of proton pump inhibitors (PPI) (>1 year) was reported by 28.6% (32/112) of the patients diagnosed with ACG and 42.5% (17/40) of the Inactive chronic gastritis (ICG) group
A higher number of cases of ICG were associated with treatment, no evidence of association between long-term use of PPI and decrease in polymorphonuclear infiltrate was found in the sample studied (p = 0.15)
Summary
The presence of Helicobacter pylori in the gastric epithelium typically leads to an antral-predominant nonatrophic active chronic gastritis (ACG) lesion, known to be one of the first pathologic markers of H. pylori infection and one of the steps preceding progression to gastric adenocarcinoma [1]. Two factors are well established in H. pylori virulence, namely the presence of the vacA s1m1 allele [5] and the cagA gene, other virulence factors have been pointed out as potentially relevant to gastric cancer development. CagE and virB11 genes, belonging to the cag pathogenicity island (cag-PAI), have been correlated with more severe lesions [6]-[10]. Some authors even consider the cagE gene a better marker of cag-PAI than the cagA gene [11]-[13]
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