Abstract
In Asia, the incidences of Helicobacter pylori infection and gastric cancer are high, but their association with autoimmune gastritis (AIG) is unclear. This was a retrospective cohort study of patients endoscopically diagnosed with chronic gastritis between 2005 and 2017. AIG was diagnosed according to anti-parietal cell antibody positivity. Laboratory, histological findings, and gastric cancer incidence were compared between AIG and non-AIG patients. The AIG group had more females and a higher rate of thyroid disease. Serum levels of gastrin were significantly higher in AIG patients (mean 1412 and 353 pg/mL, p < 0.001). The endoscopic findings included a significantly higher percentage of corpus-dominant atrophy in AIG (31.67%) than in non-AIG (7.04%) patients (p < 0.001). Clusters of ECL cells were observed in 28% of AIG patients and 7% of non-AIG patients (p = 0.032). The cumulative incidence of gastric cancer at 5 and 10 years was 0% and 0.03% in the AIG group and 0.03% and 0.05% in the non-AIG group, and no significant difference in gastric cancer incidence was observed. Despite significant differences in gastrin levels between AIG and non-AIG patients, there was no evidence of an impact of AIG on the incidence of gastric cancer.
Highlights
Chronic gastritis is a common disease in Asian countries due to the high prevalence of Helicobacter pylori (H. pylori) infection
autoimmune gastritis (AIG) is caused by an autoimmune process that leads to the destruction of gastric parietal cells and chief cells in the proximal stomach by specific autoantibodies, which leads to reductions in acid and intrinsic factor secretion, resulting in impaired vitamin B12 absorption and pernicious anemia [1]
H. pylori, CagA-positive strains, induce chronic inflammation in the stomach, which leads to the development of atrophic gastritis and intestinal metaplasia [2,3]
Summary
Chronic gastritis is a common disease in Asian countries due to the high prevalence of Helicobacter pylori (H. pylori) infection. In Western countries, the rate of H. pylori infection is much lower, and autoimmune gastritis (AIG) is the more common subtype of chronic gastritis. Impaired acid secretion is compensated by the increased activation of gastrin secretion via a negative feedback mechanism. Both enterochromaffin-like cell (ECL) hyperplasia and neuroendocrine tumor may be associated with these series of responses. H. pylori, CagA-positive strains, induce chronic inflammation in the stomach, which leads to the development of atrophic gastritis and intestinal metaplasia [2,3]. H. pylori infection is a well-established risk factor for gastric cancer, in patients with severe gastric atrophy and intestinal metaplasia [4], including in the proximal stomach. In Japan, H. pylori infection is thought to Biomedicines 2020, 8, 419; doi:10.3390/biomedicines8100419 www.mdpi.com/journal/biomedicines
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