Abstract
Gastric cancer is a leading cause of mortality worldwide. The risk of developing gastric adenocarcinoma, which comprises >90% of gastric cancers, is multifactorial, but most associated with Helicobacter pylori infection. Autoimmune gastritis is a chronic autoinflammatory syndrome where self-reactive immune cells are activated by gastric epithelial cell autoantigens. This cause of gastritis is more so associated with the development of neuroendocrine tumors. However, in both autoimmune and infection-induced gastritis, high risk metaplastic lesions develop within the gastric mucosa. This warrants concern for carcinogenesis in both inflammatory settings. There are many similarities and differences in disease progression between these two etiologies of chronic gastritis. Both diseases have an increased risk of gastric adenocarcinoma development, but each have their own unique comorbidities. Autoimmune gastritis is a primary cause of pernicious anemia, whereas chronic infection typically causes gastrointestinal ulceration. Both immune responses are driven by T cells, primarily CD4+ T cells of the IFN-γ producing, Th1 phenotype. Neutrophilic infiltrates help clear H. pylori infection, but neutrophils are not necessarily recruited in the autoimmune setting. There have also been hypotheses that infection with H. pylori initiates autoimmune gastritis, but the literature is far from definitive with evidence of infection-independent autoimmune gastric disease. Gastric cancer incidence is increasing among young women in the United States, a population at higher risk of developing autoimmune disease, and H. pylori infection rates are falling. Therefore, a better understanding of these two chronic inflammatory diseases is needed to identify their roles in initiating gastric cancer.
Highlights
Gastric cancer is the fourth leading cause of cancer related mortality with the fifth highest incidence rate worldwide (Hyuna Sung et al, 2021)
Gastric cancer is a world leading cause of cancer related mortality (Hyuna Sung et al, 2021). It has been well-established that gastric infection with Helicobacter pylori (Hp) is the major risk factor for developing gastric cancer. This bacterium still infects a large portion of the world population, but infection rates in the United States are low and incidence of Hp-negative gastric cancer is increasing (Hooi et al, 2017; Nguyen et al, 2020)
Autoimmune gastritis (AIG) has been missed as a significant risk factor for gastric cancer, but the risk associated with AIG may be just as high as with Hp infection and the major pathology-inducing immune cells are consistent in both disease settings (Smythies et al, 2000; D’Elios et al, 1997; Vannella et al, 2013; D’Elios et al, 2001)
Summary
Gastric cancer is the fourth leading cause of cancer related mortality with the fifth highest incidence rate worldwide (Hyuna Sung et al, 2021). The discrepancy with lower incidence than mortality rate may be linked to the fact that most gastric cancers are diagnosed late in disease progression due to limited premalignant signs and symptoms. In the United States, late diagnosis contributes to a 5-year survival rate of only 31% for gastric cancer (Matsuzaka et al, 2016). A combination of environmental, host behavior, genetic, and microbial factors contribute to the risk of developing gastric adenocarcinoma (Rawla and Barsouk, 2019). More thorough investigation is needed into how chronic inflammation, triggered by infection or autoimmunity, causes epithelial cells to undergo premalignant changes that can lead to gastric cancer. The high mortality and poor survival associated with gastric adenocarcinoma make it imperative to better understand disease progression to improve preventative and therapeutic strategies
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