Gastritis, Gastric Polyps and Gastric Cancer

Gastric cancer is still an important disease causing many deaths worldwide, although there has been a marked reduction in prevalence during the last few decades. The decline in gastric cancer prevalence is due to a reduction in Helicobacter pylori infection which has occurred for at least 50 years. The most probable mechanism for the carcinogenic effect of H. pylori is hypergastrinemia since H. pylori infected individuals do not have increased risk of gastric cancer before the development of oxyntic atrophy. When atrophy has developed, the carcinogenic process continues independent of H. pylori. Autoimmune gastritis also induces oxyntic atrophy leading to marked hypergastrinemia and development of ECL cell neoplasia as well as adenocarcinoma. Similarly, long-term treatment with efficient inhibitors of acid secretion like the proton pump inhibitors (PPIs) predisposes to ECL cell neoplasia of a different degree of malignancy. Contrasting the colon where most cancers develop from polyps, most polyps in the stomach have a low malignant potential. Nevertheless, gastric polyps may also give rise to cancer and have some risk factors and mechanisms in common with gastric cancer. In this overview the most common gastric polyps, i.e., hyperplastic polyps, adenomatous polyps and fundic gland polyps will be discussed with respect to etiology and particularly use of PPIs and relation to gastric carcinogenesis.

Automated summary

Despite a decrease in prevalence over the past few decades, gastric cancer remains a significant global cause of death, with Helicobacter pylori infection reduction being a key factor. The carcinogenic effects of H. pylori are likely due to hypergastrinemia and autoimmune gastritis, while long-term use of proton pump inhibitors may also predispose individuals to ECL cell neoplasia. Additionally, gastric polyps, although generally low in malignant potential, can still pose a cancer risk and share some common risk factors and mechanisms with gastric cancer.