Abstract
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.
Highlights
The prevalence of gastric cancer has had a marked reduction in prevalence during the last decades
Every condition with long-standing hypergastrinemia in every species examined predisposes to gastric neoplasia of a different degree of malignancy. This has been demonstrated in rodents including rats, mice and Japanese cotton rats [57,58,59], as well as in man with sporadic gastrinoma [60] or gastrinomas as part of multiple endocrine neoplasia type I [61], autoimmune gastritis [21], H. pylori gastritis [25], proton pump inhibitor treatment [40,43], after surgery where antral mucosa is no longer exposed to acidic gastric juice [62] and in families with an inactivation mutation in the proton pump resulting in anacidity [44,45]
The positive trophic effect of mediators released from the ECL cell, like REG protein [20,21] could induce the growth resulting in polyp formation and thereby linking the occurrence of Hyperplastic polyps (HPs) to oxyntic atrophy and hypergastrinemia
Summary
The prevalence of gastric cancer has had a marked reduction in prevalence during the last decades. It is still an important disease, globally being the third cause of cancer death [1]. The mechanism by which H. pylori causes gastric cancer is still debated, which to some extent hampers a rational prophylaxis. In the present review we will repeat and strengthen the arguments in favour of the role of gastrin in H. pylori carcinogenesis [3] and focus on the different types of gastric polyps as precursors of gastric cancer. We will further discuss the role of proton pump inhibitors (PPIs), another cause of hypergastrinemia, in the pathogenesis of gastric polyps and gastric cancer
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