Several chronic conditions of the stomach are considered to increase the risk of later gastric cancer. They matter because each carries a different rate of progression, and the rate decides how closely a patient is watched rather than whether they are treated as if they already had cancer.
Chronic atrophic gastritis
Chronic atrophic gastritis is defined as loss of the specialised glandular structure of the stomach, and it can be seen in the process of development of gastric cancers. Its annual risk of progression to gastric cancer is between 0.1 and 1% per year.
There are two types. Environmental multifocal gastritis is associated with H. pylori infection and with the formation of metaplasia. Autoimmune metaplastic atrophic gastritis is associated with anti-parietal and anti-intrinsic factor antibodies. The autoimmune form carries a lesser risk of gastric cancer than the environmental form, because the inflammation is less than the atrophy caused by the H. pylori infection.
Intestinal metaplasia and dysplasia
Intestinal metaplasia (IM) is classified into three types. Type 1 IM has mature goblet cells secreting sialomucin and absorptive cells, and is not associated with gastric cancer. Type 2 IM has less differentiated goblet cells secreting sialomucin or sulfomucin and few or no absorptive cells, and is associated with a 20-fold higher risk of gastric cancer. Type 3 IM is less differentiated still, is also associated with a 20-fold higher risk, and 45% of patients with type 3 IM progress to intestinal-type gastric cancer at 5-year follow-up.
The more advanced the change, the higher the risk. Low-grade dysplasia regresses in more than 60% of cases, while 10 to 20% of them progress to high-grade dysplasia. High-grade dysplasia of the stomach carries a 2 to 6% annual risk of cancer progression, and is commonly present together with cancer in other parts of the stomach; overall, its presence is associated with a 40-fold increase in the risk of cancer progression.
Gastric polyps
Gastric polyps are prevalent in 0.8 to 2.4% of the population and are of three main kinds. Fundic gland polyps account for 50% of them. They are generally benign and more common in patients who use proton-pump inhibitors for a long time; 5-year use of PPIs increases the risk of fundic gland polyps 4-fold. Their rate of progression to cancer is very low, less than 1%, and is confined to polyps larger than 1 cm. The exception is familial adenomatous polyposis, in which fundic gland polyps occur in 51 to 88% of cases with a high rate of dysplasia.
Hyperplastic polyps account for 40%. They are mostly benign and are mostly seen in conditions with chronic inflammation of the stomach, such as H. pylori infection, chronic gastritis or peptic ulcer disease.
Adenomatous polyps account for 10% and behave differently: in contrast to fundic gland and hyperplastic polyps, they have a very high rate of cancer progression. Cancer progression is seen in 11% of patients with gastric adenoma at 4-year follow-up, so resection of a gastric adenoma is suggested.
Previous gastrectomy and Ménétrier disease
Patients who had a gastrectomy before the age of 50 have a higher risk of gastric cancer, with a 20-year delay between surgery and cancer. Several theories attempt to explain this. One is that lesser acid production at the site of surgery predisposes to over-growth of bacteria, more production of nitrate, and more reflux of bile and pancreatic enzymes into the stomach. Ménétrier disease is also counted among the premalignant conditions.
While gastric atrophy and intestinal-type metaplasia are associated with a higher risk of gastric adenocarcinoma, there is no conclusive data showing direct cancer formation from these cells. Gastric adenocarcinoma is believed to arise from stem cells or progenitor cells within the gastric mucosa rather than from terminally differentiated metaplastic cells.