Changes in the environment of the residual stomach can promote gastric cancer

The development of cancer in the residual stomach after gastric surgery is a complex biological process, which is closely related to the changes in the gastric environment after gastrectomy and Helicobacter pylori infection.

The triggering factors caused by changes in the residual stomach environment after gastric surgery include the following two aspects:

1. Duodenal-gastric reflux

Due to anatomical and physiological changes, the remnant stomach loses the anti-reflux function of the pylorus and has varying degrees of duodenal-gastric reflux. The long-term reflux and immersion of alkaline intestinal fluid and bile in the reflux fluid causes a series of pathological changes in the gastric mucosa near the anastomosis, such as remnant gastritis, intestinal gland metaplasia, glandular cystic change, atypical hyperplasia, adenomatous change, and even cancer.

2. Bacterial overgrowth in the stomach

After subtotal gastrectomy, most of the acid-secreting glands are removed. In addition, there is varying degrees of duodenal reflux after gastrointestinal anastomosis, and the gastric pH is high. Gastric pH is the main factor determining the gastric flora. The total bacterial count in gastric juice with a pH higher than 4 is higher than that in normal people. The fecal flora in the residual stomach can catalyze the nitroso reaction and promote the formation of nitrite and N-nitroso compounds. Nitrosamines are currently recognized as one of the carcinogens.

Secondly, some bacteria in the fecal flora can also decompose the bound primary bile acid that flows back into the stomach to form free secondary bile acids, such as deoxycholic acid and lithocholic acid. The latter can not only damage the gastric mucosal barrier, but also induce mucosal cancer.