A human mode of intestinal type gastric carcinoma

Gastric cancer is a malignant tumor originating from the gastric mucosa epithelium. Intestinal type gastric cancer is frequently taken on elderly men, and there are many high incidence areas around the world. Intestinal type gastric cancer often is accompanied by gastric mucosal atrophy, intestinal metaplasia. The clinical manifestation involves hypergastrinemia, low stomach acid, PG I/II progressive decreasing, anemia, and protein energy malnutrition. The neck cells of gastric glands act as tissue stem cells to regenerate the gastric glands. In addition to secreting gastric acid and intrinsic factor, the parietal cells also have the function of inducing differentiation of themselves and gastric epithelial cells. When the function of parietal cells is normal, the neck cells differentiate into mature cells, and the glands regenerate intact. When the function of parietal cells is defective, the neck cells maybe differentiate into mature intestinal cells, and the gastric glands will regenerate in form of the intestinal metaplasia. When the function of parietal cells is lost, the neck cells can not differentiate into mature cells successfully, and the accumulation of immature cells in gastric mucosal tissue forms atypical hyperplasia of different degrees and cancers of various differentiation grades. Any factors that can reduce the function of parietal cell could result in intestinal type gastric carcinogenesis. Adrenal cortical hypofunction can make the parietal cell hypofunction, hypohematopoiesis, protein synthesis rates reducing and protein degradation rates increasing. The patients develop gastric cancer, and come with lack of gastric acid and intrinsic factor, anemia, protein energy malnutrition. Autoimmune gastritis can produce parietal cell antibodies to damage parietal cells. Patients with autoimmune gastritis gastric exhibit hypergastrinemia, lack of gastric acid and internal factor, higher incidence of gastric cancer. H. pylori can damage gastric parietal cells directly and indirectly. When declining in quantity of parietal cells, the patients exhibit hypergastrinemia, low gastric acid, mucosa atrophy, intestinal metaplasia and gastric cancer. Medicine that inhibits the function of parietal cells also could increase the risk of gastric cancer development. The distribution of mucosa atrophy, intestinal metaplasia and intestinal type gastric cancer is opposite with the distribution of parietal cells in stomach. With age the quantity of parietal cells decreases, the atrophy area of gastric mucosa extends upward from antrum to body and downward from cardia to body along lesser curvature, and the location of distal gastric cancer moves upward and the gastric cardiac cancer increase.