Understanding precancerous lesions and precancerous diseases of the stomach

  The incidence of gastric cancer remains high in China, and the incidence of gastric cancer ranked third in the incidence of cancer in both men and women in 2015 China cancer incidence statistics. Recognizing gastric precancerous lesions and precancerous diseases has important clinical significance for the prevention and treatment of gastric cancer.  What is gastric precancerous lesions and precancerous diseases What is gastric mucosal heterotypic hyperplasia? There are three degrees of gastric mucosal epithelial heterotypic hyperplasia: (1) Mild heterotypic hyperplasia: Mild heterotypic hyperplasia is an excessive proliferative response of mucosa to injury, often appearing at the edge of ulcers, or various types of gastritis, hyperplastic polyps, and loss of protein gastric disease, etc., and is mostly of regenerative type in terms of typing. Most of these lesions are reversible and do not require regular follow-up.  (2) Moderate heterogeneous hyperplasia: The histological and cytological heterogeneity of moderate heterogeneous hyperplasia is more obvious and can be seen in both atrophic gastritis, adenomatous polyps, etc., as well as in paraneoplastic mucosa. Although some cases are reversible or remain intact for a long time, some may evolve and escalate, so regular gastroscopic follow-up is required.  (3) Severe heterogeneous hyperplasia: The histological and cytological heterogeneity of severe heterogeneous hyperplasia is obvious, and sometimes it is not easily distinguished from highly differentiated carcinoma in the mucosa. Such lesions are mainly seen in adenomatous polyps with peri-mucosa carcinoma and occasionally right in the tumor foci themselves, with obvious malignant tendency and only little chance to reply to downgrading, so recent gastroscopic biopsy review and close follow-up observation should be done, and if cancer is suspected, appropriate treatment such as endoscopic mucosal resection (EMR), endoscopic mucosal dissection (ESD) or surgical treatment should be done.  Mild to moderate heterogeneous hyperplasia is a low-grade neoplasm, while severe heterogeneous hyperplasia or carcinoma in situ is a high-grade neoplasm.  What is the cancer rate of gastric mucosal epithelial heterogeneous hyperplasia? The cancer rate of gastric mucosal epithelial heterogeneous hyperplasia is a common concern, i.e., how many of these cases can become cancerous? There are two conditions that should be considered, one is that the longer the observation time of a heterogeneous hyperplasia lesion, the more cases of cancer may occur in a certain number of cases, so the percentage of cancer cannot be generally stated. In a group of cases of heterogeneous hyperplasia observed for 10 years versus another group of cases observed for 5 years, there may be more cancerous cases in the former group and relatively fewer cases in the latter group. So far, some reports (mostly adenomatous heterogeneous hyperplasia) are around 5%, some 10% or more, and some are only 1% to 3%. Another problem is related to the degree of heterogeneous hyperplasia. Obviously, the chance of carcinoma is more in severe cases than in mild or moderate cases, and the frequency of carcinoma varies.  What is intestinal metaplasia? Intestinal metaplasia, or simply intestinal metaplasia, refers to the presence of intestinal glands or intestinal-type epithelium in the gastric mucosa. It is a relatively common lesion in gastritis and is often seen in atrophic gastritis. The appearance of intestinal metaplasia is related to the damage to the gastric mucosa and the inability to completely regenerate and repair it. Helicobacter pylori (Hp) infection is an important etiology of chronic gastritis, especially seen in active chronic gastritis. This bacterium has a destructive effect on the epithelium of the gastric mucosa, and when chronic gastritis continues to develop and prolong, Hp decreases or disappears, while the gastric lamina propria gradually decreases and is replaced by intestinal metaplasia, even eventually becoming the so-called “metaplastic gastritis”.  According to the situation of mucus secretion by the intestinal metaplasia epithelium and the nature of the mucus secreted by it, intestinal metaplasia is divided into several types: Ming (1967) divided intestinal metaplasia into complete and incomplete types. The former is similar to small intestinal mucosal absorptive cells, has brush border, does not secrete mucus, has Pan cells, cup cells and absorptive cells, contains sucrase, alglucosidase and leucine-based peptidase and alkaline phosphatase; while incomplete intestinal epithelial metaplasia has inconspicuous brush border, underdeveloped microvilli, mucus-secreting granules in the cytoplasm, contains sucrase, but low aminopeptidase and alkaline phosphatase activity, and no alglucosidase. Teglbjaerg (1978) referred to enterocytes secreting acetyl sialic acid and sulfate mucins and those not secreting such mucins as large intestine type enterocytes and small intestine type enterocytes, respectively; Jass (1988), on the other hand, classified enterocytes into type I, i.e., complete type enterocytes similar to small intestine; type II enterocytes, i.e., incomplete type enterocytes with mucus-secreting cells between cup cells, and The cup-shaped cells containing salivary acid mucus and the columnar cells containing neutral mucus are called type IIA enterocytosis, and those containing sulfate mucus or saliva at the same time are called type IIB enterocytosis.  At present, many pathological researchers regard incomplete colorectal type intestinal chemosis as precancerous lesions of gastric cancer.    In conclusion, although pre-cancerous diseases and pre-cancerous lesions have the word “cancer” in them, do not be frightened by them. It is not that scary and there is no need to panic. However, we should pay attention to it, have regular gastroscopy, understand the development of the disease, and control it timely in order to achieve the purpose of cancer prevention and control.