It is believed that the occurrence of CAG is related to H. pylori infection, bile reflux, immunity, age, high salt, overheating, low vitamin diet and genetic factors, and is the result of a combination of factors.
1.Infection factors
(1) H.pylori infection
H.pylori is the main cause of CAG, the pathogenic mechanism of H.pylori is related to its own adhesion, the toxic effect of ammonia produced by the decomposition of urea, a variety of enzymes of H.pylori, the role of free radical damage, infection caused by immune deficiency, the age of the patient at the time of infection and infection caused by vitamin C deficiency and other factors.
(2) Other bacterial and viral infections
Sanduleanu et al. reported that patients on long-term acid suppression therapy can cause bacterial infections other than H. pylori, which is an independent risk factor for gastric body atrophic gastritis, and dual infections can significantly increase the risk of gastric body atrophic gastritis.
2. Bile reflux
Bile reflux causes CAG mainly by damaging the gastric mucosal barrier. H+ in the gastric lumen diffuses back into the gastric mucosa through the damaged barrier, stimulating increased secretion of histamine, which in turn increases gastric acid secretion and acts on vascular H1 and H2 receptors causing vasodilation, increased permeability, and reduced effective blood flow to the gastric mucosa, leading to the occurrence of CAG. Bile reflux is now considered to be an independent causative factor. H.pylori is not the cause of reflux, regardless of the presence or absence of H.pylori infection, the severity of bile reflux is significantly and positively correlated with the severity of mucosal inflammation and atrophy, and also with the severity of intestinal epithelial metaplasia.
3.Alteration of gastric mucosal microcirculation
It has been reported in the literature that gastric mucosal blood flow (GMBF) is significantly lower in patients with CAG than in patients with non-atrophic gastritis. The gastric mucosal blood circulation plays a vital role in maintaining the physiological function and defense mechanism of gastric mucosa. The experimental results showed that: the metabolism of gastric mucosa is more sensitive to ischemia, and the renewal of gastric mucosa is faster, so it cannot carry out effective anaerobic metabolism to replenish the energy deficiency under ischemic condition.
4.Change of vasoactive factors
At present, there are more studies such as PGE2, which is used clinically as a vasodilator and gastric mucosal protector.
5.Lack of mucosal nutrient factors
At present, there are more researched gastrin, epidermal growth factor (EGF), growth hormone (GH), vitamins, etc.
6.Hereditary factors of the host
In some countries and regions, especially in Africa, the incidence of H. pylori infection is high, but the incidence of CAG or gastric cancer is very low, this phenomenon is called “the mystery of Africa”. These phenomena suggest that host factors may play an important role. In the host genetic genes in recent years more research such as: interleukin (IL)-1β gene and tumor necrosis factor (TNF)-α gene.
7.Vitamin deficiency
The high incidence of CAG is above 50 years old, and a large amount of clinical data has clearly indicated the existence of vitamin B12 and folic acid deficiency and increased cysteine in the elderly population. Long-term H. pylori infection will inhibit the secretion of vitamin C from the gastric mucosa, so that the ability of vitamin C to scavenge oxygen free radicals and nitrite is reduced, which also aggravates the degree of CAG lesions.
8, immune factors
The gastric body atrophic gastritis and autoimmune related, in patients often detected anti-mural cell antibodies and internal factor antibodies, multifocal atrophic gastritis is also involved in immune factors, it is generally believed that the gastric mucosal damage caused by immune factors is secondary to the role of other pathogenic factors, so that the release of mural cell antigens, causing a delayed cellular immune response, followed by humoral immunity, resulting in the destruction of the mural cells, the mucosa atrophy.
9.Lifestyle
At present, scholars at home and abroad recognized the occurrence of CAG and lifestyle, dietary habits have a great relationship. Our current research is more focused on the impact of high-salt, overheated food on the gastric mucosa. Long-term overheated, salty diet can cause gastric mucosal epithelial cell regulation and proliferation and regulatory genes out of control, resulting in the formation of CAG.
10.Other
Age factor: the incidence of chronic gastritis gradually increases with age. Aging can cause distortion of the small vessels of the gastric mucosa, glassy changes in the walls of the small arteries and luminal narrowing, such local vascular factors of the stomach and degenerative changes in the semi-physiology of the gastric mucosa can make the mucosa malnutrition, decreased secretion and low function of the gastric mucosal barrier, causing atrophy, intestinalization and heterogeneous hyperplasia, is an important factor in the occurrence of CAG in the elderly.
Neuropsychiatric factors:The cerebral cortex ensures the regulation of systemic tissue and organ functions through the interaction and balance of excitation and inhibition. Excessive mental stimulation, depression, exertion and the repeated action of other mental factors cause excessive tension in the cortical nerve cells and imbalance between excitation and inhibition processes. At this time, the subcortical center loses inhibition, so that the autonomic nerves are in a long-term state of excitation and dysfunction, resulting in various pathological changes in the stomach, such as spasmodic contraction of blood vessels in the stomach wall, forming an ischemic zone, malnutrition of the gastric mucosa, abnormal secretion of the gastric glands, and even the gradual formation of glandular atrophy.
In addition, heart failure, liver cirrhosis combined with portal hypertension, malnutrition can cause chronic gastritis. Patients with diabetes, thyroid disease, chronic hypoadrenocorticism and dry syndrome with CAG are also more common.