Xiang Sha Yang Wei Pills for Gastritis? The etiology and pathogenesis of chronic gastritis remain incompletely understood. It may be associated with the following factors:
I. Residual Effects of Acute Gastritis: Persistent or recurrent lesions of the gastric mucosa following acute gastritis can lead to chronic gastritis.
II. Irritant Foods and Beverages: Foods and medications strongly irritating to the gastric mucosa, such as strong tea, hard liquor,or salicylate-based medications. Inadequate chewing of coarse foods causing repeated mucosal damage, or excessive smoking where nicotine directly affects the gastric mucosa, may also contribute.
III. Reflux of duodenal contents and long-term medication use. Studies indicate that chronic gastritis patients often experience bile reflux due to pyloric sphincter dysfunction.This often leads to bile reflux, which may be a significant pathogenic factor. Phospholipids in pancreatic juice, combined with bile and pancreatic digestive enzymes, dissolve mucus and disrupt the gastric mucosal barrier. This facilitates the backflow of H+ and pepsin into the mucosa, causing further damage. Chronic gastritis resulting from this mechanism primarily affects the gastric antrum. Gastritis due to bile reflux is very common in patients who have undergone gastroduodenal anastomosis.Nearly all peptic ulcer patients exhibit concomitant chronic gastric antral inflammation, potentially linked to pyloric sphincter dysfunction. Nicotine in tobacco relaxes the pyloric sphincter, thus long-term smokers may exacerbate bile reflux and induce antral gastritis. IV. Immunological Factors Altered immune function has gained widespread recognition in chronic gastritis pathogenesis. In atrophic gastritis,Particularly in patients with corpus gastritis, antibodies against parietal cells can be detected in blood, gastric juice, or within atrophic mucosa. In patients with gastric atrophy accompanied by pernicious anemia, antibodies against intrinsic factor are found in the blood. This suggests that autoimmune reactions may be a contributing cause in certain chronic gastritis. However, whether immune factors participate in the pathogenesis of gastritis remains inconclusive. Additionally, the gastric mucosa in atrophic gastritis exhibits diffuse lymphocytic infiltration.Abnormalities in in vitro lymphoblast transformation assays and leukocyte migration inhibition tests suggest that cellular immune responses may play a significant role in the development of atrophic gastritis. Certain autoimmune diseases, such as chronic thyroiditis, hypothyroidism or hyperthyroidism, insulin-dependent diabetes mellitus, and chronic adrenal insufficiency, may be associated with chronic gastritis. This indicates that the disease may be related to immune responses.Infection Factors In 1983, Warren and Marshall discovered significant quantities of Helicobacter pylori (H. pylori) in the mucus layer near the epithelial cell surface of the gastric antrum in patients with chronic gastritis. The positive rate reached 50-80%. Reports indicate this bacterium is not present in normal gastric mucosa. Wherever the bacterium colonizes, inflammatory cell infiltration of the gastric mucosa is observed, with the degree of inflammation positively correlated with bacterial quantity.Electron microscopy also revealed a reduction or blunting of surface microvilli on epithelial cells connected to the bacteria. Antibodies against Helicobacter pylori can be detected in patients' blood and gastric mucosa. After antibiotic treatment, symptoms and histological changes may improve or even disappear. Therefore, it is considered that this bacterium may be involved in the pathogenesis of chronic gastritis, though this remains inconclusive at present.