| disease | Chronic Gastritis |
| alias | Chronic Gestritis |
Chronic gastritis refers to the chronic inflammation or atrophic changes of the gastric mucosa caused by various disease factors. Its essence lies in the repeated damage to the gastric mucosal epithelium, which, due to the mucosa's specific regenerative capacity, leads to mucosal remodeling and ultimately results in irreversible atrophy or even disappearance of the intrinsic gastric glands. This condition is very common, accounting for approximately 80-90% of patients undergoing gastroscopy, with a higher prevalence in males than females, and the incidence gradually increases with age.
bubble_chart Etiology
The etiology of the disease has not been fully elucidated, and it is generally believed to be related to harmful factors in the surrounding environment and susceptible constitution. Long-term and repeated exposure of susceptible individuals to physical, chemical, and biological harmful factors can lead to the disease. Persistent or recurrent disease causes can result in chronic sexually transmitted disease changes.
(1) Physical factors: Long-term consumption of strong tea, hard liquor, coffee beans, excessively hot, cold, or rough food can cause injury to the gastric mucosa.
(2) Chemical factors: Long-term and excessive use of non-steroidal anti-inflammatory drugs such as aspirin and indomethacin can inhibit the synthesis of prostaglandins in the gastric mucosa, damaging the mucosal barrier. Smoking, with nicotine in tobacco, not only affects the blood circulation of the gastric mucosa but also leads to dysfunction of the pyloric sphincter, causing gall fel reflux. Various causes of gall fel reflux can damage the mucosal barrier.
(3) Biological factors: Bacterial infections, especially Hp infection, are closely related to chronic gastritis. The mechanisms include: ① Hp has a spiral shape and flagellar structure, allowing it to move freely in the mucus layer and closely adhere to mucosal cells, directly invading the gastric mucosa; ② It produces various enzymes and metabolites such as urease and its metabolite ammonia, superoxide dismutase, proteolytic enzymes, phospholipase A, etc., which can damage the gastric mucosa; ③ Cytotoxin can cause vacuolar degeneration of cells; ④ Hp antibodies can lead to autoimmune injury.(4) Immune factors: Serum from patients with chronic atrophic gastritis can test positive for parietal cell antibodies (PCA), and those with nausea anemia may also test positive for intrinsic factor antibodies (IFA). Immune complexes formed by parietal cell antigens and PCA, with the participation of complement, destroy parietal cells. IFA binding to intrinsic factor blocks the binding of vitamin B12 to intrinsic factor, leading to pernicious anemia.
(5) Others: Conditions such as heart failure, liver cirrhosis with portal hypertension, and malnutrition can also cause chronic gastritis. Patients with diabetes, thyroid disease, chronic adrenal cortical insufficiency, and Sjögren's syndrome often have concurrent atrophic gastritis. Other gastric conditions such as gastric fluid, gastric polyps, and gastric ulcers are also frequently associated with chronic atrophic gastritis. Genetic factors have also garnered attention.
bubble_chart Pathological Changes
(1) Chronic superficial gastritis is characterized by inflammatory cell infiltration in the lamina propria between gastric pits. The inflammatory cells are mainly plasma cells and lymphocytes, occasionally eosinophils. Edema, congestion, and even focal hemorrhage are commonly seen in the lamina propria. The gastric glands remain normal, without destruction or reduction, though erosion (necrosis of the lamina propria without involving the muscularis mucosae) may sometimes be observed. The superficial epithelial cells appear flattened and are often irregularly arranged. Based on the severity of inflammation, superficial gastritis can be classified into grades I, II, and III. Grade I is defined when inflammatory cell infiltration is limited to the upper 1/3 of the gastric mucosa; grade II when infiltration exceeds 1/3 but does not surpass 2/3 of the mucosal layer; and grade III when inflammatory cells infiltrate the entire mucosal thickness.
In chronic atrophic gastritis, pyloric gland metaplasia (pseudopyloric glands) and intestinal metaplasia are frequently observed. The glands in the gastric body and fundus normally contain parietal cells and chief cells. When these cells disappear and the glands transform into mucus-secreting glands resembling pyloric glands, it is termed pyloric gland metaplasia. Intestinal metaplasia is also common in chronic gastritis. In chronic superficial gastritis, intestinal metaplasia may appear in the superficial mucosa, whereas in atrophic gastritis, all gastric mucosal glands may be replaced by intestinal metaplasia. Intestinal metaplasia often begins at the neck of gastric pits, extending upward to the superficial epithelium and downward to the deeper parts of the glands. Initially focal, it may progressively coalesce into larger areas.
In atrophic lesions, if accompanied by hyperplastic changes in the glandular neck or metaplastic intestinal epithelium, granular lesions may form on the gastric mucosal surface, termed atrophic-hyperplastic gastritis.
bubble_chart Clinical Manifestations
Chronic gastritis lacks specific symptoms, and the severity of symptoms does not necessarily correspond to the extent of gastric mucosal lesions. Most patients often have no symptoms or experience varying degrees of dyspeptic symptoms such as dull epigastric pain, loss of appetite, postprandial fullness, and acid reflux. Patients with atrophic gastritis may present with anemia, weight loss, glossitis, or diarrhea. In some cases, those with mucosal erosions may have more pronounced epigastric pain and may also experience bleeding.
Gastroscopy Examination
(1) Superficial Gastritis The mucous membrane is congested, edematous, and exhibits a mottled red-and-white appearance, predominantly red, or resembling a measles-like pattern. There may be grayish-white or yellowish-white secretions attached, with localized erosions and bleeding spots.
(2) Atrophic Gastritis The mucous membrane loses its normal orange-red color and may appear light red, gray, grayish-yellow, or grayish-green. Grade III atrophy presents as grayish-white with uneven coloration. The folds become thin and flattened, and submucosal blood vessels are visible, appearing tree-like or网状. Sometimes,颗粒 formed by epithelial cell proliferation can be observed on the atrophic mucous membrane. The atrophic mucous membrane becomes more fragile and prone to bleeding, with possible erosive lesions.
(3) Chronic Erosive Gastritis Also known as verrucous gastritis or smallpox-like gastritis, it often coexists with peptic ulcers, superficial or atrophic gastritis, or may occur independently. It is primarily characterized by multiple verrucous, enlarged folds, or papule-like protrusions on the gastric mucous membrane, measuring 5–10 mm in diameter. The顶端 may show mucosal defects or umbilical-like depressions with central erosions. The surrounding area of the protrusions usually lacks a red halo but often exhibits红斑 of similar size, mostly found in the gastric antrum. It can be classified into persistent and disappearing types. In the Sydney classification of chronic gastritis, it is categorized as a special type of gastritis, endoscopically divided into raised erosive gastritis and flat erosive gastritis.
Laboratory Tests
(1) Gastric Acid Measurement In superficial gastritis, gastric acid levels are normal or slightly reduced, while in atrophic gastritis, they are significantly decreased or even absent.
(2) Serum Gastrin Level Measurement Type B gastritis usually shows normal levels, whereas Type A gastritis often exhibits elevated levels, particularly more pronounced in cases of pernicious anemia.
(3) Helicobacter Pylori Testing Detection can be performed through culture, smear, or urease testing.
(4) Other Tests In atrophic gastritis, parietal cell antibodies, intrinsic factor antibodies, or gastrin antibodies may appear in the serum. X-ray barium meal examination is not very helpful in diagnosing chronic gastritis but aids in differential diagnosis.
The diagnosis of this disease mainly relies on gastroscopy and direct visual biopsy of the gastric mucosa.
bubble_chart Treatment Measures
There is no specific treatment for chronic gastritis, and asymptomatic individuals do not require therapy.
1. Choose easily digestible, non-irritating foods, avoid smoking, alcohol, and strong tea, and chew food slowly and thoroughly.
2. For those positive for Helicobacter pylori, a triple therapy can be used: De-Nol 0.24 Bid; amoxicillin 0.5, gid or 1g Bid; and metronidazole 0.2 gid. For those with a positive penicillin test, other antibiotics such as tetracycline, erythromycin, or gentamicin may be selected.
3. For patients with dyspepsia, gastric mucosal protective agents such as sucralfate can be administered. For abdominal distension, fullness, nausea, or vomiting, gastrointestinal motility drugs such as metoclopramide, domperidone, or cisapride can be given. For symptoms of hyperacidity, medications like Roter or Tagamet can be used, but acid suppressants should be avoided in cases of atrophic gastritis. For bile reflux, sucralfate and gastrointestinal motility drugs can be administered to neutralize bile salts and prevent reflux.
4. Atrophic gastritis can be treated with Yangwei Infusion Granule, vitamin enzyme, or Weifuchun. For those with pernicious anemia, vitamin B12 and folic acid should be supplemented.
5. Surgical intervention is suitable for atrophic gastritis with grade III dysplasia or grade III intestinal metaplasia, especially in cases of large intestine-type intestinal metaplasia.
Chronic superficial gastritis has a good prognosis, with a few cases potentially progressing to atrophic gastritis. Atrophic gastritis accompanied by grade III intestinal metaplasia or (and) dysplasia may have the potential for cancerous transformation, with the cancer rate of chronic atrophic gastritis ranging from 2.55% to 7.46%.
