What Is Atrophic Gastritis?

Atrophic gastritis, also known as chronic atrophic gastritis, is characterized by atrophy of the gastric mucosa epithelium and glands, reduction of the number, thinning of the gastric mucosa, thickening of the basement of the mucosa, or pyloric and intestinal glandular metaplasia, or atypical hyperplasia. Characteristics of chronic digestive disorders. Often manifested as upper abdominal pain, fullness, belching, loss of appetite, or weight loss, anemia, etc., nonspecific. Is a multi-pathogenic disease and precancerous lesions.

Basic Information

nickname: Chronic atrophic gastritis
English name: atrophic gastritis
Visiting department: Gastroenterology

Common causes: Gastric mucosal inflammation, glandular atrophy, Helicobacter pylori infection, etc.
Common symptoms: Abdominal pain, fullness, belching, or weight loss, anemia, etc.
Contagious: no

Causes of atrophic gastritis

1. Helicobacter pylori (Hp) infection

Hp can be cultured in the gastric mucosa of 60% to 90% of patients with chronic gastritis. In 1986, the eighth session of the World Gastroenterological Society proposed that Hp infection is one of the important causes of chronic gastritis.

2. Eating habits

Smoking, drinking, food irritation, drugs that damage the gastric mucosa, etc.

3. Immune factors

In atrophic gastritis, especially gastrointestinal gastritis patients' blood, gastric juice or plasma cells in atrophic mucosa, parietal cell antibodies or internal factor antibodies can often be found, so the autoimmune response is considered to be the relevant cause of atrophic gastritis.

4. Bile or duodenal fluid reflux.

5. Physical factors

Clinical statistics show that the occurrence of this disease is significantly positively correlated with age. The older the person, the worse the "resistance" of gastric mucosal function, which is susceptible to damage from external adverse factors.

6. Genetic factors

Its role in the pathogenesis of type A atrophic gastritis has been confirmed. PCA and IFA positive rates are high in family members of malignant anemia, and atrophic gastritis is common.

7. Metal contact

Lead workers have a high incidence of gastric ulcers, and gastric mucosal biopsies have also found that the incidence of atrophic gastritis is also increased. In addition to lead, many heavy metals such as mercury, copper, and zinc have certain damage to the gastric mucosa.

8. Radiation

Radiation treatment of ulcers or other tumors can cause gastric mucosal damage or even atrophy.

9. Iron deficiency anemia

Many facts show that iron deficiency anemia is closely related to atrophic gastritis.

10. Other

The continuation of chronic superficial gastritis waited.

Clinical manifestations of atrophic gastritis

The clinical manifestations of atrophic gastritis not only lack specificity, but are not completely consistent with the extent of the disease. The following clinical manifestations often occur: gastric swollen stomach; gastric sacral pain; heartburn and indigestion; abnormal stool and weakness; anemia.

Diagnosis of atrophic gastritis

The symptoms and signs of atrophic gastritis are not specific and cannot be used as a basis for diagnosis. The diagnosis is mainly based on gastroscopy and gastric mucosal biopsy.

(1) Mostly older than middle-aged, with a long course of disease, often with a history of chronic superficial gastritis.

(2) Symptoms and signs Long-term indigestion, discomfort in the stomach bulge, poor appetite, fatigue, weight loss, anemia, etc.

(3) Gastroscopy The color of gastric mucosa becomes lighter; Submucosal blood vessels are visible; mucosal folds are small or even disappear; when atrophic gastritis is accompanied by excessive hyperplasia of glandular neck or intestinal metaplasia, the surface of the mucosa is rough and uneven It is granular or nodular, sometimes the formation of pseudopolyps, and the exposed features of submucosal blood vessels are often masked; atrophic mucosa increases fragility, easily bleeds, and may have erosions; Atrophic gastritis can be accompanied by chronic Symptoms of superficial gastritis, such as congestive erythema, adhesion of mucus, and enhanced reflection.

(4) Pathological examination Glandular atrophy inherent in gastric mucosa; Metaplasia; Hyperplasia; Canceration.

(5) Laboratory examination Gastric fluid analysis: Patients with type A CAG are mostly acid-free or low-acid, and patients with type B CAG can be normal or low-acid. Pepsinogen measurement Pepsinogen is secreted by main cells. In atrophic gastritis, blood and urine The content of pepsinogen is reduced. Determination of serum gastrin . G cells in gastric mucosa secrete gastrin. In patients with type A CAG, serum gastrin often increases significantly. In patients with type B CAG, the gastric antral mucosa atrophy directly affects the function of G cells to secrete gastrin, and serum gastrin is lower than normal. Immunological examination of parietal cell antibody (PCA), Determination of internal factor antibody (IFA) and gastrin secreting cell antibody (GCA) can be used as auxiliary diagnosis of atrophic gastritis and its typing.

Atrophic gastritis complications

1. Gastric bleeding.

2. Anemia.

3. Gastric ulcer.

4. Precancerous lesions.

Atrophic gastritis treatment

General treatment

Quit smoking and avoid alcohol, avoid using drugs that damage the gastric mucosa such as aspirin, indomethacin, erythromycin, etc., diet should be regular, avoid overheating, salty and spicy food, and actively treat chronic mouth, nose, and throat infections.

2. Weak acid treatment

The pentapeptide gastrin test confirmed that patients with low or no acid can take rice vinegar in an amount of 1 to 2 spoons each time, 3 times a day; or 0.5 to 1.0 ml of 10% dilute hydrochloric acid, taken before or during meals, while taking the stomach Protease mixture, 10ml each time, 3 times a day; multi-enzyme tablets or pancreatin tablets can also be used to improve the symptoms of indigestion.

3. Anti-Helicobacter pylori treatment

In atrophic gastritis, the acidity of the stomach is reduced or lacking, and bacteria in the stomach are born, especially the positive rate of H. pylori. Anti-Hp treatment should be performed.

4. Inhibit bile reflux and improve gastric motility

Cholestyramine complexes the bile salts flowing back into the stomach, preventing bile acids from damaging the gastric mucosal barrier. Sucralfate can be combined with bile acids and lysolecithin, and can also be used to treat bile reflux. Ursodeoxycholic acid can also be given. Metoclopramide, morphine, cisapride and other drugs can enhance gastric motility, promote gastric emptying, assist the movement of the stomach and duodenum, prevent bile reflux, regulate and restore gastrointestinal movement.

5. Increase mucosal nutrition

Albizia oleifera can increase gastric mucosal renewal, improve cell regeneration ability, enhance gastric mucosal resistance to gastric acid, and protect gastric mucosa. Activin can also be selected; or sucralfate, urea sac, progesterone, prostaglandin E, etc. can be selected.

6. Pentagastrin

In addition to promoting the secretion of hydrochloric acid by parietal cells and increasing the secretion of pepsinogen, pentagastrin also has a significant proliferation effect on the gastric mucosa and other upper gastrointestinal mucosa. It can be used to treat atrophy of low acid and acid or atrophy In patients with gastritis, intramuscular injection is given half an hour before breakfast, once a day, and once every other day in the third week, twice a week in the fourth week, and once a week in the future, and three months as a course of treatment. The application of mild to moderate atrophic gastritis has good therapeutic effect and effectively promotes gland repair.