I. What is chronic atrophic gastritis?
Chronic atrophic gastritis is a type of chronic gastritis with limited or widespread atrophy of the intrinsic glands of the gastric mucosa (reduced number and function), often accompanied by intestinal epithelial hyperplasia and inflammatory reactions, and is diagnosed mainly by gastroscopic findings and pathological findings on gastric mucosal biopsy.
What are the manifestations of atrophic gastritis?
Some patients have no symptoms, some patients have varying degrees of indigestion symptoms such as epigastric pain, gastric distension, lethargy, loss of appetite, some patients have regurgitation of acid and other symptoms, a few patients also have anemia, tongue inflammation, diarrhea, etc., individual patients with mucosal erosion, epigastric pain more obvious, and bleeding.
Gastroscopy in atrophic gastritis shows red and white mucosa, mainly white, thinning or flattening of the folds, exposure of mucosal vessels, granular or nodular mucosa, etc. There is also mucosal erosion and bleeding.
Histopathological examination of the gastric mucosa biopsy shows a decrease in intrinsic mucosal glands, replaced by pyloric glandular hyperplasia or intestinal glandular hyperplasia, with significant interstitial inflammatory infiltration.
What is the classification of atrophic gastritis?
In 1973, Strickland et al. classified atrophic gastritis into two separate types, type A and type B, based on the distribution of serum immunologic tests and lesions in the stomach.
Type A atrophic gastritis
Type A atrophic gastritis lesions are mainly found in the body of the stomach, mostly diffusely distributed, with normal sinus mucosa, positive serum mural cell antibodies, increased serum gastrin, reduced or absent gastric acid and endocannabinoid secretion, and prone to pernicious anemia, also known as autoimmune gastritis.
Type B atrophic gastritis
Type B atrophic gastritis is a simple atrophic gastritis with a multifocal distribution of lesions mostly in the gastric sinus, negative serum mural cell antibodies, normal serum gastrin, normal or mildly decreased gastric acid secretion, and no pernicious anemia, and is more likely to be complicated by gastric cancer.
In our country, type B atrophic gastritis is common, and type A atrophic gastritis is rare.
What are the reasons for the onset of atrophic gastritis?
The onset of chronic atrophic gastritis may be related to the following factors.
(1) the continuation of chronic superficial gastritis
(2) Genetic factors
The incidence of chronic atrophic gastritis is significantly higher among the first generation of relatives of patients with chronic atrophic gastritis, and the genetic factor of pernicious anemia is also evident.
(3) Heavy metal exposure
Lead, mercury, tellurium, copper and zinc all have a damaging effect on the gastric mucosa.
(4)Radiation
(5)Iron deficiency anemia
(6) Bile or duodenal fluid reflux
Due to pyloric sphincter dysfunction or after gastrojejunostomy, bile or duodenal fluid can reflux into the stomach and destroy the gastric mucosal barrier, prompting H?+ and pepsin to backscatter into the mucosa causing a series of pathological changes, leading to chronic superficial gastritis, which can develop into chronic atrophic gastritis.
(7) Immune factors
In patients with atrophic gastritis, especially gastric body gastritis, antibodies to mural cells or antibodies to internal factors are often found in the blood and gastric juice or in the plasma cells of the atrophic mucosa, so it is believed that autoimmune reactions are the relevant etiology of chronic atrophic gastritis.
(8) Helicobacter pylori (HP) infection
HP infection occurs in 60% to 90% of patients with chronic gastritis, and the degree of HP infection is positively correlated with the degree of gastric mucosal inflammation, HP infection is an important cause of chronic gastritis and atrophic gastritis.
Inappropriate diet, long-term addiction to tobacco and alcohol, drug abuse, and the removal of gastrin-secreting gastric sinus region after major gastrectomy, resulting in nutritional disorders of the gastric mucosa, etc., are likely to lead to damage to the gastric mucosa and atrophy, inflammatory changes.
How to diagnose atrophic gastritis?
Gastroscopy and pathologic biopsy are the main diagnostic tools. The gastroscopic diagnosis includes the location of the lesion, the degree of atrophy, intestinal metaplasia and atypical hyperplasia.
In addition, serum immunological examination in a few patients with pernicious anemia reveals positive mural cell antibodies (PCA) and internal factor antibodies (IFA).
Sixth, I heard that gastroscopy is unpleasant, is there any painless examination method?
The diagnosis still relies on gastroscopic pathological examination. Although conventional gastroscopy is painful and uncomfortable, sedation endoscopy (commonly known as painless endoscopy) is very easy to be accepted by patients.
In addition, it has been found that the detection of serum gastrin-17 (G17) and pepsinogen (PG) I and II can help in the diagnosis of atrophic gastritis. In patients with gastric body atrophy, serum G17 was elevated and PGⅠ/PGⅡ level was decreased, in patients with gastric sinus atrophy, G17 level was decreased and PGⅠ/PGⅡ ratio was normal, and in patients with total gastric atrophy, both were decreased. In patients with gastric cancer, the ratio is more significantly reduced.
What are the risks of atrophic gastritis?
The incidence of the disease increases with age, and the degree of lesions becomes more severe. Therefore, it is believed that chronic atrophic gastritis is a degenerative change of gastric mucosa in middle-aged and old people, which is a “semi-physiological” phenomenon. The incidence of chronic atrophic gastritis is higher in areas with a high incidence of gastric cancer than in areas with a low incidence.
Because of its slow onset, recurrence, and difficulty in healing, it is closely related to the occurrence of gastric cancer, so it is getting more and more attention.
How to follow up atrophic gastritis?
The annual cancer rate of atrophic gastritis is about 0.5% to 1%, so these patients need to be followed up regularly to improve the diagnosis rate of early gastric cancer. Those with atrophic gastritis without intestinal metaplasia and heterogeneous hyperplasia can be followed up by endoscopy and pathology every one to two years; those with moderate to severe atrophy or intestinal metaplasia can be followed up every one year; those with mild heterogeneous hyperplasia (biopsy is not taken from the cancer side) can be followed up every six months; those with severe heterogeneous hyperplasia need to be reviewed immediately by endoscopy and biopsy pathology, and if necessary, surgical treatment or endoscopic local treatment.