Pseudopyloric metaplasia

Introduction Metaplasia is divided into intestinal metaplasia (intestinal) and pseudo-pyloric gland metaplasia, the former is common in atrophic gastritis, even in superficial gastritis or even normal mucosa, while the latter is only seen in atrophic gastritis, which refers to gastric mucosa Replaced by the gastric antrum mucosa, often along the small curvature of the stomach, said the stomach sinus migration.

Cause

The etiology of chronic atrophic gastritis has not been known so far and may be related to the following factors:

(1) Continuation of chronic superficial gastritis: Chronic atrophic gastritis can be developed from chronic superficial gastritis. Six hospitals including the General Hospital of the People's Liberation Army reported 164 cases of superficial gastritis after 5 to 8 years of follow-up, of which 34 cases were converted into chronic atrophic gastritis (20.7%). The cause of chronic superficial gastritis can become a causative and aggravating factor of chronic atrophic gastritis.

(2) Genetic factors: According to the Varis survey, the incidence of chronic atrophic gastritis was significantly increased among the first generation of relatives of patients with chronic atrophic gastritis, and the genetic factors of pernicious anemia were also obvious. The incidence of relative relationships was 20 times greater than that of the control group, indicating that chronic atrophic gastritis may be related to genetic factors.

(3) Metal contact: The incidence of gastric ulcer in lead workers is high, and the incidence of atrophic gastritis is also increased in gastric mucosa biopsy. Polmer calls it excretory gastritis. In addition to lead, many heavy metals such as mercury, strontium, copper and zinc have certain damage to the gastric mucosa.

(4) Radiation: Radiation treatment of ulcer disease or other tumors can cause damage or even atrophy of the gastric mucosa.

(5) Iron deficiency anemia: Many facts indicate that iron deficiency anemia is closely related to atrophic gastritis. Badanoch reported 50 cases of iron deficiency anemia, normal gastric mucosa, superficial gastritis and atrophic gastritis accounted for 14% and 46% respectively. And 40%. However, the mechanism of anemia caused by gastritis is still unclear. Some scholars believe that gastritis is the primary disease, because gastritis is low in stomach acid, iron can not be absorbed, or due to gastric bleeding, resulting in anemia; another opinion is that there is anemia first, because the iron deficiency in the body makes the gastric mucosal renewal rate affected and easily occurs. Inflammation.

(6) Biological factors: The effects of chronic infectious diseases such as hepatitis and tuberculosis on the stomach have also attracted people's attention. Chronic liver disease patients often have symptoms and signs of chronic gastritis. Gastric mucosal staining also confirmed the presence of hepatitis B virus antigen-antibody complex in the gastric mucosa of patients with hepatitis B. Ruijin Hospital reported 91 patients with atrophic gastritis, and 24 patients (26.4%) had chronic hepatitis. Therefore, the impact of chronic infectious diseases, especially chronic liver diseases, on the stomach is worth noting.

(7) Constitutional factors: Clinical statistics show that the incidence of this disease is significantly positively correlated with age. The older the age, the worse the "resistance" of the gastric mucosal function is, and it is easily damaged by external adverse factors.

(8) bile or duodenal reflux: due to pyloric sphincter dysfunction or gastrojejunostomy, bile or duodenal juice can reflux to the stomach, and destroy the gastric mucosal barrier, promote H? + and pepsin Dissemination into the mucosa causes a series of pathological changes leading to chronic superficial gastritis and can develop into chronic atrophic gastritis.

(9) Immune factors: In atrophic gastritis, especially in the blood, gastric juice or plasma cells of atrophic mucosa in patients with atrophic gastritis, wall cell antibodies or internal factor antibodies are often found, so the autoimmune response is considered to be chronic atrophy. The cause of gastritis. In recent years, a small number of patients with gastric antrum gastritis have been found to have gastrin-secreting cell antibodies, which are special autoimmune antibodies of cells, belonging to the Ig G line. Some patients with atrophic gastritis have abnormal lymphocyte transformation test and leukocyte migration inhibition test, suggesting that cellular immune response is also important in the occurrence of atrophic gastritis.

(10) Helicobacter pylori (HP) infection: In 1983, Australian scholars Marshall and Warren first isolated HP from the gastric mucosal layer and epithelial cells of patients with chronic gastritis. Since then, many scholars have carried out a large number of experimental studies on patients with chronic gastritis, and HP is cultured in the gastric mucosa of 60% to 90% of patients with chronic gastritis, and then it is found that the degree of HP infection is positively correlated with the degree of gastric mucosal inflammation. At the eighth session of the World Gastroenterology Society in 1986, HP infection was one of the important causes of chronic gastritis.

In addition, such as improper diet, long-term tobacco and alcohol, drug abuse, chronic inflammation of the upper respiratory tract, central nervous system dysfunction, damage to the gastric mucosa, and gastric resection, the gastric antrum excretion of gastrin, resulting in the stomach Mucosal dystrophies, etc., are likely to cause damage to the gastric mucosa and atrophy and inflammatory changes.

an examination

Related inspection

Gastrin-peptone gastrin gastric juice analysis of pentagastrin gastrin gastric juice

Atrophic gastritis, smooth mucosal folds, thinning of the mucosa, cell infiltration can involve the submucosa, most of the glands disappear, and sometimes the regenerative process of the restricted tissue predominates, polyps can occur, and even can be converted to gastric cancer. When the lesion is severe, the shape of the gastric mucosa is like the small intestine (intestinal). Since most of the glands disappear and the secretion function of the stomach is reduced, the secretion of pepsin and factors of hydrochloric acid is reduced. Basic lesions of the bone mucosa:

(1) Atrophy of the gland in the gastric mucosa, to determine whether the gland has atrophy, mainly according to the following points:

1. The epithelial cells of the gland are reduced in size, and the number of cells is also reduced. Therefore, the gland volume is reduced or even disappeared, and the residual intrinsic glands are irregularly distributed.

2, fibrous tissue hyperplasia between atrophic glands, interstitial widening, which has more inflammatory cell infiltration.

3, the inherent gland is reduced, replaced by biochemical glands. The normal gland is reduced, and the more glandular metaplasia, the heavier the degree of atrophy.

4. Normal glands disappear to varying degrees and are replaced by a hyperplasia of small glands.

Anyone with any of the above lesions can be seen as a manifestation of glandular atrophy. Glandular atrophy is often focally distributed, generally first pyloric, posterior corpus, first small bend, then large curved side.

The degree of shrinkage can be divided into three levels:

Mild: The superficial gland of the antrum is focally atrophied and reduced, while the large and small curved glands are normal.

Moderate: The antrum and small curved glands have atrophy, reduction, and the range of cut is mild.

Severe: most of the antrum of the antrum is atrophied and reduced. Only a few original glands remain, and the size and bending of the gland are atrophy. Or the mucosa is significantly thinner, and the original gland is completely atrophied and disappeared, and replaced by metaplastic glands. .

(2) Metaplasia: refers to the intrinsic gland of various parts of the gastric mucosa, and becomes the gland of other types of gastric glands or intestines. Such as intestinal metaplasia, pyloric gland metaplasia.

1. Intestinal metaplasia, intestinal gland metaplasia: refers to any gland of the gastric mucosa that becomes the gland of the small intestine. Start with the epithelium of the glandular neck and then develop deep into the epithelium and glands of the mucosal surface. Intestinal metaplasia (intestinal metaplasia) is a small intestinal metaplasia, which differs from the large intestine gland in the presence of Paneth cells.

2, false pyloric gland metaplasia: is a change in the body and stomach gland atrophy. If the biopsy is taken from the body of the stomach. There is a pyloric gland in the mucosa, which can be considered as metaplasia. In particular, the mucosa taken from the large curved part, if there is a pyloric gland, is definitely a metaplasia.

(3) Hyperplasia: When the gland has atrophy and disappearance, it is often accompanied by the proliferation of the neck gland, which is a repair and compensation phenomenon for the injury.

Differential diagnosis

According to the site of atrophic gastritis, combined with immunological changes, including autoimmune tests and serum gastrin determination, Strick land divides atrophic gastritis into two types, A and B.

Type A atrophic gastritis is an autoimmune disease that is positive for autoantibodies. Since autoimmune damage occurs in parietal cells, the lesion is heavier in the body of the stomach, and the glandular gland is destroyed and atrophied. Therefore, the acid secretion function of the stomach is significantly reduced or acid-free, and thus the serum gastrin level is increased. Can develop into gastric atrophy. In food, VitB12 binds to the inner factor (IF) secreted by parietal cells into an internal factor vitamin B12 complex, which contributes to the absorption of Vit B12. Intracellular factor antibody (IFA) can be found in the serum of patients with type A atrophic gastritis, mainly IgG, with binding and blocking types. The binding type IFA can bind to the internal factor or the internal factor vitamin B12 complex, while the blocked type IFA blocks the binding of the inner factor to the vitamin B12, thereby affecting the absorption of vitamin B12. Type A patients are often associated with pernicious anemia (16%), and 60% of them have blocked IFA. Atrophic gastritis in China is mainly found in the antrum of the stomach, and occurs in the corpus, which is consistent with the rare cases of pernicious anemia in China.

Type B atrophic gastritis is not an immune disease and is negative for autoantibodies. The onset of the disease is related to duodenal fluid reflux or other chemical and physical damage. The mucosa of the antrum is more permeable than the mucosa of the stomach (the ability of H+ reverse dispersion is 20 times stronger than the bottom of the stomach). Because the mucosal barrier of the gastric antrum is smaller than other parts, it is susceptible to the reflux of the duodenal juice and its contents, so the antrum is most susceptible. Gastric body lesions are light, so the gastric acid function is generally normal. Gastric sinus lesions damage G cells in the pyloric gland, and gastrin secretion is reduced, so the general serum gastrin level is low. The cancerous atrophic gastritis is mainly type B, and its carcinogenesis can last for more than 10 years or more.

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