thickening of gastric mucosa
Introduction
Introduction Gastric mucosal thickening is one of the clinical manifestations of "chronic atrophic gastritis" (intestinal, atypical hyperplasia), and chronic atrophic gastritis is a common gastric disease. Arteriosclerosis, insufficient blood flow to the stomach, and hobby of tobacco and tea are all likely to impair the barrier function of the gastric mucosa and cause chronic atrophic gastritis. In atrophic gastritis, the gastric mucosa is atrophied and replaced by intestinal epithelial cells, ie intestinal metaplasia; inflammation continues to evolve, cell growth is not typical, and even cell proliferation and carcinogenesis.
Cause
Cause
What causes the thickening of the gastric mucosa?
(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 after gastrectomy, gastric antrum excision, resulting in the stomach Mucosal dystrophies, etc., are likely to cause damage to the gastric mucosa and atrophy and inflammatory changes.
Examine
an examination
Related inspection
Fiberoptic gastroscopy
How should the gastric mucosal thickening be diagnosed?
(1) The color of the gastric mucosa becomes lighter: it is light red and grayish yellow, and the heavy one is gray or grayish blue. It can be diffuse or localized with plaque distribution. The border of Zhou is unclear. It can be expressed as red and white, mainly white, which is the earliest manifestation of mucosal atrophy.
(2) submucosal vascular permeability: mucosal atrophy makes the submucosal blood vessels visible. In the early stage of atrophy, dark red reticular small blood vessels in the mucosa can be seen, and in severe cases, blue dendritic veins of the mucosa can be seen. Vascular exposure is an important endoscopic feature of chronic atrophic gastritis. However, it should be noted that when the stomach is over-inflated at the bottom of the normal stomach and the intragastric pressure is too high, the gastric mucosa can penetrate the vascular network.
(3) Mucosal folds are small or even disappear. When the gas is injected into the stomach, the wrinkles disappear quickly. After the air is removed, the wrinkles recover slowly, and the secretions in the stomach are less, sometimes the mucous membranes are dry and the reflection is weakened.
(4) When chronic atrophic gastritis is associated with glandular neck transitional hyperplasia or intestinal metaplasia, the mucosal surface is rough and uneven, granular or nodular, sometimes showing the formation of pseudopolyps, while the characteristics of submucosal vessels are often revealed. Covered. Microscopic observation under the microscope can initially determine intestinal metaplasia, but it must be confirmed by gastric mucosal pathology.
(5) The atrophic mucosa is increased in fragility, easy to bleed, and may have erosive lesions.
(6) Chronic atrophic gastritis can be accompanied by the manifestations of chronic superficial gastritis, such as congestion of erythema, adhesion of mucus, and enhanced reflection. If the change is superficial gastritis, it is called superficial atrophic gastritis. The main change is chronic atrophic gastritis, which is called atrophic superficial gastritis.
Laboratory inspection
1 gastric juice analysis: patients with type A CAG are mostly acid-free or low-acid, and patients with type B CAG can be normal or low in acid.
2 Pepsinogen assay: Pepsinogen is secreted by the main cell, and the content of pepsinogen in blood and urine is reduced in chronic atrophic gastritis.
3 serum gastrin assay: G cells of the gastric antrum mucosa secrete gastrin. In patients with type A CAG, serum gastrin is often significantly increased; gastric mucosa atrophy in patients with type B CAG directly affects the secretion of gastrin by G cells, and serum gastrin is lower than normal.
4 immunological examination: wall cell antibody (PCA), internal factor antibody (IFA), gastrin secretion cell antibody (GCA) determination, can be used as a secondary diagnosis of chronic atrophic gastritis and its classification.
(3) X-ray examination: X-ray stomach barium meal examination Most patients with atrophic gastritis have no abnormal findings. Air sputum double contrast can show that the gastric mucosa folds flat and thin, the serrated mucosal folds of the corpus callosum become thin or disappear, the bottom of the stomach is smooth, and some gastric antrums can be serrated or mucous membranes. .
(4) Gastroscope and biopsy: gastroscopy and biopsy are the most reliable diagnostic methods. Gastroscopic diagnosis should include the extent of the lesion, degree of atrophy, intestinal metaplasia and degree of dysplasia. The mucosa of the atrophic gastritis was mostly pale or grayish, and the folds became thin or flat. The mucous membranes can be red and white, and in severe cases there are scattered white patches. Submucosal blood vessels are characterized by atrophic gastritis. Red reticular arterioles or capillaries can be seen, and severe atrophic gastritis can be seen. Epithelial cells proliferate to form fine particles or larger nodules. There are also mucosal erosions and bleeding. Gastric mucosal biopsy pathology mainly causes glandular atrophy and disappearance, and is replaced by pyloric gland metaplasia or intestinal gland metaplasia, and interstitial inflammation infiltration is significant.
Diagnosis
Differential diagnosis
What are the symptoms of gastric mucosal thickening that are easily confused?
Differential diagnosis of gastric mucosal thickening:
Type A atrophic gastritis: an autoimmune disease, 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: not an immune disease, the autoantibody is negative. 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.
symptom
(1) The color of the gastric mucosa becomes lighter: it is light red and grayish yellow, and the heavy one is gray or grayish blue. It can be diffuse or localized with plaque distribution. The border of Zhou is unclear. It can be expressed as red and white, mainly white, which is the earliest manifestation of mucosal atrophy.
(2) submucosal vascular permeability: mucosal atrophy makes the submucosal blood vessels visible. In the early stage of atrophy, dark red reticular small blood vessels in the mucosa can be seen, and in severe cases, blue dendritic veins of the mucosa can be seen. Vascular exposure is an important endoscopic feature of chronic atrophic gastritis. However, it should be noted that when the stomach is over-inflated at the bottom of the normal stomach and the intragastric pressure is too high, the gastric mucosa can penetrate the vascular network.
(3) Mucosal folds are small or even disappear. When the gas is injected into the stomach, the wrinkles disappear quickly. After the air is removed, the wrinkles recover slowly, and the secretions in the stomach are less, sometimes the mucous membranes are dry and the reflection is weakened.
(4) When chronic atrophic gastritis is associated with glandular neck transitional hyperplasia or intestinal metaplasia, the mucosal surface is rough and uneven, granular or nodular, sometimes showing the formation of pseudopolyps, while the characteristics of submucosal vessels are often revealed. Covered. Microscopic observation under the microscope can initially determine intestinal metaplasia, but it must be confirmed by gastric mucosal pathology.
(5) The atrophic mucosa is increased in fragility, easy to bleed, and may have erosive lesions. (6) Chronic atrophic gastritis can be accompanied by the manifestations of chronic superficial gastritis, such as congestion of erythema, adhesion of mucus, and enhanced reflection. If the change is superficial gastritis, it is called superficial atrophic gastritis. The main change in chronic atrophic gastritis is atrophy? Superficial gastritis.
Laboratory inspection
1 gastric juice analysis: patients with type A CAG are mostly acid-free or low-acid, and patients with type B CAG can be normal or low in acid.
2 Pepsinogen assay: Pepsinogen is secreted by the main cell, and the content of pepsinogen in blood and urine is reduced in chronic atrophic gastritis.
3 serum gastrin assay: G cells of the gastric antrum mucosa secrete gastrin. In patients with type A CAG, serum gastrin is often significantly increased; gastric mucosa atrophy in patients with type B CAG directly affects the secretion of gastrin by G cells, and serum gastrin is lower than normal.
4 immunological examination: wall cell antibody (PCA), internal factor antibody (IFA), gastrin secretion cell antibody (GCA) determination, can be used as a secondary diagnosis of chronic atrophic gastritis and its classification.
(3) X-ray examination: X-ray stomach barium meal examination Most patients with atrophic gastritis have no abnormal findings. Air sputum double contrast can show that the gastric mucosa folds flat and thin, the serrated mucosal folds of the corpus callosum become thin or disappear, the bottom of the stomach is smooth, and some gastric antrums can be serrated or mucous membranes. .
(4) Gastroscope and biopsy: gastroscopy and biopsy are the most reliable diagnostic methods. Gastroscopic diagnosis should include the extent of the lesion, degree of atrophy, intestinal metaplasia and degree of dysplasia. The mucosa of the atrophic gastritis was mostly pale or grayish, and the folds became thin or flat. The mucous membranes can be red and white, and in severe cases there are scattered white patches. Submucosal blood vessels are characterized by atrophic gastritis. Red reticular arterioles or capillaries can be seen, and severe atrophic gastritis can be seen. Epithelial cells proliferate to form fine particles or larger nodules. There are also mucosal erosions and bleeding. Gastric mucosal biopsy pathology mainly causes glandular atrophy and disappearance, and is replaced by pyloric gland metaplasia or intestinal gland metaplasia, and interstitial inflammation infiltration is significant.
