Classification and etiology of chronic atrophic gastritis

  Chronic atrophic gastritis is a type of chronic gastritis that presents 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. The incidence of the disease increases with age, and the degree of the lesion becomes more severe, so it is believed that chronic atrophic gastritis is a degenerative change of the gastric mucosa in middle-aged and elderly people, 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.  The clinical manifestations of this disease include loss of appetite, nausea, belching, epigastric fullness or dull pain, and in a few patients, upper gastrointestinal bleeding, emaciation, anemia, brittle nails, tongue inflammation or tongue papillary atrophy. Because of the high incidence of this disease, and often recurrent clinical episodes, not easily cured, and closely related to the occurrence of gastric cancer, chronic atrophic gastritis is increasingly important to people.  In 1973, Strickland et al. divided atrophic gastritis into two separate types, type A and type B, based on serum immunological examination and distribution of lesions in the stomach. type A atrophic gastritis lesions are mainly found in the body of the stomach, with diffuse distribution, generally normal mucosa of the gastric sinus, positive serum mural cell antibodies, increased serum gastrin, and reduced or absent gastric acid and endocrine secretion. Type B atrophic gastritis is a simple atrophic gastritis with a multifocal distribution of lesions mainly in the gastric sinus, a negative serum mural cell antibody, normal serum gastrin, normal or mildly decreased gastric acid secretion, no pernicious anemia, and more likely to be complicated by gastric cancer. Thereafter, Glass called the atrophic gastritis involving both the gastric sinus and the gastric body as AB type.  In China, according to Strickland’s classification, type B atrophic gastritis is common and type A atrophic gastritis is rare, and some patients with atrophic gastritis have both sinus inflammation and wall cell antibodies, which cannot be included in the above two types, so many domestic scholars have proposed a classification method suitable for our specific situation, and chronic atrophic gastritis is divided into type A1, A2, B1 and B2. type B2. The type A is divided into two subtypes, type A1 for those with no lesions in the gastric sinus and type A2 for those with lesions in the gastric sinus and gastric body. type B is divided into type B1 (heavier lesions in the gastric sinus than in the gastric body) and type B2 (heavier lesions in the gastric body than in the gastric sinus or similar lesions in the gastric body and gastric sinus) according to the severity of lesions in the gastric body and sinus. The two subtypes are classified as B1 (sinus lesions heavier than gastric weight) and B2 (gastric body lesions heavier than gastric sinus or similar gastric body and sinus lesions).  In conclusion, there is no completely uniform classification of chronic atrophic gastritis, and it is still customary to follow the Strickland classification, which divides chronic atrophic gastritis into type A and type B.  The etiology of chronic atrophic gastritis has not been understood to date and may be related to the following factors: 1. The continuation of chronic superficial gastritis: chronic atrophic gastritis can develop from chronic superficial gastritis. The PLA General Hospital and six other hospitals reported 164 cases of superficial gastritis after 5-8 years of follow-up observation, of which 34 cases turned into chronic atrophic gastritis (20.7%). The etiology of chronic superficial gastritis can be a causative and aggravating factor of chronic atrophic gastritis.  2, genetic factors: according to Varis survey, 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. The incidence rate with relatives is 20 times greater than the control group, indicating that chronic atrophic gastritis may be related to genetic factors.  Polmer called it excretory gastritis. In addition to lead, many heavy metals such as mercury, tellurium, copper and zinc have certain damaging effects on the gastric mucosa.  4, radiation: radiation therapy ulcer disease or other tumors, can make the gastric mucosa damage or even atrophy.  5, iron deficiency anemia: many facts show that iron deficiency anemia and atrophic gastritis are closely related, Badanoch reported 50 cases of iron deficiency anemia, normal gastric mucosa, superficial gastritis and atrophic gastritis accounted for 14%, 46% and 40% respectively. However, the mechanism of gastritis caused by anemia is not known. Some scholars believe that gastritis is the primary cause, because gastritis gastric acid low iron can not be absorbed, or due to gastric bleeding to form anemia; another opinion that the first anemia, because the body iron deficiency in the gastric mucosa renewal rate is affected and prone to inflammation.  6, biological factors: chronic infectious diseases such as hepatitis, tuberculosis and other effects on the stomach has also attracted attention. Patients with chronic liver disease often have signs and symptoms of chronic gastritis, and gastric mucosal staining has also confirmed the presence of antigenic antibody complexes of hepatitis B virus in the gastric mucosa of hepatitis B patients. Ruijin Hospital reported 91 cases of atrophic gastritis, 24 cases (26.4%) were combined with chronic hepatitis. So chronic infectious diseases, especially chronic liver disease on the stomach is worth noting.  7, physical factors: clinical statistics show that the occurrence of this disease and age is significantly positively correlated. The older the stomach mucosa function “resistance” is poorer, easily affected by external adverse factors and cause damage.  8, 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, resulting in chronic superficial gastritis, and can develop into chronic atrophic gastritis.  9, immune factors: in atrophic gastritis, especially gastric gastritis patients with blood, gastric juice or in the plasma cells of the atrophic mucosa, can often find wall cell antibodies or endogenous factor antibodies, it is believed that the autoimmune response is the cause of chronic atrophic gastritis. In recent years, a few patients with gastric sinus gastritis were found to have antibodies to gastrin-secreting cells, which are specific autoimmune antibodies to cells and belong to the IgG lineage. Some patients with atrophic gastritis have abnormal in vitro lymphocyte transformation test and leukocyte movement inhibition test, suggesting that cellular immune response is also important in the development of atrophic gastritis.  10, Helicobacter pylori infection: In 1983, Australian scholars Marshall and Warren first isolated HP from the mucus layer and epithelial cells of the gastric sinus in patients with chronic gastritis. since then many scholars have conducted a large number of experimental studies on patients with chronic gastritis and cultured HP in the gastric mucosa of 60-90% of patients with chronic gastritis, and then found that In 1986, the 8th meeting of the World Society of Gastroenterology suggested that HP infection is one of the important causes of chronic gastritis.  In addition; such as improper diet, long-term addiction to tobacco and alcohol, drug abuse, chronic inflammation of the upper respiratory tract, central nervous system dysfunction, damage to the gastric mucosa, as well as after major gastrectomy, gastric secretion of the gastric sinus region removed, resulting in gastric mucosa nutrient disorders, etc., are prone to damage to the gastric mucosa and atrophy, inflammatory changes.  Reaction is the relevant etiology of chronic atrophic gastritis. In recent years, a few patients with gastric sinus gastritis were found to have antibodies to gastrin-secreting cells, which are specific autoimmune antibodies to cells and belong to the IgG lineage. Some patients with atrophic gastritis have abnormal in vitro lymphocyte transformation test and leukocyte movement inhibition test, suggesting that cellular immune response is also important in the development of atrophic gastritis.