Overview of chronic atrophic gastritis
Chronic atrophic gastritis is divided into two types: type A and type B. Type A atrophic gastritis, also known as autoimmune gastritis, is caused by autoimmune dysfunction, that is, the body’s immune cells launch an attack on their own gastric mucous membrane wall cells, resulting in gastric mucous glands atrophy and reduction, the main lesions are distributed in the body of the stomach; this type of gastritis leads to severe gastric acid secretion is low, and due to the reduction of the secretion of the internal factors will occur malignant anemia and neurological lesions.
Etiology
The cause of the disease is unknown and is mainly related to autoimmune abnormalities.
Symptoms
The lesions are more severe in the body of the stomach. Due to vitamin B12 malabsorption caused by internal factor deficiency, in addition to the manifestations of anemia, there may be dyspepsia, etc.; some patients present with neurological symptoms such as abnormal sensation in the limbs, loss of deep sensation in the lower limbs, ataxia, and spastic paralysis, and often consult the neurology department, and are diagnosed with subacute spinal cord syndromic degenerative lesion, which mainly involves the posterior cord of the spinal cord, pyramidal tracts, and peripheral nerves, and also involves the white matter of the brain.
Examination
1. Laboratory examination
① Red blood cell count or hemoglobin content, white blood cell count and platelet count in peripheral blood are all reduced, but bone marrow image shows significant hyperplasia of megaloblastic erythrocytes. ② Positive serum mural cell antibodies and autoantibodies to endogenous factors. ③Serum unconjugated bilirubin may be mildly increased due to the easy destruction of megaloblasts in the bone marrow.
2. Endoscopy, pathologic and histologic examination
It shows that the mucosa of gastric sinus is normal, while the mucosa of gastric body is atrophic, and gastric acid is reduced or absent.
3. Urea breath test
The patient takes urea containing the isotope 13C or 14C, the urease produced by H. pylori breaks down the urea to produce CO2 labeled with the isotope, which can be detected in the subject’s exhaled gas and is one of the gold standards for H. pylori infection screening.
Diagnosis
The following indicators are helpful in the diagnosis of this disease: ① Positive antibodies to mural cells and internal factors. ② Absence of gastric acid secretion. Gastroscopy and histopathology suggest that the mucosa of the gastric sinus is basically normal, while the atrophy of the gastric body is obvious. Serum pepsinogen (PG) Ⅰ content is obviously decreased. If the pyloric gland of the gastric sinus extends to the gastric body and pseudo-pyloric glandular metaplasia occurs, the PG Ⅱ content is also increased, resulting in a significant decrease in both PG Ⅰ and PG Ⅰ / PG Ⅱ ratio. ⑤ Serum vitamin B12 level <200ng/L is definitely vitamin B12 deficiency (normal value 300～860ng/L). ⑥ Vitamin B12 absorption test: detect the absorption of vitamin B12 in the terminal ileum. (7) Fasting serum gastrin is often >500ng/L (normal <100ng/L).
Differential diagnosis
It should be differentiated from type B atrophic gastritis, which is a non-immune disease with negative autoantibodies. It is a non-immune disease with negative autoantibodies. Its pathogenesis is mostly seen in the gastric sinus, which causes G-cell damage and reduced gastrin secretion, so the serum gastrin level is low. Gastric body lesions are mild, and the function of gastric acid secretion is generally normal.
Treatment
Vitamin B12 replacement therapy can be applied to this disease. Patients with occult pernicious anemia should also be given regular vitamin B12 therapy to prevent the occurrence of pernicious anemia and neurological lesions. Gastric cancer is more common in chronic type A atrophic gastritis combined with pernicious anemia, and should be followed up regularly.