chronic non-atrophic gastritis

Introduction

Introduction to chronic non-atrophic gastritis Chronic non-atrophic is a chronic gastritis that is not associated with atrophic changes of the gastric mucosa and is infiltrated by chronic inflammatory cells mainly composed of lymphocytes and plasma cells in the gastric mucosa. Gastric sinusitis, gastritis, and total gastritis are mainly gastric antrum or total gastritis. Helicobacter pylori infection is the main cause of chronic non-atrophic gastritis. The prevalence of chronic non-atrophic gastritis varies with the prevalence of H. pylori infection in different countries and regions. basic knowledge The proportion of illness: 0.025% Susceptible people: no specific population Mode of infection: non-infectious Complications: gastric cancer, gastric bleeding, anemia, gastric ulcer

Cause

Causes of chronic non-atrophic gastritis

1, Helicobacter pylori infection

Helicobacter pylori infection is the most important cause of chronic non-atrophic gastritis. The relationship between the two is in line with Koch's four basic requirements for determining the pathogen's etiology of infectious diseases, that is, the pathogen is present in the patient's pathogen distribution. Consistent with the distribution of lesions in the body, the disease can be improved after removal of the pathogen, and the pathogen can induce a disease similar to humans in an animal model.

There are two prominent types of Helicobacter pylori-related chronic non-atrophic gastritis: the antrum is the main gastritis and the stomach is the main gastritis. The former gastric acid secretion can be increased, thus increasing the risk of duodenal ulcer; the latter reduces gastric acid secretion, which increases the risk of gastric ulcer and gastric cancer.

2, other factors

When the pyloric sphincter dysfunction, the duodenal juice containing bile and pancreatic juice flows back into the stomach, which can weaken the gastric mucosal barrier function, so that the gastric mucosa is affected by the digestive juice, causing inflammation, erosion, hemorrhage and epithelial metaplasia. Other exogenous factors, such as alcoholism, taking NSAIDs, and other irritating foods, can repeatedly damage the gastric mucosa.

Prevention

Chronic non-atrophic gastritis prevention

1, quit smoking and alcohol, diet rules, should not be excessive.

2. Avoid eating irritating foods such as coffee, tea, and pepper.

3, eat too hard, too rough, too hot or too cold food.

4. Eat less sweet and sour foods and fruits such as chocolate, ice cream, apples and oranges.

5, eat less prone to gas, such as sweet potato, glutinous rice, potatoes and so on.

Complication

Chronic non-atrophic gastritis complications Complications, gastric cancer, stomach bleeding, anemia, gastric ulcer

1, stomach bleeding.

2, anemia.

3, stomach ulcers.

4, the early stage of gastric cancer.

Symptom

Chronic non-atrophic gastritis symptoms Common symptoms Heartburn, acid reflux, abdominal discomfort, bloating, left upper abdominal pain, nausea, loss of appetite, hunger, upper abdominal pain, early suffocation

Most patients with chronic non-atrophic gastritis have no symptoms, lack of specificity in clinical manifestations, and the severity of symptoms is not exactly the same as the degree of mucosal lesions. Most patients do not have any clinical symptoms or only symptoms of dyspepsia such as abdominal pain, bloating, nausea, acid reflux, loss of appetite. Individual patients with mucosal erosion have more obvious upper abdominal pain and may have bleeding. There are also some patients with neuropsychiatric symptoms such as insomnia, anxiety, irritability, palpitation, and suspicion. Some patients are always skeptical about their own stomach cancer and seek medical treatment everywhere, repeatedly asking for a gastroscopy.

Examine

Chronic non-atrophic gastritis examination

1, gastroscope and biopsy

Gastroscopic examination and simultaneous biopsy for histological pathology are the most reliable diagnostic methods. Endoscopic chronic non-atrophic gastritis can be seen in erythema (point, flaky, strip), rough mucosa, bleeding point (plaque), mucosal edema and exudation and other basic manifestations; sometimes visible erosion and bile reflux. Because the endoscopic findings are often inconsistent with the pathological findings of biopsy, the two should be combined at the time of diagnosis, and the biopsy diagnosis should be based on the full biopsy.

2, Helicobacter pylori detection

H. pylori can be detected simultaneously in histopathological examination, and one more tissue can be taken for endoscopic examination for rapid urease test to increase the reliability of diagnosis. After eradication of Helicobacter pylori treatment, the above examination can be repeated during gastroscopy, and non-invasive examination methods such as 13C or 14C urea breath test, Helicobacter pylori antigen test and serological examination (qualitative detection of serum anti-pylorus) can also be used. Helicobacter IgG antibody). However, the recent application of antibiotics, proton pump inhibitors, expectorants and other drugs will make the above tests (except serological tests) false negative.

Diagnosis

Diagnosis and diagnosis of chronic non-atrophic gastritis

diagnosis

In view of the fact that most patients with chronic gastritis have no symptoms, symptoms and lack of specificity, and lack of specific signs, it is difficult to make a correct diagnosis of chronic gastritis based on symptoms and signs. The diagnosis of chronic non-atrophic gastritis depends mainly on endoscopy and histological examination of gastric mucosal biopsy, especially the latter is more diagnostic.

The diagnosis of chronic gastritis should be clear to determine the cause. Helicobacter pylori infection is the main cause of chronic non-atrophic gastritis, so it should be used as a routine test for the diagnosis of chronic gastritis.

Correlation analysis between endoscopy and gastric mucosal histology and symptoms of chronic gastritis showed that the patient's symptoms were not specific, and the presence or absence of symptoms and severity were not positively correlated with endoscopic findings and histological grades. .

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