Diagnostic criteria and precautions for erythematous gastritis

Gastric disease has gradually become an obstacle to the health of many people. It is basically divided into two categories: acute simple gastritis and chronic gastritis. The main causes of gastritis are mostly excessive intake of coffee, liquor, long-term use of ammonium sulfate, antibiotics and other chemical substances, or frequent consumption of cold, too hot food or infection with bacterial toxins. More and more people are suffering from the disease. Chronic gastritis is generally divided into two categories: chronic superficial gastritis and chronic atrophic gastritis. The human body sometimes suffers from these two diseases at the same time. Most people think that as long as the stomach and abdomen feel uncomfortable, painful, stomach acid, nausea, etc., they are gastritis, but they ignore one point, which is classification. As mentioned above, gastritis is divided into two categories. Only by diagnosing which specific category it is can we prescribe the right medicine. Today we will talk about the treatment and protection methods of erythematous gastritis, one of the chronic superficial gastritis in chronic gastritis.

1. Diagnosis and differential diagnosis

The diagnosis of chronic gastritis mainly depends on endoscopic examination and histological examination of gastric mucosal biopsy, especially the latter which has greater diagnostic value. Routine testing for Helicobacter pylori is recommended. In chronic gastritis, in patients with gastric body atrophy, the serum gastrin G17 level is significantly increased, and the pepsinogen I or the ratio of pepsinogen I and II is decreased; in patients with antral atrophy, the former is decreased, and the latter is normal; in patients with complete gastric atrophy, both are decreased. Therefore, the detection of serum gastrin G17 and pepsinogen I and II can help determine whether the gastric mucosa is atrophied and the location of the atrophy. Atrophic gastritis can be caused by Hp infection or autoimmunity. For those suspected of being caused by autoimmunity, it is recommended to monitor serum gastrin, vitamin B12, parietal cell antibodies, intrinsic factor antibodies, etc.

(II) Diagnostic criteria and relevant precautions for chronic gastritis pathology:

1. Common lesions of chronic gastritis are mainly divided into atrophic and non-atrophic, and the term "superficial" is no longer used. Because "superficial" corresponds to "deep", it is a term used to divide depth and cannot reflect the number of gastric mucosal glands.

2. Chronic gastritis is divided into antral gastritis, gastric body gastritis and pangastritis according to the location of the lesion.

3. A small number of chronic gastritis are special types of gastritis, such as chemical gastritis, lymphocytic gastritis, granulomatous gastritis, eosinophilic gastritis, collagenous gastritis, radiation gastritis, infectious (bacterial, viral, fungal and parasitic) gastritis and Menetrier's disease.

4. Gastric mucosal atrophy refers to the reduction of gastric intrinsic glands, and there are two types histologically. (1) Metaplastic atrophy: The lamina propria of the gastric mucosa is partially or entirely composed of intestinal epithelial glands. (2) Non-metaplastic atrophy: The number of glands in the lamina propria of the gastric mucosa decreases, and the replacement components are fibrous tissue, fibromuscular tissue, or inflammatory cells (mainly chronic inflammatory cells).

5. As long as the pathological biopsy of chronic gastritis shows atrophy of the intrinsic glands, it can be diagnosed as chronic atrophic gastritis, regardless of the number and degree of atrophy in the biopsy specimen. Clinicians can make a judgment on the scope and degree of atrophy based on the pathological results and endoscopic findings.

6. Chronic gastritis observation includes 5 histological changes and 4 grades. The five histological changes include H. pylori infection, chronic inflammatory response (mononuclear cell infiltration), activity (neutrophil infiltration), atrophy (reduction of intrinsic glands), and intestinal metaplasia (intestinal metaplasia). The 4 levels include: 0 indicates none, + indicates mild, ++ indicates moderate, and ++++ indicates severe.

3. Treatment

The goal of treating chronic gastritis is to relieve clinical symptoms and improve the inflammatory response of the gastric mucosa; treatment should be targeted at the cause as much as possible and follow the principle of individualization. Chronic non-atrophic gastritis without clinical symptoms and Hp-negative does not require special treatment; however, for chronic atrophic gastritis, especially severe chronic atrophic gastritis or accompanied by intraepithelial neoplasia, care should be taken to prevent its malignant transformation.

There is no consensus on whether Hp should be eradicated in all cases of Hp-related gastritis. The domestic consensus on the treatment of Hp infection recommends eradication of Hp in patients with gastric mucosal atrophy, erosion, or clinical symptoms of indigestion. The main clinical symptom of chronic gastritis is dyspepsia, which should be classified as functional dyspepsia. Eradication therapy can provide long-term relief of clinical symptoms in patients with Hp-positive functional dyspepsia. Eradication of H. pylori can improve gastric mucosal histology, which is of great significance for preventing peptic ulcers and gastric cancer, and also has cost-effectiveness advantages in improving or eliminating clinical symptoms of dyspepsia. For patients with gastric mucosal erosion and/or clinical symptoms such as acid reflux and upper abdominal pain, antacids, H2 receptor antagonists or proton pump inhibitors can be selected according to the severity of the disease or clinical symptoms.

For patients with upper abdominal fullness, nausea or vomiting as the main clinical symptoms, prokinetic drugs such as mosapride, itopride hydrochloride and domperidone can be used. For patients with bile reflux, prokinetic drugs and/or gastric mucosal protective agents that bind bile acid, such as aluminum carbonate preparations, can be used. For patients with significantly improved clinical symptoms of indigestion such as eating-related abdominal distension and loss of appetite, digestive enzyme preparations such as compound azintamide, Aspergillus oryzae pancreatin, and various pancreatic enzyme preparations may be considered.