Surface Gastritis

　　The occurrence and development of superficial gastritis is a chronic process, and the disease is caused by the combined effects of multiple factors.

　　(1) Helicobacter pylori infection

　　Helicobacter pylori is the main cause of chronic gastritis, and the reasons are: ① The majority of chronic active gastritis patients can detect Helicobacter pylori in the gastric mucosa; ② The distribution of Helicobacter pylori in the stomach is consistent with the distribution of gastric inflammation; ③ Eradication of Helicobacter pylori can cause regression of gastric mucosal inflammation; ④ Chronic gastritis caused by Helicobacter pylori infection can be replicated in volunteers and animal models. Helicobacter pylori has flagella and can penetrate the mucus layer in the stomach to move towards the gastric mucosa. The adhesins secreted by it can make it adhere to epithelial cells. It releases urease to decompose urea, producing ammonia to maintain a neutral environment around the bacteria, which is conducive to its colonization on the surface of the gastric mucosa. Helicobacter pylori can cause cell damage and a strong inflammatory response through ammonia production and secretion of toxins, induce immune response, and lead to chronic inflammation of the gastric mucosa.

　　(2) Dietary and environmental factors

　　Stimulative foods, such as long-term consumption of strong alcohol, strong tea, coffee, spicy and rough foods, as well as irregular dietary patterns such as overeating or under-eating, can all damage the protective barrier of the gastric mucosa and cause gastritis. Epidemiological studies have shown that high salt intake and a lack of fresh vegetables and fruits in the diet are closely related to the occurrence of gastric mucosal atrophy, intestinal metaplasia, and gastric cancer.

　　(3) Autoimmune

　　Autoimmune gastritis can produce autoantibodies that attack parietal cells, reducing the total number of parietal cells and leading to reduced or lost secretion of gastric acid; the intrinsic factor antibody binds to intrinsic factor, obstructing the absorption of vitamin B12, thus causing pernicious anemia.

　　(4) Other factors

　　When the pyloric sphincter function is incomplete, duodenal juice containing bile and pancreatic juice can reflux into the stomach, which can weaken the protective function of the gastric mucosal barrier. Other exogenous factors, such as alcoholism, taking NSAIDs and other drugs, and certain刺激性 food, can repeatedly damage the gastric mucosa. Theoretically, these factors can individually or in synergy with Helicobacter pylori infection cause or exacerbate chronic inflammation of the gastric mucosa, but there is currently a lack of evidence from systematic studies.

　　Long-term chronic symptoms of the stomach, disordered digestion and absorption, can lead to the intrinsic lesions of the stomach and systemic effects on nutrition metabolism, autonomic nerve function regulation, endocrine hormone release levels, growth and development, and overall immune function, becoming an important potential factor for the occurrence of complications. The complications of superficial gastritis include:
　　(1) Precancerous stage of gastric cancer
　　The carcinogenesis of chronic gastritis is closely related to gastritis-related hyperplasia, especially in patients with chronic gastritis accompanied by pernicious anemia and atrophic inflammation with intestinal metaplasia and severe atypical hyperplasia. If the damage to the gastric mucosa of patients cannot be treated in time, it can cause disorders of the vasodilation and vasoconstriction function of the gastric mucosal blood vessels, reduce the blood flow of the gastric mucosa, destroy the protective function of the gastric mucosal barrier, exacerbate the chronic inflammatory reaction of the gastric mucosa, and eventually lead to atrophy, intestinal metaplasia, and atypical hyperplasia of the gastric mucosa.
　　(2) Gastric ulcer
　　Superficial gastritis can cause the mucosa to atrophy and thin due to long-term obvious inflammatory stimulation, leading to erosion and ulceration.
　　（3）Anemia
　　Patients with superficial gastritis may develop nutritional anemia or pernicious anemia due to decreased digestive function, reduced dietary intake, and vitamin absorption disorders. Anemia can also occur after secondary gastrointestinal bleeding.

　　Patients with superficial gastritis often have no obvious symptoms; some patients may manifest as upper abdominal pain or discomfort, abdominal distension, early satiety, belching, nausea, and other dyspeptic symptoms, without obvious rhythm. These symptoms are generally more severe after eating. The presence and severity of these symptoms are not necessarily related to the endoscopic findings and histopathological changes of chronic gastritis.
　　（1）Epigastric pain is the most common symptom of superficial gastritis, accounting for about 85%. The upper abdominal pain in patients with superficial gastritis is usually irregular, unrelated to diet, and is generally diffuse epigastric burning pain, hidden pain, or distension. Symptoms may worsen after eating cold, hard, spicy, or other刺激性 foods, and a few are related to changes in weather.
　　（2）Abdominal distension is also a common symptom, accounting for about 70%. It is often caused by gastric dysfunction due to gastritis, leading to gastric retention, delayed emptying, and poor digestion.
　　（3）Burping, about 50% of patients have this symptom, feeling an increase in gastric gas, which is temporarily relieved after being expelled through the esophagus.
　　（4）Other symptoms, including loss of appetite, acid regurgitation, nausea, vomiting, fatigue, constipation, or diarrhea. Patients with superficial gastritis often have reduced appetite or fluctuating conditions. Inflammatory gastric mucosa is stimulated by physical, biological factors, and gastric motility disorders, as well as retrograde peristalsis, causing nausea and vomiting. Most patients have constipation symptoms, while diarrhea is relatively rare.

　　The prevention of superficial gastritis should start from daily life and diet, actively avoid and eliminate various pathogenic factors. Specific precautions include:
　　1. Have a balanced diet: The diet of gastritis patients should be light, nutritious, and have fewer meals. They should also avoid stimulants such as strong tea, coffee, spices, raw garlic, and horseradish that can damage the gastric mucosa. They should also avoid eating hard, sour, spicy, cold, hot, and excessively rough foods. Patients should quit smoking and drinking to prevent further damage to the gastric mucosa.
　　2. Increase nutrition appropriately: The selection of food should pay attention to choosing high-nutrient protein foods and soft foods rich in vitamins, such as milk, tofu, carrots, and some fermented foods. Food should be chewed slowly. Dietary notes should be paid to food pairing, and it is best to have both dry and wet foods, as well as a combination of protein foods and a small amount of staple foods.
　　3. Have regular meals: Patients should have regular and quantitative meals, avoid overeating and binge eating, develop good eating habits, and this can reduce the burden on the stomach.
　　4. Relax your mood: Patients should avoid mental stress, depression, and overexertion during the convalescence period. They should live a disciplined life, combine work and rest, and maintain an optimistic mood. They can strengthen physical exercise according to their physical condition to enhance their physical fitness and gastrointestinal motility function.
　　5. Actively treat systemic diseases that can lead to chronic gastritis, such as: Liver, gallbladder, pancreas, heart, kidney diseases, and endocrine lesions, etc.
　　6. Be cautious or avoid taking刺激性 drugsCommon drugs that cause significant damage to the gastric mucosa include aspirin, sodium salicylate, paracetamol, phenacetin, tetracycline, indomethacin, ibuprofen, morphine, phenylbutazone, aminopyrine, prednisone, dexamethasone, cortisone, and others.

　　Common examination items for superficial gastritis include:
　　(1) Gastroscopy and biopsy examination
　　Gastroscopy examination combined with pathological examination of living tissue is the most reliable method for diagnosing chronic gastritis. Endoscopic superficial gastritis is manifested as punctate, patchy, or striated erythema of the gastric mucosa, rough and uneven mucosal surface, which may be accompanied by bleeding spots or hemorrhagic macules, mucosal edema, and exudation. The main findings of the histopathological examination of gastric mucosal living tissue are the degeneration of gastric mucosal epithelial cells, hyperplasia of crypt epithelium, and inflammatory cell infiltration in the lamina propria. Occasionally, there may be metaplasia of the surface epithelium and crypt epithelium, without a decrease in the固有腺体.
　　(2) Helicobacter pylori detection
　　During endoscopic examination, it is possible to take another piece of living tissue for rapid urease test to increase the reliability of the diagnosis of Helicobacter pylori infection. Helicobacter pylori antibody detection uses colloidal gold technology to qualitatively detect antibodies against Helicobacter pylori in human serum, plasma, or whole blood. When the patient's sample contains specific antibodies against Helicobacter pylori, they form an antigen-antibody-antigen colloidal gold particle complex with the antigen on the detection line (T line), and a red line is displayed. The use of a breath test instrument for Helicobacter pylori testing is simple, has no adverse reactions, and is currently one of the ideal testing methods. The sensitivity of the test results is over 95%, and it is currently the gold standard in the medical field for detecting HP.
　　(3) Related examinations for autoimmune gastritis
　　For those suspected of having autoimmune gastritis, blood PCA and IFA should be tested. A positive result suggests the presence of autoimmune factors. The determination of serum vitamin B12 concentration and vitamin B12 absorption test can help diagnose pernicious anemia.
　　(4) Determination of serum gastrin G17, pepsinogen I, and II
　　Serum gastrin and pepsinogen detection are non-invasive examinations that help determine the presence and distribution of gastric mucosal atrophy, as well as its degree.

　　The onset of superficial gastritis is often related to dietary factors, therefore, dietary adjustment should be made. The diet should be non-irritating, contain low fiber, easy to digest, and rich in nutrition; eat less but more frequently; relax and maintain a pleasant mood during meals. At the same time, avoid long-term consumption of strong alcohol, strong tea, coffee, excessive spicy seasonings, and foods that are too salty, sour, or rough, which can repeatedly stimulate the gastric mucosa. More importantly, unreasonable dietary habits, irregular diet, overeating, or long-term deficiency of protein and B-group vitamins can lead to the denaturation of the gastric mucosa.
　　(1) Regular dietDiet should be light and non-irritating to the gastric mucosa, with a regular diet schedule, avoiding both extreme hunger and overeating. The principle is to eat less but more frequently. For those with reduced gastrointestinal function or the elderly, it is best to have 4 to 5 meals a day, with each meal being about 60 to 70% full. Pay attention to the proportion of sugar, fat, and protein in the food, and the content of vitamins and other essential nutrients for the body.
　　(2) Avoid spicy and刺激性 food: Harmful substances in alcohol and smoke can affect the function of the gastric mucosa and cause significant damage to the gastric mucosa. Therefore, superficial gastritis patients need to quit smoking and drinking to avoid exacerbating the condition.
　　(3) Avoid cold, hot, and hard food: Cold food and cold drinks can cause stomach cramps, contraction of gastric mucosal blood vessels, and are not conducive to the regression of inflammation; overly hot food and drinks can directly scald or stimulate the gastric mucosa after ingestion. Too hard and rough food, rough vegetables, fried or grilled food with oil, after eating, can increase the mechanical digestion burden on the stomach, cause friction and damage to the gastric mucosa, and exacerbate the inflammatory changes of the mucosa.

　　Superficial gastritis can be treated with drugs to suppress gastric acid secretion, protect the gastric mucosa, control Helicobacter pylori (HP) infection, and improve bile reflux to remove the cause of the disease and cure the disease.

　　(1) Gastric parietal cell receptor antagonists: H2 histamine receptor, gastrin receptor, and acetylcholine receptor antagonists can all reduce gastric acid secretion and are used for the treatment of gastritis, especially suitable for those with high gastric acid. Commonly used drugs include Cimetidine, Ranitidine, Famotidine, and others. Omeprazole, Rabeprazole, Pantoprazole, and other drugs are proton pump inhibitors that can effectively inhibit gastric acid secretion.

　　(2) Drugs for protecting the gastric mucosa: This type of drug can quickly establish a protective layer for the gastric mucosa, resist acid erosion, and prevent further damage to the gastric mucosa. Common drugs include Sucralfate, Colloidal Bismuth Subcitrate, Maitaolin-S Granules, and others.

　　(3) Controlling Helicobacter pylori infection: Helicobacter pylori is closely related to superficial gastritis, and drugs that kill Helicobacter pylori are beneficial for the treatment of superficial gastritis. Common drugs include Omeprazole, Metronidazole, Amoxicillin, Clarithromycin, Bismuth potassium citrate, and others. Generally, three to four drugs are used in combination to enhance the effect of clearing Helicobacter pylori.

　　(4) Drugs for controlling and improving bile reflux: Bile reflux can cause gastritis by destroying the gastric mucosal barrier, so drugs such as Stomach Comfort, Antivert, Metoclopramide, Cisapride, and Cholestyramine can be used for treatment to control and improve bile reflux.