Chronic atrophic gastritis

　　The incidence of chronic atrophic gastritis is very high, and the cause is not yet clear, which may be related to the following factors:

　　(1) Genetic factors: According to Varis' survey, the incidence of chronic atrophic gastritis in the first-generation relatives of patients with chronic atrophic gastritis is significantly increased, and the genetic factors of pernicious anemia are also very obvious. The incidence rate among relatives is 20 times higher than that of the control group, indicating that chronic atrophic gastritis may be related to genetic factors.

　　(2) Continuation of chronic superficial gastritis: Chronic atrophic gastritis can develop from chronic superficial gastritis. Reports from the General Hospital of the People's Liberation Army and other 6 hospitals show that among 164 cases of superficial gastritis followed up for 5 to 8 years, 34 cases (20.7%) transformed into chronic atrophic gastritis. The etiology of chronic superficial gastritis can all become pathogenic and aggravating factors for chronic atrophic gastritis.

　　(3) Metal contact: Workers in lead operations have a high incidence of gastric ulcers, and gastric mucosal biopsy findings show an increased incidence of chronic atrophic gastritis. Polmer calls it excretory gastritis. In addition to lead, many heavy metals such as mercury, tellurium, copper, and zinc also have certain damaging effects on the gastric mucosa.

　　(4) Radiation: Radiation therapy for peptic ulcer disease or other tumors can cause damage to the gastric mucosa, even atrophy.

　　(5) Iron deficiency anemia: Many facts show that iron deficiency anemia is closely related to chronic atrophic gastritis. Badanoch reported that among 50 cases of iron deficiency anemia, normal gastric mucosa, superficial gastritis, and atrophic gastritis accounted for 14%, 46%, and 40% respectively. However, the mechanism by which anemia causes gastritis is still unclear. Some scholars believe that gastritis is the primary disease because low gastric acid in gastritis leads to poor absorption of iron, or because of gastric bleeding leading to anemia; another opinion is that anemia occurs first because iron deficiency in the body affects the renewal rate of the gastric mucosa and makes it easy to develop inflammation.

　　(6) Biological factors: The influence of chronic infectious diseases such as hepatitis and tuberculosis on the stomach has also attracted people's attention. Chronic liver disease patients often have symptoms and signs of chronic gastritis, and gastric mucosal staining also confirms the presence of hepatitis B virus antigen-antibody complexes in the gastric mucosa of hepatitis B patients. The Renji Hospital reported that among 91 patients with atrophic gastritis, 24 cases (26.4%) had chronic hepatitis. Therefore, the influence of chronic infectious diseases, especially chronic liver disease, on the stomach deserves attention.

　　(7) Constitution factors: Clinical statistics show that the occurrence of the disease is significantly positively correlated with age. The older the age, the worse the function of the gastric mucosal 'resistance', and it is easy to be damaged by external adverse factors.

　　(8) Immune factors: In chronic atrophic gastritis, especially in patients with corpus gastritis, it is often found that parietal cell antibodies or intrinsic factor antibodies can be found in the blood, gastric juice, or plasma cells in the atrophic mucosa, therefore, it is believed that autoimmune reaction is related to the etiology of chronic atrophic gastritis. In recent years, it has been found that a few patients with antral gastritis have gastrin-secreting cell antibodies, which are special autoimmune antibodies of the IgG system. Some patients with chronic atrophic gastritis have abnormal results in vitro lymphocyte transformation tests and white blood cell migration inhibition tests, indicating that cell immune response also plays an important role in the occurrence of chronic atrophic gastritis.

　　1. Gastric ulcer: Gastric ulcer coexists with superficial gastritis and erosive gastritis, with obvious inflammatory stimulation, gastric mucosal atrophy becomes thin, and complications such as erosion and ulceration occur. It is necessary to undergo gastroscopy in a timely manner to avoid delay in diagnosis and treatment.

　　2. Gastric hemorrhage: Gastric hemorrhage in atrophic gastritis is not uncommon: mucosal atrophy becomes thin, blood vessels become visible, rough food abrasion, mucosal erosion and hemorrhage, mainly manifested as black stools. If the hemorrhage is large, it may suddenly vomit blood, and severe cases may have dizziness, palpitations, dark vision, profuse sweating, and even shock.

　　3. Anemia: After a large amount of bleeding in atrophic gastritis, two types of anemia may occur:

　　(1) Megaloblastic anemia, also known as pernicious anemia, patients have anemia symptoms, such as dizziness, fatigue, palpitations, and pale complexion.

　　(2) Iron deficiency anemia, which is caused by chronic blood loss; secondly, due to reduced food intake and malnutrition in patients with atrophic gastritis; thirdly, due to lack of gastric acid;

　　4. Precancerous stage of gastric cancer: According to the World Health Organization, in areas with a high incidence of gastric cancer, after 10-20 years of follow-up, the average incidence rate of gastric cancer is 10%, and their development path is: superficial gastritis - atrophic gastritis - intestinal metaplasia or atypical hyperplasia - gastric cancer. The canceration of atrophic gastritis is closely related to gastritis-related hyperplasia. There are two types of atrophic gastritis that are prone to canceration: 1. Atrophic gastritis with pernicious anemia, the incidence rate of canceration is more than 20 times higher than that of other gastrointestinal diseases, which should be paid attention to by gastrointestinal disease patients. 2. Atrophic gastritis with intestinal metaplasia and severe atypical hyperplasia.

　　Chronic atrophic gastritis usually develops from chronic superficial gastritis, with clinical manifestations including abdominal distension, upper abdominal pain or discomfort, early satiety, which becomes more pronounced with slight overeating, and may even lead to belching, nausea, poor digestion, fatigue, weight loss, anorexia, anemia, and other symptoms. The clinical manifestations of chronic atrophic gastritis are not specific and do not always correspond to the degree of lesion. In clinical practice, some patients with chronic atrophic gastritis may have no obvious symptoms, but most patients may experience burning, distending, dull pain, or fullness and oppression in the upper abdomen, especially after eating. Symptoms such as loss of appetite, nausea, belching, constipation, or diarrhea may occur, and in severe cases, weight loss, anemia, brittle nails, glossitis, or atrophy of the lingual papillae may occur. A few patients with gastric mucosal erosion may be accompanied by upper gastrointestinal bleeding, among which A-type atrophic gastritis complicated with pernicious anemia is rare in China. This disease has no specific signs, and there may be mild tenderness in the upper abdomen. Most patients with chronic atrophic gastritis have no obvious自觉 symptoms. Those with symptoms also lack specificity. Generally speaking, the following clinical manifestations often occur:

　　(1) The color of the gastric mucosa becomes pale: it is light red, gray yellow, and in severe cases, it is gray white or gray blue. It can be diffused or present as localized patchy distribution, with unclear peripheral boundaries, and can be red and white intermingled, mainly white. It is the earliest microscopic manifestation of mucosal atrophy.

　　(2) Visibility of submucosal vessels: mucosal atrophy makes the submucosal vessels visible. In the early stage of atrophy, there are dark red reticular small vessels in the mucosa, and in severe cases, there are larger blue tree-like veins in the mucosa. The visibility of vessels is an important endoscopic feature of chronic atrophic gastritis. However, it should be noted that when the gastric pressure is too high due to excessive inflation of the gastric base in normal cases, the vascular network of the gastric mucosa can be visible.

　　(3) The mucosal folds are small and even disappear. When gas is injected into the stomach, the folds quickly disappear. After the air is discharged, the folds recover slowly, and there is little gastric secretion. Sometimes the mucosa is dry, and the reflection is weakened.

　　(4) When chronic atrophic gastritis is accompanied by hyperplasia of the gland neck or intestinal metaplasia, the mucosal surface is rough and uneven, showing granular or nodular, and sometimes pseudo-polyps may be formed. However, the characteristic of exposed submucosal vessels is often concealed. Although it is possible to make an initial judgment of intestinal metaplasia under microscopic observation, it must be confirmed by pathological examination of the gastric mucosa.

　　(5) Increased friability of atrophic mucosa, easy to bleed, and may have erosion foci.

　　(6) Chronic atrophic gastritis may be accompanied by the manifestations of chronic superficial gastritis, such as congestion and erythema, mucous adhesion, and enhanced reflection. If the changes of superficial gastritis are predominant, it is called superficial atrophic gastritis; if the changes of chronic atrophic gastritis are predominant, it is called atrophic superficial gastritis.

　　With the wide application of inspection instruments, if chronic atrophic gastritis can be detected early and treated correctly in time, the atrophic glands can be restored, which has changed the previous understanding that chronic atrophic gastritis is irreversible.

　　Controlling emotions is very important in preventing chronic atrophic gastritis.

　　There are many factors affecting chronic atrophic gastritis, especially emotional factors such as anger, worry, fear, or being anxious all day long, pessimistic and disappointed, mentally depressed, and easily annoyed, etc. These factors are bound to cause endocrine disorders in the body, functional disorders of the internal organs, decreased immune function, which not only promotes the progression and aggravation of the disease, but also affects the normal therapeutic effect.

　　Therefore, it is necessary to cultivate an optimistic attitude, be patient and determined during treatment, and do everything possible to exclude and avoid factors that stimulate the disease.

　　Do not forget healthy eating to prevent atrophic gastritis.

　　Maintain regular eating habits, have a moderate diet, do not overeat or undereat, do not eat food that irritates the stomach, and opt for easily digestible and nutritious food. Promote smoking and alcohol cessation, pay attention to rest and good sleep, moderately engage in physical exercise, enhance physical fitness, improve the quality of life, and it is conducive to the recovery of the disease.

　　In addition to emotions and diet, attention should also be paid to the following points:

　　First, regular check-ups, and gastroscopy when necessary.

　　Second, in case of symptoms such as exacerbation, weight loss, anorexia, melena, etc., it is necessary to seek medical attention in a timely manner.

　　Third, moderate drinking, do not smoke, to avoid the damage of nicotine to the gastric mucosa; avoid long-term use of anti-inflammatory and analgesic drugs.

　　Fourth, the food eaten should be fresh and nutritious, ensuring sufficient intake of protein, vitamins, and iron. Eat on time, avoid overeating and under-eating, do not eat cold or hot food, and use or minimize the use of刺激性调味品 such as chili powder.

　　(I) Laboratory examination

　　① Gastric juice analysis: Patients with type A CAG often have no acid or low acid, while patients with type B CAG can have normal or low acid.

　　② Pepsinogen measurement: Pepsinogen is secreted by chief cells. In chronic atrophic gastritis, the content of pepsinogen in blood and urine decreases.

　　③ Serum gastrin measurement: G cells in the gastric antrum secrete gastrin. In patients with type A CAG, serum gastrin is often significantly increased; in patients with type B CAG, the atrophy of the gastric antrum mucosa directly affects the function of G cells to secrete gastrin, resulting in serum gastrin being lower than normal.

　　④ Immunological examination: the measurement of parietal cell antibody (PCA), intrinsic factor antibody (IFA), and gastrin-releasing cell antibody (GCA) can be used as auxiliary diagnostic methods for chronic atrophic gastritis and its classification.

　　(II)

　　Gastroscopy and biopsy are the most reliable diagnostic methods. Gastroscopy diagnosis should include the location of the lesion, degree of atrophy, intestinal metaplasia, and degree of atypical hyperplasia. Normal gastric mucosa is orange-red,呈灰白、灰黄或灰绿色 when atrophic, with mucosa showing alternating red and white, predominantly white. Severe cases may have scattered white plaque-like folds, which become finer or flat. The range of atrophy of the gastric mucosa is also inconsistent, with some being diffuse, some localized, and even small focal lesions. Submucosal blood vessels are a feature of atrophic gastritis, and red reticular small arteries or capillaries can be seen. In severe atrophic gastritis, there may be epithelial cell hyperplasia forming fine granules or larger nodules. There may also be mucosal erosion and bleeding. After atrophy of the glands, the glandular pits may hyperplasia and elongate or show signs of intestinal metaplasia, with the mucosal layer becoming thicker. At this time, submucosal blood vessels cannot be seen, and only the rough and uneven mucosal surface, granules, or nodules are visible, with a sense of stiffness and a change in luster.

　　Gastric mucosal biopsy mainly shows varying degrees of atrophy of the固有腺体, thickening of the mucosal muscle layer, inflammation of the固有膜, formation of lymphoid follicles, and metaplasia of pseudo-pyloric glands or intestinal glands in place of them.

　　Chronic atrophic gastritis is a common digestive system disease, more common in middle-aged and elderly people. The clinical manifestations of chronic atrophic gastritis include upper abdominal fullness, discomfort, or pain, which are more obvious after meals, accompanied by other symptoms of poor digestion, such as belching, acid regurgitation, nausea, vomiting, and loss of appetite. Sometimes, due to the destruction of gastric factors, poor absorption of vitamin B12 can lead to anemia. Endoscopy and biopsy are the only means to diagnose chronic atrophic gastritis. The formation of this disease is related to poor dietary habits, smoking, drinking, bile reflux, low immunity, and Helicobacter pylori infection.

　　Patients with chronic atrophic gastritis have a thinning gastric mucosa, reduced secretion of gastric acid, poor gastric motility, low digestive function, and poor nutrient absorption ability. Therefore, medication alone cannot completely work, and nutritional treatment should be combined. Food should be eaten at regular intervals and in moderate portions, and it is advisable to eat foods rich in protein with low fat content, avoiding hard and irritating foods. Avoid eating foods that are too cold or too hot, and use fewer or no irritant seasonings. When there is little gastric acid, some acidic foods can be eaten in moderation. Meat soup, chicken soup, fish soup, etc., can not only increase appetite but also stimulate the secretion of gastric acid, increasing the concentration of gastric acid.

　　Carbonated drinks are actually a solution of carbon dioxide in water (with sugar and spices). By sealing in about 2-3 atmospheres of carbon dioxide in the sugar water, some of the carbon dioxide gas will dissolve in the water, forming carbonic acid in the water. The stimulating taste of carbonated drinks is due to the carbonic acid.

　　In the scorching summer heat, people like to drink ice-cold carbonated drinks. This is because the temperature of ice-cold carbonated drinks is lower, and they contain more carbon dioxide, making them feel cooler and more refreshing. Although carbonated drinks can quench thirst and relieve summer heat, they should not be drunk in large quantities at one time, otherwise they will dilute the gastric juice, reduce the digestive ability and bactericidal action of the gastric juice, and affect appetite. Large amounts of ice-cold carbonated drinks can cause abdominal pain due to the strong cold stimulation to the stomach, and may even trigger gastritis. Spicy foods mainly include chili, pepper, mustard powder, ginger, curry powder, and slightly less irritating garlic, Sichuan pepper, and scallions. Eating a moderate amount of spicy food can adjust the taste and enhance appetite. However, patients with atrophic gastritis should avoid spicy foods.

　　Eating spicy food and carbonated drinks at the same time can cause bloating in the stomach, as a large amount of carbonated drinks can lead to stomach bloating. Spicy food is irritating to the gastric mucosa and can cause increased stomach pain. It is a basic principle for chronic gastritis patients to avoid cold, spicy, and hard-to-digest foods. Patients with chronic atrophic gastritis with hyperplasia and intestinal metaplasia should not smoke, drink strong tea, or strong alcohol. The taste should be light, and foods with too much salt should not be eaten. It is also important to pay attention to food hygiene and avoid using drugs that irritate the stomach.

　　(1) General treatment: For patients with chronic atrophic gastritis, regardless of the cause, they should abstain from smoking and drinking, avoid using drugs that damage the gastric mucosa such as Aspirin, Indomethacin, Erythromycin, etc. Diet should be regular, avoid hot, salty, and spicy foods. Actively treat chronic infections in the mouth, nose, and throat.

　　(2) Treatment with weak acid: Patients with hypochlorhydria or achlorhydria confirmed by the pentagastrin test can take a moderate amount of vinegar. 1 to 2 spoons per time, 3 times a day; or 10% dilute hydrochloric acid 0.5 to 1.0 ml, taken before or during meals, while taking pepsin hydrochloride mixture, 10 ml per time, 3 times a day; or you can choose to take DPP or Pancreatin tablets for treatment to improve the symptoms of dyspepsia.

　　(3) Treatment against Helicobacter pylori: In chronic atrophic gastritis, the decrease or absence of gastric acid allows bacterial proliferation in the stomach, especially the high detection rate of Helicobacter pylori. The use of antibiotic drugs has a certain therapeutic effect on improving the symptoms of chronic atrophic gastritis. The commonly used method for clearing Helicobacter pylori is: Trisodium dicitrate bismuth (TDB De-NOL), 120 mg per time, 4 times a day, taken for 4 to 6 weeks; Amoxicillin capsules, 0.5 g per time, 4 times a day; Furazolidone (Tetramidine) 100 mg, 3 to 4 times a day. These drugs not only clear Helicobacter pylori but also help to alleviate and eliminate concomitant active gastritis. Other drugs with therapeutic effects on Helicobacter pylori include Gentamicin, Berberine, Metronidazole, Tetracycline, Norfloxacin, etc.

　　(4) Inhibition of bile reflux and improvement of gastric motility: Cholestyramine can complex bile salts refluxing into the stomach, preventing bile acids from destroying the gastric mucosal barrier. The dosage is 3 to 4 grams per time, 3 to 4 times a day. Sucralfate can combine with bile acids and lysophosphatidylcholine, and can also be used to treat bile reflux. The dosage is 0.5 to 1 gram, 3 times a day. Ursodeoxycholic acid (UDCA) can also be administered, 100 mg per time, 3 times a day. Stefaniwsky believes that the most toxic bile acids to the gastric mucosa in bile are deoxycholic acid and lithocholic acid. In the gastric juice of patients with bile reflux, bile acids are mainly cholic acid and deoxycholic acid, with UDCA accounting for only 1%. Taking UDCA, the bile acids in the gastric juice are mainly UDCA (can account for 43±15%), while the concentrations of cholic acid, deoxycholic acid, and lithocholic acid are significantly reduced, thereby reducing the damaging effects of the latter two on the gastric mucosa. Medications such as Metoclopramide, Domperidone, Cisapride can enhance gastric peristalsis, promote gastric emptying, assist in the movement of the stomach and duodenum, prevent bile reflux, and regulate and restore gastrointestinal motility. Specific application methods: Metoclopramide 5 to 10 mg, 3 times a day; Domperidone 10 mg, 3 times a day; Cisapride 5 mg, 3 times a day.

　　(5) Adding Mucosal Nutrition: Acacia frangipani leaf ester can increase the renewal of the gastric mucosa, improve the cell regeneration ability, enhance the resistance of the gastric mucosa to gastric acid, and achieve the protective effect of the gastric mucosa, with a dose of 50-60mg, taken three times a day. It can also be chosen to take活血素, with a dose of 80-90mg per day; or choose to take sucralfate, urea, gasterone, prostaglandin E, and others.

　　(6) Pentagastrin and Hormones: Pentagastrin, in addition to promoting the secretion of hydrochloric acid by parietal cells and increasing the secretion of pepsinogen, also has a significant proliferative effect on the gastric mucosa and other upper gastrointestinal mucosa. It can be used to treat chronic atrophic gastritis patients with low or no acid or atrophic corpus of the stomach, with a dose of 50μg, intramuscular injection half an hour before breakfast, once a day. After three weeks, it is changed to every other day. In the fourth week, it is changed to twice a week. Thereafter, once a week, with a course of 3 months.

　　The onset of chronic atrophic gastritis is related to autoimmune factors, so short-term prednisone can be tried as immunosuppressive therapy. This method is particularly suitable for chronic atrophic gastritis patients with PCA positivity and pernicious anemia, but the clinical effect is not very definite.

　　(7) Other Symptomatic Treatments: Including antispasmodic analgesics, antiemetics, digestive aids, anti-anxiety, and improving anemia. For anemia, if it is due to iron deficiency, iron supplements should be taken. For macrocytic anemia, supplementation with vitamin B12 or folic acid is given according to the deficiency. The method is vitamin B12, 50-100μg/day, for 20-30 days; folic acid 5-10mg, three times a day, until symptoms and anemia are completely resolved.

　　(8) Surgical Treatment: Chronic atrophic gastritis patients over middle age, if ulcers, polyps, bleeding, or even no obvious lesions are found during treatment or follow-up. However, if there are moderate to severe atypical hyperplasia in the pathological examination of gastroscopy, partial gastrectomy can be considered in combination with the patient's clinical condition. Early gastric cancer may be detected in the resection specimens of these patients.