Chronic gastritis in the elderly

　　The causes of senile chronic gastritis are numerous and can be divided into non-specific and specific. Non-specific gastritis is the most common, while specific gastritis refers to the mucosal inflammatory changes caused by various bacteria (tuberculosis, syphilis), viruses (cytomegalovirus, herpes virus, HIV), parasites (ameba, schistosoma), and fungi (candida, histoplasma, cryptococcus, mucor). The pathogenesis of chronic gastritis caused by different reasons is as follows:
　　1. Helicobacter pylori
　　Helicobacter pylori (HP) is spiral-shaped and has flagellar structures. The detection rate of HP in patients with chronic gastritis is related to the activity of gastritis. Research data from outside China shows that the detection rate of HP in patients with chronic active gastritis is relatively high, reaching up to 90%, while it is lower in patients with non-active lesions. The detection rate of HP in different parts of the gastric mucosa is not completely the same. The detection rate in the antrum is higher than that in the corpus. There is no significant relationship between HP infection and the clinical symptoms of chronic gastritis. The detection rate of HP in asymptomatic chronic gastritis can be as high as 35% to 72%, while in patients with obvious chronic gastritis symptoms, the detection rate of HP may not be very high. The severity of clinical symptoms is related to various factors. However, more research data show that the pathological and histological changes of gastritis are related to the severity of HP infection. The severity of inflammation in the gastric mucosa is related to the number of HP infections. The mechanisms of action of HP on the gastric mucosa include several aspects:　　
　　2. Immune factors
　　In patients with chronic gastritis mainly characterized by atrophic gastritis, serum parietal cell antibodies (PCA) and intrinsic factor antibodies (IFA) can often be detected. Both are autoantibodies, and their detection rate is quite high in patients with atrophic gastritis complicated with pernicious anemia. Chronic gastritis gradually extends from the superficial layer to the glandular area, followed by the destruction and reduction of glands leading to atrophy.
　　3. Chronic superficial gastritis
　　The inflammatory cell infiltration of superficial gastritis is limited to the surface of gastric pits and the superficial layer of the lamina propria of the mucosa, while the glands remain intact. The inflammatory cells are mainly adenocytes and lymphocytes, with occasional eosinophils. The lamina propria commonly shows edema, congestion, and even focal hemorrhage. There is no destruction of gastric glands and no reduction in the number of glands. There may be mucosal erosion, mucus accumulation, congestion and edema of the lamina propria, and even focal hemorrhage. The superficial epithelial cells become flattened, and their arrangement is often irregular. According to the degree of inflammation, superficial gastritis can be divided into mild, moderate, and severe. The inflammatory cell infiltration is limited to the upper 1/3 of the gastric mucosa for mild cases, exceeding 1/3 but not more than 2/3 of the full layer for moderate cases, and reaching the full layer for severe cases.
　　4, Chronic atrophic gastritis
　　The pathological changes of chronic atrophic gastritis include not only the lesions of chronic superficial gastritis, but also involve the glands, gland atrophy, a decrease in the number of glands, and common thickening of the mucosal muscle. Due to gland atrophy or disappearance, the gastric mucosa becomes thinner to varying degrees.
　　In the gastric mucosa of chronic atrophic gastritis, there are often pyloric gland metaplasia (pseudo-pyloric glands) and intestinal gland metaplasia. The glands in the gastric body and fundus mucosa contain parietal cells and chief cells. Once such cells disappear, the glands become mucous glands and are similar to pyloric glands, and are then called pyloric gland metaplasia. In chronic gastritis, intestinal gland metaplasia is also very common. During chronic superficial gastritis, intestinal metaplasia can appear in the superficial layer of the mucosa. During atrophy, it is possible that all gastric mucosal glands are replaced by intestinal gland metaplasia. Intestinal metaplasia often starts from the top of the gastric pit, and can extend upwards to the superficial epithelium and downwards to the deep part of the glands. Initially, it may be focal, and as the lesion progresses, intestinal metaplasia can connect into a sheet.

　　If elderly chronic gastritis is complicated with gastric mucosal erosion, it may be accompanied by upper gastrointestinal bleeding, mainly manifested as melena; chronic atrophic gastritis may cause poor digestion and absorption, weight loss, and megaloblastic anemia when the gastric body atrophies.

　　The most common symptoms of chronic gastritis are upper abdominal pain and fullness. In contrast to peptic ulcer disease, it is more comfortable on an empty stomach, but uncomfortable after eating, which may be due to dysfunction of accommodation and relaxation, feeling full even though not much food is eaten. Patients often complain of 'weak stomach' or 'soft stomach'. Symptoms are often caused or exacerbated by cold food, hard food, spicy food, or other irritant foods. These symptoms are not easily relieved by antacids or antispasmodics. Most patients report loss of appetite.

　　In addition, bleeding is also one of the symptoms of chronic gastritis, especially when combined with erosion. It can be recurrent small amount of bleeding, or even massive bleeding. Emergency gastroscopy suggests that acute and chronic gastritis account for 20% to 40% of the causes of upper gastrointestinal bleeding. Bleeding is often manifested as melena, usually stops spontaneously after 3 to 4 days, and can recur after several months or years. The pathological changes of gastritis are not consistent with the symptoms. There are two possibilities for the discrepancy between symptoms and biopsy findings: ①Blind biopsy may not have reached the lesion site, and the positive rate of biopsy under direct vision of fiberoptic gastroscopy has reached 80% to 90%; ②The symptoms may not originate from the stomach, but may be caused by diseases of the liver, gallbladder, and biliary system. Moreover, the issue of asymptomatic 'healthy people' with positive biopsies should still be diagnosed as gastritis. Because many diseases can be asymptomatic or have mild symptoms, such as ulcers, liver cirrhosis, liver cancer, and lung cancer, which are discovered only after health checks. Therefore, it is not surprising that some patients with gastritis have no symptoms. According to clinical studies, the infection of HP (Helicobacter pylori) and the severity of clinical symptoms are not significantly related.

　　Elderly people should remove the causes of acute gastritis as early as possible, avoid using non-steroidal anti-inflammatory drugs such as aspirin and indomethacin alone, and treat chronic infections in the oral cavity and throat as soon as possible. For patients with chronic liver, biliary diseases, uremia, or systemic diseases, treatment should be aimed at the primary disease. It is necessary to avoid hard, cold, spicy, rough, and irritating foods, not to overindulge in alcohol, and to regulate diet, making it easy to digest, regular, and quantitative, while ensuring the supply of nutrition.
　　In elderly life, it is best to avoid mental stress, maintain an open-minded attitude, and stable emotions, which are conducive to the prevention and treatment of gastritis and can regulate the function of the digestive system; pay attention to the combination of work and rest and changes in climate, do not catch a cold. During an attack, avoid physical labor and night shifts, and severe patients can also take appropriate rest; in terms of diet, avoid raw, cold, sour, spicy, hard, and fried foods, eat small and frequent meals, process coarse grains finely, and this will help stabilize the condition and prevent acute onset or recurrence of the disease; patients should quit smoking, alcohol, and strong tea habits.
　　Lifestyle adjustment:
　　1. Foods should be easy to digest, eat small and frequent meals, process coarse grains finely, and try to minimize the stimulation to the gastric mucosa.
　　1. Develop the habit of eating slowly and chewing thoroughly. Quit drinking and smoking.
　　2. Control the amount of food intake during meals, do not overeat due to favorite foods, and make sure to eat small and frequent meals to enhance nutrition and reduce the burden on the stomach.
　　3. Avoid eating and taking drugs that strongly stimulate the gastric mucosa, quit smoking and alcohol. Pay attention to dietary hygiene and prevent overeating and overdrinking.
　　

　　According to symptoms such as postprandial upper abdominal fullness, pain, and thick, greasy tongue coating, the presence of gastritis may be suspected. However, for a definitive diagnosis and further clarification of the location and extent, it is necessary to undergo gastroscopy and histological examination. It is also essential to exclude peptic ulcer disease, gastric cancer, chronic liver disease, and chronic cholecystopathy, and one should not be satisfied with a diagnosis of gastritis. Referring to the Sydney classification of chronic gastritis, the diagnosis of chronic gastritis should include etiology, site of lesion, histomorphology (including inflammation, activity, atrophy, intestinal metaplasia, and the presence of Helicobacter pylori), and grading of the lesion (none, mild, moderate, severe). In parallel with histology, classification and grading of endoscopic findings should also be performed.
　　1. Laboratory Examination
　　1. Gastric acid In superficial gastritis, the level of gastric acid is normal or slightly low, whereas in atrophic gastritis, it is significantly reduced, and fasting often shows no acid.
　　2. Pepsinogen Secreted by chief cells, it can be detected in gastric juice, blood, and urine. The level of protease is basically parallel to gastric acid. However, chief cells are more numerous than parietal cells, so in pathological conditions, the secretion of gastric acid is often lower than that of pepsinogen. Joske observed that the level of pepsinogen in gastric juice and blood often corresponds to the results of histological pathological changes, and those with low pepsinogen levels often have atrophic gastritis on histological examination.
　　3. Intrinsic Factor (IF)IF is secreted by parietal cells, and a decrease in IF secretion is also associated with a decrease in parietal cells, indicating a strict parallelism between the two. The normal secretion level is an average of 7700U/h. The examination of IF is helpful for the diagnosis of atrophic gastritis, gastric atrophy, and pernicious anemia. A significant reduction in IF is conducive to the diagnosis of the above three diseases.
　　4. Gastrin Gastrin is secreted by G cells in the antrum. Gastrin can promote the secretion of gastric juice, especially gastric acid. Due to feedback, the secretion of gastrin increases when the gastric acid is low, and decreases when the gastric acid is high. In addition, the level of serum gastrin is closely related to whether there is a lesion in the antral mucosa. Patients without acid should have increased gastrin, but if it is not high, it indicates severe lesions of the antral mucosa with a decrease in G cells.
　　5. Parietal cell antibody (PCA)PCA has a higher positive rate in type A gastritis, and the detection of this antibody is helpful for the classification of chronic gastritis, and is helpful for understanding the pathological process and treatment of chronic gastritis.
　　6. Gastrin secretion cell antibody (GCA)
　　II. Other auxiliary examinations
　　1. Endoscopic examination Generally, the endoscopic findings of superficial gastritis are macular erythema like the skin of a measles patient (or called red and white intermingled), and in the vertical part of the small curvature, it is linear erythema at the top of the longitudinal folds; followed by increased mucus secretion, adhering to the mucosa and not easily peeled off, often causing redness or erosion of the mucosal surface after falling off, the swallowed or regurgitated mucus often contains bubbles and flows with peristalsis, which is not difficult to distinguish; followed by edema, with pale mucosa, obvious small depressions, and strong reflection; finally, erosion, due to the erosion of the epidermis above the glandular pit, often accompanied by bleeding, and can be divided into 3 types: ① Papular elevation with central depression covered with dark brown effusion or white scab, surrounded by erythema like skin lesions of smallpox, often occurring at the top of the folds in the antrum. ② Flat type almost consistent with the level of the mucosa, with an uneven surface covered with brown or white secretions. ③ Concave type is the most common, lower than the normal mucosa. The surface is rough or has secretions or even bleeding, with a range or large or small, a few millimeters to several centimeters, often irregular in shape. It may be localized or diffused. The endoscopic examination of atrophic gastritis has two prominent findings: ① Color change, often gray, gray-white, gray-yellow, or gray-green, the depth of the same area may be inconsistent, the boundary is often unclear, the range may be large or small. There may also be residual red spots in the atrophic area. ② Due to the thinning of the mucosa and the inflation, the submucosal blood vessels are often visible, with mild vascular networks and severe branching like tree branches. Dark red with a slight blue tinge, easy to confuse with folds, can be distinguished according to the direction of the blood vessel course perpendicular to the long axis of the stomach.
　　2. X-ray examination Surface gastritis shows no positive findings on X-ray. Atrophic gastritis may show small or absent folds, and reduced tension.

　　Older people with stomach problems should follow the following dietary principles:
　　1. Prefer mild and precise:Mildness means not to eat too much at one time and not to overeat. It is not advisable to drink water when extremely thirsty, and to drink water in moderate amounts. Dinner should be light. Precision refers to eating less rough and fibrous foods, especially for patients with poor digestion, who require food to be well-prepared and rich in nutrition.
　　2. Prefer mild and clean:It is advisable for patients with stomach problems to avoid overeating cold fruits and vegetables, and not to consume hot and烫 food due to fear of coldness, as this can also cause great damage to the esophagus and stomach. Cleanliness refers to the fact that people with stomach problems have poor stomach resistance, and they should prevent food from being contaminated, and pay attention to the hygiene of eating utensils.
　　3. Fresh and light:Fresh refers to eating a moderate amount of fresh vegetables and fruits, which can prevent cancer, and also refers to eating fresh food, not eating decayed and deteriorated food. Light refers to eating light vegetarian food. In traditional Chinese medicine, light taste is considered to nourish the stomach. Light vegetarian food is easy to digest and absorb, and conducive to the recovery of gastric diseases, and can also make people live a long life. Fresh vegetables and grains are all good for the stomach, but they should not be eaten in excess.
　　4. Soft and slowIt is advisable to eat soft foods such as rice, vegetables, and fish, which should be soft and not fried, fried, or half-cooked, nor hard foods, as they are difficult to digest and may cause damage to the gastric meridians. It is advisable to chew slowly and thoroughly, with a large amount of saliva secretion, which is beneficial for the digestion and absorption of food and can also have the effects of preventing cancer and anti-aging.

　　There is no effective treatment for senile chronic gastritis. Generally, it is advocated that asymptomatic patients do not need treatment. If symptoms occur, the following methods can be referred to for treatment:
　　I. Treatment
　　1. Diet therapy
　　The cause should be eliminated, such as the long-term consumption of strong liquor, strong tea, strong coffee. Those with a habit of eating sour, spicy, or hot food should quit. Easy-to-digest foods such as milk, fresh fruits, and vegetables should be consumed, and pickled foods should not be eaten, and the intake of salt should be reduced. Nutrients such as beta-carotene, vitamin C, vitamin E, folic acid, and antioxidant vitamins, as well as trace elements such as zinc and selenium, may help reverse atypical hyperplasia and intestinal metaplasia of the gastric mucosa.
　　2. Eliminate the cause
　　Gastritis caused by the use of hormone drugs and non-steroidal anti-inflammatory drugs. First, stop the use of drugs that stimulate. For gastritis caused by oral infections, anti-inflammatory treatment should be administered. For patients with systemic diseases, treatment of the primary disease should be carried out, such as: heart failure, diabetes, uremia.
　　3. Drug treatment
　　(1) Eradication of HP (Helicobacter pylori) infection: Since HP infection is a pathogenic factor for chronic gastritis and a risk factor for tumor occurrence, it is very important to eradicate HP.
　　Due to the low HP environment in the stomach, most antibacterial drugs have low activity and cannot penetrate the mucus layer to reach the bacteria, making it difficult to eradicate HP infection. The treatment plans for eradicating HP can be roughly divided into two major categories: those based on proton pump inhibitors (PPI) and those based on colloidal bismuth agents. One is PPI combined with clarithromycin, amoxicillin, or tetracycline, metronidazole, or tinidazole. Two of the three antibacterial drugs make up a triple therapy. The other is colloidal bismuth agents combined with two of the aforementioned antibacterial drugs.
　　There are reports that the resistance rate of HP strain to metronidazole is rapidly increasing. The antibacterial effect of furazolidone against HP is enhanced. HP is not easy to produce resistance, and furazolidone can replace metronidazole, with a dose of 200mg/d, taken twice a day. H2R can be used instead of PPI to reduce costs, but the efficacy is also reduced. For patients who fail to respond to initial treatment, a quadruple therapy combining PPI colloidal bismuth agent with two antibacterial drugs can be used. One week is a course of treatment, and the percentage of HP-negative after one course of treatment is the clearance rate. A re-examination 4 weeks after discontinuation of medication is necessary. The absence of HP infection is the eradication rate. Since HP is classified as a type I carcinogen, eradication of HP treatment is very important.
　　(2) Increase gastric motility drugs: Gastric motility is an important factor that promotes gastric emptying, promotes digestion, and maintains normal physiological function. If the motility is weakened, it can cause symptoms such as bile reflux, nausea, belching, bloating, early satiety, etc. Gastric motility drugs can be taken.
　　4. Optimal Treatment Plan
　　The occurrence of chronic gastritis is closely related to Helicobacter pylori infection. Currently, it is internationally recognized that HP is classified as a class I carcinogen. Therefore, the eradication of HP treatment is very important in the treatment of chronic gastritis and the prevention of tumors. Currently, it is reported abroad that the resistance of HP to metronidazole is gradually increasing and has been gradually eliminated. On the other hand, some patients have gastrointestinal reactions to metronidazole, so it is not suitable for first-line treatment. Two treatment plans are recommended:
　　(1) Bismuth potassium citrate + furazolidone + amoxicillin. Two weeks is one course of treatment.
　　(2) PPI (proton pump inhibitor) + furazolidone + clarithromycin + bismuth potassium citrate. One week is one course of treatment.
　　Bismuth potassium citrate 480mg/d, furazolidone 0.2/d, amoxicillin 2.0/d, PPI 40mg/d, clarithromycin 0.5-1.0/d, among which the second method is used for the radical HP treatment after the failure of the first treatment plan.

　　II. Prognosis
　　In the long-term course of chronic gastritis, the condition is sometimes good and sometimes bad, but most have no obvious progression, only a few patients have persistent symptoms that are difficult to heal, and there is progressive histological change. Although chronic gastritis has the evolution process of superficial inflammation → atrophy → intestinal metaplasia → atypical hyperplasia → gastric cancer, this process is extremely slow, and it can be completely cured if detected at the early stage of gastric cancer, and surgery or endoscopic resection can be performed. It is an undeniable fact that chronic atrophic gastritis can lead to cancer, with a cancer rate of 2% to 10% or more, but this process can last up to 10 years, and only total atrophic gastritis is closely related to gastric cancer, mainly developing into intestinal-type gastric cancer, while the relationship between local atrophy and gastric cancer has not been confirmed. Close monitoring is required for chronic atrophic gastritis, and endoscopy is the best method, and attention should be paid to multi-point biopsy of suspicious lesions. For patients with total atrophic gastritis, follow-up should be carried out once every 6 to 12 months, the interval between follow-up should be appropriately extended for local atrophy, and superficial inflammation does not require emphasis on endoscopic examination.