Chronic gastritis in the elderly
Introduction
Introduction to chronic gastritis in the elderly Chronic gastritis (chronicgastritis) refers to chronic inflammation or atrophic lesions of the gastric mucosa caused by repeated action on different causes. The essence is that after the gastric mucosal epithelium suffers repeated damage, due to the specific regeneration ability of the mucosa, the mucosa is remodeled, and eventually the irreversible intrinsic gastric gland shrinks or even disappears. basic knowledge The proportion of illness: 0.03% Susceptible people: the elderly Mode of infection: non-infectious Complications: anemia, upper gastrointestinal bleeding, abdominal pain, gastric perforation
Cause
Causes of chronic gastritis in the elderly
Helicobacter pylori (30%):
Helicobacter pyloi (HP) is infected with HP in a spiral shape and has a flagellar structure. The detection rate of HP in patients with chronic gastritis is related to the activity of gastritis. Research data at home and abroad indicate that HP is detected in patients with chronic active gastritis. The rate of outflow is high, up to 90%, and the rate of non-active lesions is lower. The detection rate of HP in different parts of the stomach is not exactly the same. The detection rate of gastric antrum is higher than that of the stomach, HP infection and There is no obvious relationship between the clinical symptoms of chronic gastritis. The detection rate of HP in asymptomatic chronic gastritis can be as high as 35% to 72%. However, in patients with obvious chronic gastritis, the detection rate of HP is not necessarily high, because of the severity of clinical symptoms. Many factors are related, but more research data show that the histopathological changes of gastritis are related to the severity of HP infection. The severity of inflammation of gastric mucosa is related to the number of HP infection. The mechanism of action of HP on gastric mucosa includes several aspects: 1HP has a spiral shape with a flagella structure, which can move freely in the mucus layer and closely contact with mucosal cells to directly invade the gastric mucosa.
2 the production of a variety of enzymes and metabolites, such as urea acid and metabolite ammonia, superoxide dismutase, proteolytic enzymes, phospholipase A, etc., can destroy the gastric mucosa.
3 cytotoxin can cause cell vacuolation.
4HP antibody can cause autoimmune damage, HP infection can also damage the gastric mucosal protective barrier, a large number of neutrophil inflammatory infiltration to form a glandular abscess, causing chronic changes in gastric mucosa.
Immunity factor (20%):
The detection of parietal cell antibody (PCA) and endogenous factor antibody (IFA) in serum of chronic gastritis patients with corpus atrophy, both of which are autoantibodies, is comparable in patients with atrophic gastritis with pernicious anemia. high.
(1) PCA antibody: PCA is present in blood and gastric juice. The PCA in serum is mainly IgG or IgA. The antigen is present on the microvilli membrane of the parenchyma of parietal cells. PCA is cell-specific and only reacts with parietal cells. No species specificity, the positive rate of PCA in patients with pernicious anemia can reach more than 90%. In patients with atrophic gastritis without pernicious anemia, the positive rate of PCA can reach more than 90%, without atrophy of pernicious anemia. In patients with gastritis, the positive rate of PCA is between 20% and 60%, but the detection rate is low in domestic reports. The serum PCA titer decreases or even disappears in 4-6 months after total gastrectomy. PCA can also be detected in a few healthy people. Out, the positive rate is 2% for those under 20 years old, and 16% for those over 60 years old. In addition, the positive rate of PCA in other autoimmune diseases is 20% to 30%.
(2) IFA: IFA belongs to IgG in serum, IFA can be divided into "blocking" antibody (type I) and "binding" antibody (type II). Type I antibody can block vitamin B12 and internal binding after binding with internal factors. The factors form a complex, so that vitamin B12 can not be absorbed, the latter binds to the internal factor vitamin B12 complex to block their absorption in the ileal wall, and the positive rate of type I IFA in patients with pernicious anemia is 53%, type II IFA The positive rate is about 30%. IFA is present in the serum and gastric juice of the patient. However, the antibody in the gastric juice is stronger, and the antibody in the blood is weak. The presence of IFA in the blood does not determine whether or not the absorption of vitamin B12 is disordered. IFA has Specificity is usually only seen in patients with gastric atrophy and pernicious anemia.
(3) Gastrin-secreting cell antibody: Patients generally believe that type A atrophic gastritis has little to do with immune factors, but in 1979, Vandelli, et al found that some patients with type A atrophic gastritis have gastrin-secreting cell antibodies (GCA). ), is an autoantibody against gastrin cytoplasm, 8 of 106 patients are positive, and 35 of A-type atrophic gastritis and 51 cases of pernicious anemia are negative. The pathogenic role of GCA is still unclear. More research data confirmed.
(4) duodenal reflux pylorus: sphincter dysfunction can make duodenal juice reflux, while duodenal juice contains bile, intestinal fluid and pancreatic juice, change the acidic environment of gastric mucosa, weaken the barrier function of gastric mucosa, The gastric mucosa is susceptible to the damage of gastric juice pepsin. Bile salts can reduce the permeability of the gastric mucosal barrier to ions. Bile salts can stimulate G cells to release gastrin in the antrum of the stomach, increase gastric acid secretion, and H+ through the damaged mucosa. Barrier anti-dispersion into the gastric mucosa causes inflammation changes, bile reflux gastritis, occurs in the antrum of the stomach.
(5) Bacterial and viral infections: Inflammation of the gastric mucosa after acute gastritis can be repeated to form chronic gastritis. The bacteria and toxins of the oral and sinus lesions can be swallowed into the stomach for long-term stimulation to form chronic inflammation.
(6) Dietary factors: long-term heavy drinking, spicy food, rough food, long-term chronic stimulation, long-term use of hormones, non-steroidal drugs, can cause chronic gastritis.
(7) Other factors: The elderly are prone to chronic atrophic gastritis. Some people even think that chronic atrophic gastritis is a kind of senile change, which may be related to a certain degree of degenerative changes in the gastric mucosa, malnutrition caused by insufficient blood supply, and low secretion function. And mucosal barrier dysfunction factors, in addition, gastric mucosal trophic factors, such as gastrin, reduction of epidermal growth factor, etc. is also one of the causes of chronic gastritis, chronic diseases, right heart failure, cirrhosis portal hypertension, and Diseases such as uremia also make the gastric mucosa susceptible to damage.
Pathology: Chronic gastritis is a process that gradually spreads from superficial to deep, to glandular destruction, followed by gland destruction and reduced atrophy.
Chronic superficial gastritis (20%):
The inflammatory cell infiltration of superficial gastritis is confined to the surface layer of the gastric pituitary and mucosal lamina propria, and the gland is intact. The inflammatory cells are mainly glandular lymphocytes, occasionally eosinophils, and the intrinsic membrane is often edematous, hyperemic, and even foci. Sexual hemorrhage, no damage to the glandular gland and decreased number of glands, may have mucosal erosion, mucus accumulation, intrinsic membrane congestion and edema, and even focal hemorrhage, superficial epithelial cells become flat, the arrangement is often irregular, superficial according to the degree of inflammation Gastritis can be divided into mild, moderate and severe, inflammatory cell infiltration is limited to the upper third of the gastric mucosa is mild, inflammatory cells exceed 1/3 of the mucosa but not more than 2/3 of the full layer is moderate Inflammatory cells infiltrate to the full layer is severe.
Chronic atrophic gastritis (10%):
Pathological changes of chronic atrophic gastritis include lesions of chronic superficial gastritis, lesions also involve glands, glandular atrophy, number decreased, mucosal muscles are often thickened, and gastric mucosa has varying degrees due to atrophy or disappearance of glands Thinning.
In the gastric mucosa of chronic atrophic gastritis, pyloric gland metaplasia (false pyloric gland) and intestinal gland metaplasia are common, and the glands of the corpus and body bottom mucosa contain parietal cells and main cells, once such cells disappear The gland becomes a mucous gland and is similar to the pyloric gland. It is called pyloric gland metaplasia. In chronic gastritis, intestinal gland metaplasia is also very common. In chronic superficial gastritis, intestinal superficial metaplasia can occur in the superficial mucosa. In the case of atrophy, it is possible that all glands of the gastric mucosa are replaced by intestinal metaplasia. The intestinal metaplasia often begins at the top of the stomach, and the upward development can extend to the superficial epithelium, which can be moved down to the gland. In the deep, it can be focal at first. As the lesion progresses, the intestinal gland metaplasia can be connected into pieces.
Intestinal metaplasia is mainly composed of absorbing cells and goblet cells. The former is the absorption cells of the small intestinal mucosa, the free surface has a striate edge, and the latter contains acidic mucus. According to the morphology of the intestinal epithelial cells and the composition of mucus and enzymes involved. Chemical characteristics, the intestinalization is divided into complete and incomplete types, complete intestinalization contains absorption cells, goblet cells and Pameth cells, trehalase, leucine aminopeptidase, alkaline phosphatase, invertase , maltase staining is positive, goblet cells do not contain sulfuric acid mucus, but oxygenated acetylated sulphonic acid mucin (o-acetyl sialomucin) and sulfuric acid mucus, like the large intestinal mucosa, it is also called large intestine intestinal, large intestine Intestinalization is related to the occurrence of gastric cancer. It is considered to be a precancerous lesion of gastric cancer. The degree of atrophy of chronic atrophic gastritis is also divided into mild, moderate, severe, mild: normal gastric mucosal thickness, only a few or focal gland atrophy, The glandular reduction is no more than 1/3 of the original, moderate: the gastric mucosa becomes thinner, the gland is arranged disorderly, because there is an increase in connective tissue in the membrane, the mucosal muscles are thickened, the gland is reduced by about half, and the severity: the gastric mucosa is obviously changed. Reduce more than half of the gland, mucosal muscle thickening.
In atrophic lesions, such as hypertrophy of the glandular neck or intestinal metaplasia, a granular lesion is formed on the surface of the gastric mucosa, called atrophic proliferative gastritis.
Prevention
Elderly chronic gastritis prevention
Chronic gastritis is preventable, and good habits are the key to prevention.
Primary prevention: keep the mouth clean and avoid swallowing, throat, oral lesions bacteria or viruses invading the stomach, causing bacterial or viral infection, but the amount of drinking hard alcohol, strong tea, coffee, less kimchi and too hot, too hard, Rough food, eat less spicy food, do not over-smoking, such as taking drugs that are irritating to the stomach, such as aspirin, non-steroidal anti-inflammatory drugs, need to take after meals, reduce the stimulation of the stomach on the drug, pay attention to diet In the nutrition, intake of enough protein and vitamins.
Secondary prevention: early gastroscopy for early abdominal distension, belching, acid reflux, nausea, early satiety, loss of appetite, anemia, weight loss, glossitis, tongue atrophy, diarrhea, early diagnosis, early and timely Radical cure, regular review of patients with improved symptoms.
Tertiary prevention: Patients with clear diagnosis should be treated aggressively to eliminate the cause and prevent complications, especially for patients with chronic atrophic gastritis, hypertrophic gastritis, and patients with intestinal metaplasia. Find precancerous lesions and take early treatment to prevent the disease from worsening.
Community intervention: In the prevention of the elderly, we should give full play to the advantages of the community, visit the elderly living in the community regularly, and find elderly people with digestive tract symptoms, upper abdominal discomfort, loss of appetite, anemia, abdominal distension, and weakness. Timely early inspection, and at the same time do a good job of publicity activities on health knowledge, such as: matters needing attention for the elderly, common sense of food hygiene, removing bad habits, and taking prevention as the main policy, and organizing senior citizens to participate in collective cultural activities to cultivate optimism The attitude of life helps the elderly to solve their difficulties in life.
Complication
Chronic gastritis complications in the elderly Complications anemia upper gastrointestinal bleeding abdominal pain gastric perforation
Anemia, gastric mucosal erosion, upper gastrointestinal bleeding, precancerous lesions, etc.
Symptom
Chronic symptoms of chronic gastritis in the elderly Common symptoms Weakness, loss of appetite, loss of appetite, nausea, pale, sticky, abdominal tenderness, upper gastrointestinal bleeding, dizziness, blackness
The course of chronic gastritis is prolonged, most of which have no obvious typical clinical symptoms. The most common clinical manifestations are upper abdominal fullness discomfort, severe symptoms after eating, and no obvious regular pain, belching, acid reflux, burning sensation, loss of appetite, nausea Vomiting, common in eating cold, hard, spicy or other irritating foods can induce symptoms worsening, some patients may have loss of appetite, dizziness, fatigue, weight loss, anemia, tongue inflammation, tongue atrophy and peripheral neuropathy, such as Abnormal limbs, such as chronic gastritis with gastric mucosal erosion can occur a small amount or a large number of upper gastrointestinal bleeding, urinary tract usually stops after 3 to 4 days, such as long-term bleeding can cause anemia, which type A gastritis loss of appetite, weight loss, Anemia, fatigue, clinical manifestations of peripheral neuropathy are more serious, the clinical manifestations of chronic gastritis are often inconsistent with the pathological changes of the mucosa, and can not reflect the true condition of the disease to do a series of clinical examinations to determine the condition.
Clinical signs
The signs of chronic gastritis are not typical. Some patients have a feeling of tenderness in the upper abdomen when examining the body. For example, when the chronic gastritis is acute, the signs are more obvious. In particular, the severity of gastritis cannot be judged from the signs, which can be used as an aspect to distinguish from other diseases.
2. Classification
As early as 1728, Stahl first proposed the concept of chronic gastritis. In the middle of the 20th century, Schindler classified chronic gastritis into superficial, atrophic, hypertrophic gastritis and gastritis with other diseases according to gastroscopic morphology. The so-called hypertrophic gastritis was used in the past. The gastroscopy diagnosis has not been confirmed by biopsy pathology. Therefore, the term has been abandoned. Wood has classified chronic gastritis into superficial, atrophic and gastric atrophy. The study of gastritis has been deepened since the advent of fiber gastroscope. Whitehead, 1973 From the pathological point of view, according to the location, degree, activity and the presence or absence of intestinal gland metaplasia, in 1973, Strickland et al. advocated the detection of chronic atrophic gastritis as type A based on the detection of serum-cell antibody in the lesion site. Gastric inflammatory disease, wall cell antibody positive) and type B (antral sinusitis, wall cell antibody negative), in 1982 China's chronic gastritis academic conference divided it into chronic superficial gastritis, chronic atrophic gastritis, 1990 Misiewice et al. Endoscopic findings and biopsy pathology combined with the Sydney system classification method, which shows that there are many classification methods for chronic gastritis, so far A, only in respect of the following Strickland Sydney classification and classification systems make a profile (Table 2).
Examine
Examination of chronic gastritis in the elderly
1. Determination of gastric acid
Superficial gastritis gastric acid secretion can be normal or slightly reduced, while atrophic gastritis gastric acid is significantly reduced, its acid secretion function with the atrophy of the gastric gland, the degree of intestinal gland metaplasia is reduced.
(1) pentapeptide gastrin gastric acid secretion test: subcutaneous or intramuscular injection of pentagastrin (6 g / kg body weight) can cause the maximum acid secretion of the stomach, thereby making a rough estimate of the number of parietal cells in the gastric mucosa, The amount of acid for 1 h after stimulation with pentagastrin was the maximum acid amount (MAO), and the sum of the highest acid amount of 2 consecutive 15 min times 2 was the peak acid amount (PAO). According to the domestic literature, the normal human MAO, PAO value For 16~21mmol/h, the number of parietal cells is estimated to be 700-800 million, which is slightly less than that of westerners. The MAO and PAO values can be reduced in chronic gastritis, especially in atrophic gastritis. After stimulation with pentagastrin gastrin, For example, gastric juice pH>7.0 is called no gastric acid, >3.5 is called low gastric acid, and atrophic gastritis is not gastric acid secretion.
(2) Continuous monitoring of pH in the stomach for 24 hours: The pH of the stomach can be continuously measured by the microelectrode in the gastric cavity, and the pH change in the stomach can be understood. The pH of the stomach in normal people is less than 2 in the stomach for 24 hours, the pH after the meal is increased, and the nighttime pH is The lowest, but began to rise in the early morning, chronic gastritis patients with pH> 3 time longer, especially at night, some patients have a long-lasting pH increase after eating, suggesting that gastric acid secretion is reduced in patients with chronic gastritis, because pH represents H+ The activity is not the concentration, so the pH measurement does not reflect the amount of acid, and there is no substitute for MAO and PAO.
2. Pepsinogen determination
Pepsinogen is a digestive enzyme precursor secreted by the fundus. According to its electrophoretic mobility, it can be divided into pepsinogen I and pepsinogen II. The former is secreted by the main cell and cervical mucus cells, and the latter is divided by the aforementioned cells. The Brunner gland, which is also derived from the gastric antrum and duodenum, can be detected in gastric juice, blood and urine, and its activity is basically parallel with gastric acid. The drug that inhibits gastric acid can also inhibit pepsinogen activity. The ratio of serum pepsinogen I and I/II in atrophic gastritis is significantly reduced, and the degree of reduction is opposite to the extent and degree of atrophy of the fundic gland. The results of a biopsy are often consistent. Therefore, the detection of aprotinin is atrophic. The conclusion and follow-up of gastritis has a certain significance.
3. Gastrin determination
Gastrin is secreted by gastric antrum G cells and pancreatic D cells. It is an important paracrine hormone that can stimulate wall cells to secrete hydrochloric acid, improve gastric mucosal blood circulation, nourish gastric mucosa, and maintain gastric cardia tension and prevent stomach. The contents are refluxed to the esophagus and have various physiological functions. The normal human fasting serum gastrin content is 30-120pg/ml, and the serum gastrin level of patients with atrophic gastritis can reflect the degree of antral inflammation in a certain extent. Gastric sinus mucosal inflammation is often severe, gastrin is often reduced, and the gastric antrum mucosa is basically normal, its fasting serum gastrin levels are often increased, gastric atrophy with pernicious anemia, fasting serum gastrin can be as high as 500 ~ 1000pg / ml .
4. Determination of internal factors
Intrinsic factors are secreted by parietal cells, and the decrease of parietal cells also leads to a decrease in the secretion of endogenous factors. Since the amount of internal factors secreted by normal human parietal cells greatly exceeds the amount required to promote the absorption of vitamin B12, gastric mucosal damage in patients with chronic gastritis leads to gastric acid. When the secretion is reduced, the secretion of internal factors can still maintain the body's needs. Because of the anti-inner factor antibody in the serum of patients with gastric atrophy and pernicious anemia, it combines with the internal factor or the internal factor-vitamin B12 complex, resulting in the absorption of vitamin B12. Therefore, the measurement of the internal factors contributes to the diagnosis of pernicious anemia. The detection of the internal factors can be carried out by the vitamin B12 absorption double radionuclide test by intramuscular injection of vitamin B12 while orally taking 57Co-vitamin B12-internal factor and 58 Co. - Vitamin B12, and then the radioactivity of 57 Co and 58 Co in 24 h urine was measured separately. If 58 Co radioactivity was low and 57 Co radioactivity was normal, it indicated the presence of an intrinsic factor deficiency.
5. Autoantibody detection
Patients with squamous atrophic gastritis may be positive for PCA and IFA, which may be helpful for diagnosis. The positive rate of serum IFA is lower than that of PCA. The detection of both is helpful for the classification and treatment of chronic gastritis. In addition, the gastric antrum GCA in patients with atrophic gastritis can be positive, while patients with pernicious anemia are often negative.
6.HP detection
(1) Rapid urease test: In the endoscopy tester, the simplest HP diagnostic method for mucosal biopsy carries out a rapid urease test.
(2) Histopathological section staining: Warthin-Starry silver staining and modified Giemsa staining were the most widely used. HP monoclonal antibody was prepared in several units in China, but its application value was deeply evaluated.
(3) Isolation and culture: Separation and culture positive is HP's gold standard, but its operation is complicated, time-consuming and sensitive, and requires special equipment, making it lack of application value, so it is not a simple diagnostic method.
(4) Polymerase chain reaction (PCR) and related technologies: PCR is considered to be the most sensitive technology for the detection of HP. Several HP/mg tissues can be detected, but the study believes that it is not compared with the isolated culture method. The obvious advantages, and the high technical requirements of PCR, due to its high sensitivity, are also easy to specimen, and the contamination of the device is false positive.
(5) Serology: Serology is a simple and widely used diagnostic method. If the anti-HP-IgG is elevated in untreated patients, it indicates that there is HP infection, which is considered to have the same accuracy as histology. However, when used to judge the therapeutic effect, it should be noted that the positive titer of the antibody after HP eradication can last for 2 years, and the standard ELISA method is recommended for serological diagnosis.
(6) Urea breath test: UBT breath test (UBT) is to detect the actual live HP in the stomach by measuring the activity of urease. It has high sensitivity and specificity compared with other methods, and can detect very small amounts. HP, and is suitable for long-term follow-up after eradication of HP treatment, efficacy judgment.
7. Barium meal inspection
The use of oral tincture to detect the passage of tincture through the stomach under X-ray is characterized by a simple and easy method, which can be generally carried out in clinical practice.
8. Radionuclide imaging
Radionuclide imaging can accurately reflect esophageal transit time, gastric emptying time, intestinal transit time, gastroesophageal reflux, duodenogastric reflux, and is widely used in clinical practice as a gold for gastrointestinal motility examination. The standard", because of its accuracy, non-invasiveness, reproducibility, and physiological requirements, is of great significance for the diagnosis of postprandial discomfort, belching, acid reflux, and gastrointestinal dysfunction.
9.CT, MRI section imaging examination
CT and MRI are clinically applied to the examination of cavity organ diseases in the digestive tract, which is later than the abdominal organ examination. However, due to its tomographic imaging and thin section, high-density resolution makes it a problem for many digestive diseases. Diagnosis provides new information, such as the deep layer structure of the smooth muscle of the esophagus and stomach, and changes in lymph nodes, which have important diagnostic implications.
CT, especially spiral CT and electron beam CT, can obtain three-dimensional data, and can be reconstructed to obtain high-quality images of gastrointestinal lesions. At the same time, it provides reliable signs for the staging of esophageal and rectal tumors. In this respect, the superiority of CT Sex can achieve MRI level, but MRI can perform intrarectal imaging of the rectum, which is beyond the reach of CT. CT can scan the abdominal blood vessels, plus three-dimensional reconstruction, which can provide reliable blood supply to the digestive system. Information, 4. gastroscopy
(1) superficial gastritis: mucosal congestion, edema, variegated red and white changes, and mainly red, or measles-like appearance, with gray or yellow-white secretions attached, may have localized erosion and bleeding point.
(2) Atrophic gastritis: the mucous membrane loses its normal orange-red color, which may be light red, gray, grayish yellow or grayish green, with severe atrophy and grayish white. The color is different in depth, wrinkles are thin and flat, and the submucosal blood vessels are seen like branches. Or mesh, sometimes on the atrophic mucosa to see the proliferation of epithelial cells, atrophic mucosal fragility increased, easy to hemorrhage, there may be erosion.
(3) chronic erosive gastritis: also known as verrucous gastritis or pox-like gastritis, it is often associated with peptic ulcer, superficial or atrophic gastritis, can also occur alone, mainly in the presence of multiple gastric mucosa Braided, swollen or papular-like bulge, diameter 5 ~ 10mm, mucosal defect or umbilical depression at the top, erosion in the center, no redness around the bulge, but often accompanied by erythema of similar size, more common in the stomach sinus, It is a persistent type and a disappearing type. It is a special type of gastritis in the Sydney system classification of chronic gastritis. The endoscopic classification is bulging erosive gastritis and flat erosive gastritis.
Diagnosis
Diagnosis and diagnosis of chronic gastritis in the elderly
Diagnostic criteria
In 1990, Misiewice and Tytgat proposed a new classification of gastritis at the 9th World Congress of Gastroenterology in Sydney. It consists of two parts: histology and endoscopy. The histology is centered on the lesion. Basic diagnosis: 1 acute gastritis; 2 chronic gastritis; 3 special types of gastritis, and prefixed by etiology and related factors, morphological description as suffix, and degree of inflammation, mobility, atrophy, intestinal metaplasia and HP infection respectively Grading, the endoscopic part is mainly based on the description of the naked eye, and distinguishes the degree of lesions. Seven endoscopic gastritis diagnoses are established. This classification incorporates the etiology, related pathogens, histology and endoscopy into the diagnosis. Chronic gastritis is divided into atrophic and superficial, and glandular atrophy is regarded as one of the pathological changes of chronic gastritis, which makes the diagnosis more comprehensive and complete, and is also conducive to the standardization of clinical and pathological research. However, the Sydney classification is not typical. Proliferative precancerous lesions are included, and clinically accurate etiological diagnosis is difficult to achieve, so there are still further questions (Table 3).
The preferred method for the diagnosis of chronic gastritis is endoscopic and gastric mucosal biopsy. The complete diagnosis should include: 1 etiological diagnosis; 2 endoscopic diagnosis; 3 histological diagnosis; 4 pathophysiological diagnosis, such as acid secretion, gastric motility , Helicobacter pylori, etc.
The incidence of chronic gastritis is very high. One is because there are many causes of gastric mucosal inflammation. Many factors are difficult to avoid completely; the second physician has insufficient understanding of endoscopic and histological changes of gastric mucosal inflammation, lacking uniform standards, resulting in There is inflammation everywhere in the endoscope. Any mucosal inflammatory cell infiltration is inflammation. This chapter simply defines the normal gastric mucosa in histology and endoscopy. It needs further research in the future, especially the need to establish normal age groups. Gastric mucosal standards.
The symptoms of chronic gastritis are non-specific, and many digestive tract diseases can occur. The diseases to be identified include peptic ulcer, gastroesophageal reflux disease, early gastric cancer, cholecystitis, gallstones, etc. Non-erosive gastritis is non-ulcerative digestion. The bad category is divided into reflux type, ulcer type, movement disorder type, special hairstyle and so on.
