chronic gastritis
Introduction
Introduction to chronic gastritis Chronic gastritis (chronicgestritis) refers to chronic inflammation or atrophic lesions of the gastric mucosa caused by different causes. The essence is that after repeated damage of the gastric mucosa epithelium, due to the mucosal specific regenerative capacity, the mucosa is remodeled and eventually leads to irreversible intrinsic The atrophy of the stomach gland even disappears. The disease is very common, accounting for 80-90% of patients undergoing gastroscopy. Men are more than women, and the incidence increases with age. Chronic superficial gastritis, atrophic gastritis, and chronic erosive gastritis are the two most common chronic gastritis. The clinical incidence of chronic gastritis in children and chronic gastritis in the elderly has gradually increased in recent years. basic knowledge The proportion of illness: 15% Susceptible people: no special people Mode of infection: non-infectious Complications: gastric bleeding anemia iron deficiency anemia gastric ulcer gastric cancer
Cause
Causes of chronic gastritis
It has been clarified that Hp infection is the most important cause of chronic gastritis. Some people call it Hp-related gastritis, but other physical, chemical and biological harmful factors can cause this disease for a long time. Chronic lesions can be formed by persistence or recurrence. A random sampling method for gastric mucosal examination in rural Finland confirms that chronic atrophic gastritis is a chronic progressive disease with superficial inflammation and eventually irreversible atrophy. Inflammation, from clinical observations, there is also evidence to explain this problem. Young people are mostly superficial gastritis, and the elderly are mostly atrophic gastritis; superficial gastritis and atrophic gastritis often exist in the same patient at the same time; Mucosal biopsy has also found that some superficial gastritis can become atrophic gastritis after several years. It is currently believed that chronic gastritis is caused by many factors.
Helicobacter pylori infection (20%):
In 1982, Marshall and Warren first isolated a micro-aerobic, catalase-positive, Gram-negative spirochete with urease activity, 3 m × 0.5 m in size, curved or S-shaped, with 2 to 6 sheaths at one end. Flagella, active gastritis 95% of this bacterial infection, originally named Campylobacter-like microorganism (CLO), later renamed pylobacter pylori, in 1989 changed its name to pyloric screw according to its biochemical and morphological characteristics Bacteria, we have confirmed through clinical studies that the detection rate of Hp in chronic active gastritis is 98%-100%, indicating that chronic gastritis, especially chronic active gastritis is closely related to Hp infection, Marshall, 1985, Morris II, 1987 Humans themselves as volunteers oral Hp caused acute gastritis, cured by antibiotic treatment, in 1987 Lam bert successfully established an animal model of Hp gastritis with suckling pigs, so Hp has basically met Koch's criteria for pathogenic bacteria.
The main mechanism of Hp causing gastritis is as follows:
1. Hp is spiral and has a flagella structure, which can move freely in the mucus layer.
2. Hp has a target site on the mucus, which can bind to the glycoprotein and glycolipid targets of epithelial cells and mucus.
3, close contact with mucosal cells, and "attachment pedestal"-like structure with epithelial cells, so that the microvilli fall off and the cytoskeleton is destroyed.
4, the production of a variety of enzymes and metabolites, such as urease and its products ammonia, superoxide dismutase, proteolytic enzymes, phospholipase A2 and C, our experiments confirmed that Hp positive individuals gastric mucosa and gastric juice ammonia is significantly higher than Hp Negative individuals, indicating that urease hydrolyzes large amounts of urea in the stomach to produce large amounts of ammonia, which can cause significant gastric mucosal damage in animal experiments.
5. Cytotoxin can cause vacuolar degeneration of cells.
6. After Hp infection, gastric epithelial cells release IL-1, 8 and other cytokines and TNF2 factors, causing neutrophils to migrate from the blood vessels to the gastric epithelium and activate them, which can release metabolites and proteolytic enzymes. It can damage the gastric mucosa, and it can also cause activation of monocytes, basophils, eosinophils, etc., further aggravating the damage of the gastric mucosa.
7. Immune response: Hp infection can cause or aggravate the formation of gastritis by cellular immunity, humoral immunity (production of antibodies) and induction of autoimmune reactions in the body.
Due to the infection of Hp, a large number of mononuclear cells infiltrate in the lamina propria, and the destruction of epithelial cells is directly proportional to the degree of bacterial infiltration and the closeness of bacterial contact with cells. When neutrophils appear, they are indicators of inflammatory activity, and surface mucus disappears. Cell degeneration and necrosis, a large number of neutrophils pass through the glandular neck into the glandular fossa, forming a glandular abscess (tubular), which greatly affects the regeneration of the gland. When the neutrophil infiltration is obvious, the bacteria and cells The decrease in contact rate may be the result of an immune response, and the surface of the bacteria is surrounded by IgG to prevent contact with the cells.
Genetic factors (10%):
The genetic predisposition of type A gastritis (gastric gastritis) Vars and Siurala have done a lot of work. They found that the incidence of gastritis in the first-degree relatives of pernicious anemia is significantly higher than that of the general population. The risk of severe atrophic gastritis is random. 20 times of the population, they believe that it plays an autosomal dominant gene. The study of gastric antrum gastritis also shows family aggregation. Therefore, the genetic susceptibility of the human body plays a role in the pathogenesis of chronic gastritis. .
Age (10%):
Clinical statistics show that the incidence of chronic gastritis is significantly positively correlated with age. The older the age, the worse the gastric mucosal function, the "resistance", and the damage caused by external adverse factors.
Smoking (10%):
The incidence of gastritis in severe smokers can be increased. Eward found that 40% of people who smoked more than 20 cigarettes per day had gastric mucosal inflammation, and Oddson et al's gastric mucosal biopsy also showed this link.
Drinking (10%):
Beaumont passed the first observation of alcohol in patients with stomach cramps to produce flaky flushing of the gastric mucosa. Later, it was confirmed by gastroscopic observation, but it was restored after stopping drinking. Wood used blind biopsy to observe 51 cases of chronic alcoholics. Superficial gastritis, but it stops when drinking is stopped. If it persists for a long time, it can develop into chronic atrophic gastritis. Palmer also found that soldiers who drink alcohol have superficial inflammation of the stomach. After stopping drinking for 3 weeks, inflammation can disappear. Wolf Through 1006 cases of investigation, it has not been found that drinking is closely related to gastritis. Most cases with inflammation are older, so age is also an important factor in addition to alcohol. Animals with high concentration of alcohol can form acute gastric injury but cannot form. Chronic gastritis, low concentration of alcohol is not only harmless but also protective. It is speculated that low concentration of alcohol can increase the prostaglandin level of gastric mucosa. Prostaglandins have protective effect on gastric mucosa. Our observational materials suggest chronic gastritis drinkers. Not much to see.
Food stimulation (10%):
Various condiments and irritating foods promote the secretion of gastric acid, but have not been proven to cause chronic gastritis.
drug
Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and phenylbutazone can cause gastric mucosal erosion, chronic gastritis can be left behind after erosion, and some antibiotics also have some damage to the gastric mucosa, but there is no evidence that long-term Taking can cause atrophic gastritis.
Iron deficiency anemia
Many facts indicate that iron deficiency anemia is closely related to atrophic gastritis. Badanoch reported 50 cases of iron deficiency anemia, normal gastric mucosa, superficial gastritis and atrophic gastritis accounted for 14%, 46% and 40%, respectively, but anemia caused gastritis The mechanism is still unclear. Some authors believe that gastritis is the primary disease. Because gastritis is low in gastric acid, iron can not be absorbed, or hemorrhage due to gastritis. Another opinion is that anemia is first caused by iron deficiency in the body. The rate is affected by inflammation, or the lack of iron causes the lack of iron-containing enzyme system, affecting the metabolism of gastric mucosa, can be restored after treatment with iron. Some people think that iron deficiency anemia is a syndrome, the reasons are many, except In addition to the above mentioned reasons, it can also be related to immune and genetic factors.
Metal contact
The incidence of gastric ulcer in lead workers is high. According to the author's biopsy of gastric mucosa, the incidence of atrophic gastritis is also increased. Polmer calls it excretion gastritis. Many heavy metals such as mercury, antimony and copper are removed. And zinc and other have a certain damage to the gastric mucosa.
temperature
Cold or overheated foods or beverages or ice water for gastric lavage can cause gastric mucosal damage. Hirai can induce gastritis by feeding animals at 46 °C for a long time. Roshitoshi injects 300 ml of water at 50-58 °C into the stomach. In the first half of the year, at least 72 times, some dogs can cause inflammation of the gastric mucosa. On the contrary, Perry can feed the animals with ice or hot water, which can cause acute inflammation. In severe cases, it can cause death. One survivor has no acid for a long time. Ewards It is found that drinking hot tea is closely related to gastritis. Long-term thermal damage may be a factor in chronic inflammation.
radiation
Radiation therapy for ulcer disease or other tumors can damage or even atrophy the gastric mucosa, but it cannot explain the cause of atrophic gastritis.
Gastric retention
Long-term gastric retention caused by any cause can cause gastritis, often superficial inflammation of the antrum of the stomach, but it can also be widely present.
Duodenal reflux
When performing gastroscopy on patients with chronic gastritis, it is often found that there are yellow-green bile in the mucus pool. In addition, when the pylorus is open, bile reflux can be seen and even sprayed into the stomach. Siurula and Tawast have found sodium taurocholate and other surface tensions in gastric juice. Reduce the substance, these substances are normally present in the bile, because bile reflux into the stomach, indicating that gastritis is closely related to bile, and some people use 99Tc labeled food to observe the reflux of the stomach and duodenum, and found that some patients with gastritis have Backflow, feeding the mice with 0.01% hyodeoxycholic acid, each 25mg/d, can cause chronic atrophic gastritis, or can be used as a gallbladder stomach fistula can also have the same result, Black confirmed that bile can destroy the gastric mucosa The barrier causes gastritis, partial gastrectomy, and bile reflux into the stomach after gastrointestinal anastomosis. The incidence of gastritis is also increased. Lawson has confirmed that reflux of duodenal juice, especially when mixed with pancreatic juice, can form lysolecithin. It has a destructive effect on the gastric mucosal barrier, so some people call it reflux gastritis, de Plessis and determine the pathological diagnostic criteria of reflux:
1. The epithelial hyperplasia is papillary;
2, glandular atrophy - especially the pyloric gland, the glandular fossa is extended;
3, the stomach body pseudo-pyloric gland metaplasia, cupped cells appear;
4, inflammatory cell infiltration;
5, histochemical staining PAS substance reduction, clinical diagnosis is difficult to master, when the gastroscope is found to contain yellow-green bile in gastric juice, and even gastric sinus mucosa yellow stain for clinical diagnosis reference, but the following conditions are required:
(1) No medication is used before surgery;
(2) Patient cooperation, smooth operation, no nausea;
(3) No gas is injected.
Immune factor
In recent years, there have been many reports on the relationship between immunity and chronic special atrophic gastritis. The initial discovery is an intrinsic factor antibody (IFA), which is divided into two types. Type I IFA, also known as blocking antibody, can prevent vitamin B12. Combined with internal factors, B12 can not be absorbed, the positive rate of this antibody in patients with pernicious anemia is as high as 60%, and the positive rate of patients with general atrophic gastritis is very low. Strikland reported that only 70 cases of IFA-positive atrophic gastritis were only in type II, type II. IFA also known as binding antibody, can bind to the internal factor-B12 complex to hinder its absorption. This type of antibody has a positive rate of 30% in patients with pernicious anemia. Although both types of antibodies can interfere with B12 absorption, the antibody in gastric juice is the most effective. Strong, the role of antibodies in the blood is weak, such as the presence of both antibodies, the effect is stronger.
In the past, it was thought that malignant anemia was caused by lack of internal factors, and it was actually mucosal atrophy, IFA positive, and blockade of B12 absorption.
Followed by PCA, Irvin first reported in 1963, PCA in the serum and stomach homogenate of patients with pernicious anemia, the highest positive rate of up to 90%, generally atrophic gastritis in the range of 20% to 60%, the hospital data is 11%, The PCA titer decreased or even disappeared 4 to 6 months after total gastrectomy.
Thyroid disease, diabetes and iron deficiency anemia can also be positive.
In 1979, Vandelli found gastrin-secreting cell antibody (GCA) in patients with type B atrophic gastritis, 8 of which were positive in 106 cases; none of 35 cases were positive in type A, and 51 cases were all negative in malignant anemia (multiple combined type A atrophy) Gastritis), 2 cases of other autoimmune diseases were positive in 121 cases. All the 115 blood transfusions as control were negative. In addition, cell-mediated immunity was also found. Various immune indicators such as lymphocyte transformation, macrophage movement inhibition, various Skin tests and tumor cell killing tests have confirmed the existence of cellular immunity. Animal immune cells and gastric mucosal lesions occur simultaneously, while autoimmune antibodies must appear 4 to 8 weeks after the onset of the disease. Humoral immunity is more important in explaining the pathogenesis.
Injecting allogeneic or heterogeneous gastric juice, gastric mucosa homogenate, PCA or IFA to various animals including rats, rabbits, dogs and monkeys, atrophic lesions can occur in animal gastric mucosa, PCA is positive after 4-8 weeks, stomach acid Low secretion but no obvious inflammatory cell infiltration.
Glass has proposed the hypothesis that the immune response damages the gastric mucosa. Various harmful factors cause damage to the gastric mucosa, release the antigen and sensitize the immune cells to cause an immune reaction. Then the round cells tend to produce the antibody, ie PCA, and the PCA forms antigenic antibodies in the parietal cells. The complex damages the parietal cells, because the cells continue to release the antigen and the antibody is continuously released, causing the inflammation to become chronic. If the reaction continues, the antigen is depleted due to gastric mucosal atrophy (gastric atrophy), and the immune response is also exhausted. Termination, due to low cell turnover rate, resulting in intestinal metaplasia and pseudo-pyloric gland metaplasia.
Other bacteria, virus infection
Various acute infectious diseases can cause acute gastritis. The influence of chronic infectious diseases such as hepatitis and tuberculosis on the stomach has also attracted people's attention. Patients with chronic liver disease often have symptoms and signs of chronic gastritis. Gastric mucosal histochemical staining has also confirmed in patients with hepatitis B. There is an antigen-antibody complex of hepatitis B virus in the gastric mucosa. In 1954, Palmer also suspected that chronic gastritis was associated with hepatitis, but gastric mucosal biopsy was performed on 160 patients with hepatitis, limited to the conditions at the time, and other viral infections such as Herpes simplex virus infection is also associated with gastritis.
According to the above facts, it is not difficult to see that chronic gastritis is formed by various harmful factors acting on susceptible human body. Although the etiology is different and the pathological process may be similar, from mild to heavy, from superficial to atrophy, superficial gastritis inflammatory cell infiltrating gland There are many necks, and pathologically, inflammatory cells can pass through the glandular neck. The author believes that this pathological change is of great significance in the pathological process of gastritis development. The glandular neck is the germinal center of the gland, and the inflammation causes the glandular neck cells. The destruction, the rate of cell renewal, causes irreversible changes in the gland, and eventually forms atrophic gastritis. Therefore, atrophic gastritis can be regarded as the final outcome of various factors causing gastric mucosal lesions.
Pathogenesis
The pathological changes of chronic gastritis are mainly confined to the mucosa, and there are a series of basic lesions. The extent of these lesions can be divided into superficial gastritis and atrophic gastritis.
1, the basic lesions
The pathological changes of chronic gastritis are mainly in the mucosal layer, with the following changes:
(1) Cell infiltration: There is only a very small amount of monocytes in the lamina propria of normal gastric mucosa. If it is obvious that it is pathological, lymphocyte plasma cells are common in chronic inflammation, neutrophils are common in acute inflammation, or chronic inflammation. During the active period, eosinophils are relatively rare.
(2) leukocyte migration (1eucopedesis): between the glandular epithelium or glandular epithelial cells, it can be seen that 3 to 5 clusters of white blood cells move outward, and the surrounding cells are clear, and finally discharged to the glandular fossa or stomach cavity. The phenomenon indicates that inflammation is active.
(3) Cast: There are 3 types of tube:
1 is mainly composed of neutrophils. When acute inflammation occurs, white blood cells migrate and are discharged to the glandular fossa.
2 glandular cell degeneration is discharged into the glandular fossa. It is also believed that the glandular cell cast is artificial. Since the mucosa was squeezed by biopsy forceps during biopsy, the author used the isolated stomach to do the experiment, at the same site, and at the same time with biopsy. The forceps were taken from the forceps and the scalpel. As a result, both tissues had a tube shape, indicating that the tube type was not squeezed by the forceps.
3 Mucous tube type is formed by excessive secretion of mucus and accumulation in the gland.
(4) mitotic figures: 1 mitotic image is seen in every 12 glandular fossa of normal mucosa, mostly in the neck, and mitotic figures increase significantly in inflammation or other injuries, indicating that cell division is accelerated.
(5) cystic changes: due to destruction of the gland, repair, atrophy and fibrosis, obstruction of the neck of the gland, causing secondary simple expansion of the gland to form a sac, occasionally visible in normal, in atrophic gastritis Most often seen.
(6) Capillaries in the neck and glandular fossa of the gland are very fragile. Vasodilatation or hemorrhage can often be seen by the influence of inflammation. Small bleeding spots or hemorrhagic erosion can be seen by the naked eye. For example, a wide range of bleeding can cause the blood vessels of the lamina propria of the neck. Widely ruptured, the former is of little significance, the latter can cause erosion or massive bleeding.
(7) progressive necrosis of the neck of the gland: acute inflammation, postoperative or chronic inflammatory activity, common neck cell necrosis, the range is large or small, while neutrophil infiltration, severe mucosal detachment above the neck, Formation of large or small erosion, common casts in the gland, so the cast is often a clue to neck necrosis.
(8) Glandular atrophy: the number of glands becomes shorter, and the cells of the main cell wall decrease or even disappear.
(9) Fibrosis: The gastric mucosa is also like other mucosa. Fibrosis is the repair process after tissue destruction. It is most common in glandular atrophy. Although the normal lamina propria has a very small amount of collagen fibers and fibroblasts, but no fiber. Performance.
(10) glandular fossa hyperplasia: the glandular layer is distorted, not neat, usually after atrophy of the gland tube.
(11) False pyloric gland metaplasia: After the atrophy of the corpus callosum, a mucous gland similar to the pyloric gland often appears, which is called a pseudo-pyloric gland.
(12) intestinal metaplasia: chronic gastritis, especially atrophic gastritis often accompanied by intestinal metaplasia, a few found in superficial gastritis, occasionally seen in normal mucosa, light and heavy but typical and intestinal villi are no different.
(13) Retention disease: In the lamina propria of the fundus mucosa of patients with hemochromatosis, hemoglobin deposition is observed, but there is no inflammation, pigment is also visible in the main cells, amyloid deposition is observed in the mucosa of patients with amyloidosis, and even The formation of tumor-like nodules, the primary often accompanied by glandular atrophy, but no inflammation, atrophic gastritis or the elderly often have fat deposition.
(14) Lymphoid follicle hyperplasia: normal lymphoid follicles are visible in the mucosal basal part, and lymphoid follicles proliferate after atrophy of the gland, and the surface is nodular.
2, the degree of disease
According to the extent and extent of the disease, chronic gastritis has been divided into superficial and atrophic types in the past. Whitehead believes that these two types of gastritis are different stages of the same pathological process, but the degree of disease is different.
(1) superficial gastritis: the lesion is confined to the upper third of the mucosa, that is, in the glandular layer without affecting the glandular part, due to inflammation, the epithelial layer is degenerated and necrotic, and the severe exfoliation forms erosion or even hemorrhage, and the mitotic image is obvious. Increased, epithelial thickening, most cells infiltrate in the lamina propria, white blood cells migrate, there are various casts in the gland fossa, in addition to congestion or hemorrhage, neck cell necrosis, glandular cell exfoliation to form erosion, occasionally Visible cystic changes.
(2) Atrophic gastritis: The change of inflammation is similar to that of superficial gastritis, but the expansion of the range can affect the whole layer of the mucosa; the main lesion is the reduction or even disappearance of the number of glands, and Whitehead divides the atrophic gastritis into 3 degrees:
One group of 1 to 2 glandular ducts disappeared slightly.
2 All disappeared or only 1 to 2 groups of glands were severe.
3 is moderate between the two (domestic classification see gastric mucosal biopsy).
Plasma cell infiltration is mainly in the upper layer, lymphocytes and follicles are mainly in the lower layer, and most plasma cells belong to IgG. In severe cases, especially those with malignant anemia, plasma cells with IgG are also seen, and Russel is also common (developed from plasma cells). Eosinophils, in which glycoproteins indicate plasma cell dysfunction.
Sometimes glandular atrophy is not obvious, but cell infiltration affects the whole layer of mucosa. Some people call it interstitial gastritis. After atrophy of the gland tube, the space is filled with monocytes. It is often seen that the connective tissue collapses with the reticulum fiber staining. It is easy to determine by this method. The gland is atrophied, and the disappearance of the gland is replaced by a pseudo-pyloric gland that secretes the mucosa.
Intestinal metaplasia is common in atrophic gastritis. In the light, only a small number of cup cells are seen. In severe cases, a large number of typical intestinal villus epithelium can be seen. In addition, there are also Pannet cells and argyrophil cells, and the glandular fissure prolongation and mucosa. The muscles are normal or thickened, and the mucosa is thinned.
The atrophy changes can be very broad, can be expressed as total gastric atrophy, that is, gastric atrophy, can also be limited to one, also known as focal atrophy, in addition to the accumulation of fat cells.
The above-mentioned superficial and atrophic gastritis pathological changes refer to the inflammation of the stomach, such as inflammation occurs in the antrum of the stomach, because the normal gastric antrum mucosa can see more monocytes, determine whether there are inflammatory cells Infiltration is more difficult, Benedict opinion that cell infiltration must be more than 2/3 of the mucosa. It is more difficult to determine atrophic gastritis, because the normal pyloric gland is 1/2 of the entire mucosa, and the gland is short and sparse, so the diagnosis Atrophic gastritis should be sure that one third of the glands disappear. The lesion is confined to the sinus. Some people call it antral sinusitis. This diagnosis can only explain the location of the lesion, and it cannot explain the nature and extent of the lesion.
3, lesion activity
The term activity refers to the infiltration of neutral polymorphonuclear cells into the lamina propria of the gastric mucosa, the pituitary epithelium and surface epithelium. Severe infiltration can form lacuna abscess and epithelial degeneration, mucus formation is reduced, and activity can be dependent on neutrophils. The degree of infiltration is graded. Mild means that infiltration involves 1/3 of the gastric pits and surface epithelium, 1/3 to 2/3 is moderate, and 2/3 or more is called severe. The term "inactive" is Refers to no or few neutral polymorphonuclear cell infiltration.
4, the presence or absence of bacteria
Staining with the Warthin-Starry method, chronic gastritis often has the presence of Hp infection.
There are many classification methods for chronic gastritis, and it is difficult to introduce them one by one. The Schindler, Wood, Whitehead, Strickland classification methods and the classification of the Sydney World Gastroenterology Conference are briefly introduced.
(1) Schindler divides chronic gastritis into primary and secondary. Unexplained patients are primary, with gastric ulcer, gastric cancer and gastric surgery are secondary, primary is divided into superficial , atrophy and hypertrophy type 3, on the problem of hypertrophic gastritis, the results of many years of practice can not be confirmed by biopsy, it is not commonly used.
(2) Wood uses the blind attraction method to take the mucosa, and the chronic gastritis is divided into 3 types: 1 superficial type; 2 atrophic type; 3 gastric atrophy, although this method is simple, but can not be positioned when taking mucous membrane, affecting the accuracy of diagnosis After the fiber gastroscope is gradually promoted, the blind attraction law is about to complete its historical mission.
(3) Whitehead is classified according to the location of the lesion, tissue changes and rapid lesions.
(4) Strickland classifies chronic gastritis into two types, A and B. The basis is: parietal cell antibody (PCA) is positive, inflammation is mainly in type A in the stomach, PCA is negative, and inflammation is mainly in the antrum of the stomach. Type, 100 cases of atrophic gastritis in our hospital found that no matter whether PCA negative or positive inflammation is limited to the gastric antrum or corpus, it is not completely consistent with the Strickland classification. Therefore, this standard is not completely consistent with the domestic situation.
The significance of Strickland classification: 1 to explain the pathogenesis of atrophic gastritis, think that type A gastritis is an autoimmune disease; 2 related to prognosis, type B gastritis has a 10% malignant rate, while type A is less cancerous; Caucasian PCA positive was closely related to malignant anemia, and 16% of patients with malignant anemia were found during follow-up.
(5) In 1988, Wyatt and Dixon classified chronic gastritis into autoimmune, bacterial, and chemical damage.
(6) Sydney World Gastroenterology Society Classification: In August 1990, at the Ninth World Congress of Gastroenterology, Misiewicz et al. proposed the Sydney system, a new classification of gastritis, which is composed of histology and The endoscope consists of two parts. The histology is centered on the lesion and three basic diagnoses are identified:
1 acute gastritis;
2 chronic gastritis;
3 special types of gastritis.
Prescribing the etiology and related factors, the histomorphology is described as a suffix, and the intestinal epithelial metaplasia, inflammation activity, inflammation, glandular atrophy and Hp infection are graded separately, and the endoscopic part is seen by the naked eye. Describe the main, and distinguish the extent of the lesion, determine the diagnosis of 7 endoscopic gastritis:
1 erythema exudative gastritis.
2 flat erosive gastritis.
3 uplifting erosive gastritis.
4 atrophic gastritis.
5 hemorrhagic gastritis.
6 reflux gastritis.
7 wrinkle hypertrophic gastritis.
The Sydney classification incorporates the cause, related pathogens, histology (including Hp) and endoscopy into the diagnosis, making the diagnosis more comprehensive and complete. The items are detailed and require specific, which is conducive to the standardization of clinical and pathological studies of gastritis, but also There are some problems that need to be further resolved: how to resolve the contradictions that are often not completely consistent with clinical diagnosis and pathological diagnosis; endoscopic description requirements are too detailed and specific, although it contributes to the standardization of endoscopic diagnosis, but it is not easy for clinicians to do The cause of chronic gastritis is diverse, and it is difficult to make an accurate diagnosis by a clinician's comprehensive clinical and various auxiliary examinations. Therefore, the cause of the disease as a prefix for histological diagnosis needs further study.
In 1994, 20 pathologists from different countries in the world re-evaluated the four-year Sydney system in Houston for two purposes. One was to establish a unified gastritis standard, and the second was to define the definition and work hard to resolve the system with Sydney. Apply related questions.
In order to accurately determine the presence or absence of Hp, the biopsy site should be performed in at least 5 areas: antral curvature of 2 to 3 cm from the pyloric wheel, small curvature of the antrum (A1, A2); body about 4 cm from the stomach angle Small bend (B1); large curvature of the middle part of the stomach (B2) about 8 cm from the cardia; and stomach angle notation (IA), can be added as needed.
Prevention
Chronic gastritis prevention
1, to maintain a happy spirit: depression or excessive tension and fatigue, easy to cause pyloric sphincter dysfunction, bile reflux and chronic gastritis.
2, harmful components in tobacco can promote the increase of gastric acid secretion, harmful stimulation of the gastric mucosa, excessive smoking can cause bile reflux. Excessive drinking or long-term drinking of spirits can make the gastric mucosa congestion, edema, and even erosion, and the incidence of chronic gastritis is significantly increased. You should quit smoking and avoid alcohol.
3, with caution, avoid using drugs that have damage to the gastric mucosa. Long-term abuse of such drugs can cause damage to the gastric mucosa, causing chronic gastritis and ulcers.
4, active treatment of oropharyngeal infections, do not swallow sputum, nasal discharge and other bacterial secretions into the stomach leading to chronic gastritis.
5, too acidic, too spicy and other irritating foods and cold and difficult to digest food should be avoided, eat slowly, so that the food is fully mixed with saliva, is conducive to digestion and reduce stomach irritation. Diet should be quantitative, nutrient-rich, foods containing more vitamins A, B, and C. Avoid stimulating drinks such as strong tea and espresso.
Complication
Chronic gastritis complications Complications, gastric bleeding, anemia, iron deficiency, anemia, gastric ulcer, gastric cancer
First, stomach bleeding: chronic gastritis hemorrhage is not uncommon: mucosa atrophy and thinning, blood vessels are exposed, coarse food smashing, mucous membrane erosion, black stool as the main performance, if the amount of bleeding can suddenly vomit blood, severe dizziness, Pain, sleep, sweat, and even shock.
Second, anemia: chronic gastritis with a large number of blood loss accompanied by two kinds of anemia:
1, megaloblastic anemia, that is, pernicious anemia, patients with anemia, dizziness, fatigue, palpitations, pale,
2, iron deficiency anemia, one is caused by chronic blood loss; second, chronic gastritis patients eat less, caused by insufficient nutrition; third is the lack of stomach acid.
Third, gastric ulcer: gastric ulcer and superficial gastritis, erosive gastritis, there is obvious inflammatory stimulation, gastric mucosa atrophy and thinning, and erosion, ulcers, should be timely gastroscopy, so as not to delay diagnosis and treatment.
4. Precancerous gastric cancer: According to the statistics of the International Health Organization, in the high incidence area of gastric cancer, after 10-20 years of follow-up, the average incidence rate of gastric cancer is 10%. Their developmental context is: superficial gastritis - chronic gastritis - intestinal metaplasia or not Typical hyperplasia - gastric cancer, cancer of chronic gastritis is closely related to gastritis hyperplasia, there are two cases of chronic gastritis easy to cancer:
1, chronic gastritis with malignant anemia, the incidence of cancer is more than 20 times higher than other gastrointestinal diseases, to cause attention to patients with gastroenterology.
2, atrophic inflammation with intestinal metaplasia and severe dysplasia.
Symptom
Chronic gastritis symptoms Common symptoms Stomach pain, chronic bleeding, gastric mucosal damage, black appetite, loss of indigestion, upper gastrointestinal bleeding, upper abdominal pain, thinness after eating, diffuse...
1, symptoms
The most common symptoms of chronic gastritis are upper abdominal pain and fullness. Compared with ulcer disease, it is more comfortable on the fasting stomach. After meals, discomfort may be due to diastolic dysfunction. Although there are not many foods but fullness, patients often complain of stomach weakness. Or "soft stomach", often caused by cold food, hard food, spicy or other irritating foods or symptoms, these symptoms are not easy to relieve with antacids and antispasmodic drugs, most patients complain of loss of appetite.
In addition, bleeding is also one of the symptoms of chronic gastritis, especially combined with erosion, can be repeated small amount of bleeding, but also for major bleeding, emergency gastroscopy suggests that in the cause of upper gastrointestinal bleeding, acute and chronic gastritis accounted for 20% to 40 %, hemorrhage is more common in black stools, usually lasts 3 to 4 days after the automatic hemostasis, recurrence after several months or years, the pathological changes of gastritis and symptoms are not consistent, Zaveronik found that patients with dyspeptic symptoms confirmed by biopsy 42% of patients with gastritis; on the contrary, health school girls with no stomach symptoms, biopsy confirmed 29% of patients with chronic gastritis, the hospital has similar data, 548 patients with symptoms of stomach disease for blind aspiration biopsy, the results have 58.6% had inflammatory changes, 41.1% had no abnormalities, and there were two possibilities for symptoms to be inconsistent with biopsy:
(1) The blind biopsy failed to obtain the lesion site. At present, the biopsy under the direct view of the fiber endoscope has a positive rate of 80% to 90%;
(2) Symptoms are not caused by the stomach, may be caused by diseases of the liver and gallbladder system, and the asymptomatic "healthy person" biopsy positive problem, should still diagnose gastritis, because many diseases can be asymptomatic or mild symptoms such as ulcer disease, Liver cirrhosis, liver cancer and lung cancer have been discovered after a health check, so it is not surprising that some patients with gastritis are asymptomatic.
According to clinical studies, there is no significant relationship between Hp infection and the severity of clinical symptoms.
2, signs
Most patients have yellow, white thick greasy tongue coating, simple ulcer patients without tongue coating or thin white moss, is the difference between the two stomach diseases, the upper abdomen may have tenderness, a small number of patients are thin, anemia, in addition to no special signs.
3, classification
(1) Chronic superficial gastritis: Chronic superficial gastritis is the most common type of chronic gastritis. It is characterized by upper abdominal pain, most of the pain is irregular, abdominal distension, hernia, repeated bleeding and so on. Most patients are asymptomatic.
(2) Atrophic gastritis: clinical manifestations are not only lack of specificity, but also not completely consistent with the extent of the disease. Clinically, some patients with chronic atrophic gastritis have no obvious symptoms. However, most patients may have burning pain, pain, dull pain or fullness, suffocation in the upper abdomen, especially after eating, loss of appetite, nausea, belching, constipation or diarrhea.
(3) Chronic erosive gastritis: can occur at any age and gender. The onset is often more urgent and heavier, there is bleeding in the upper digestive tract, hematemesis, melena, shock, and often relapse after bleeding stops.
(4) Chronic gastritis in children: the symptoms are not specific, and most of them have different degrees of dyspepsia. The severity of clinical manifestations is not consistent with the degree of gastric mucosal lesions, and the course of disease is prolonged.
(5) Chronic gastritis in the elderly: The usual symptoms may be mild, and some may be discovered when complications such as hemorrhage or cancer appear.
Examine
Chronic gastritis examination
Laboratory inspection
1, stomach acid
Superficial gastritis has normal or slightly lower gastric acid, while atrophic gastritis is significantly lower. Fasting is often acid-free. Burhol used histamine method to observe the maximum gastric secretion of 47 cases of superficial gastritis. The average gastric secretion was 17.4mmol, 46 cases of atrophy. The average gastritis was 5.6 mmol, and the normal control 44 was an average of 19.8 mmol.
100 cases of atrophic gastritis in a hospital, 91 cases of gastric acid by pentapeptide gastrin and histamine method: 13 cases without acid; 18 cases of low acid; 60 cases of normal acid, 31 cases of acid and low acid, accounting for 34.1 %.
2, pepsinogen
Secreted by the main cells, it can be measured in gastric juice, blood and urine. The level of protease is basically parallel with gastric acid, but the main cells are more than the number of parietal cells. Therefore, in the pathological state, gastric acid secretion is often lower than that of proproteinase.
Joske observed that the levels of gastric juice and blood pepsinogen were consistent with the results of histopathological changes. The biopsy of patients with low protease was mostly atrophic gastritis.
3. Internal factor (IF)
IF is secreted by parietal cells, and IF secretion is reduced by parietal cells. The two are strictly parallel. The normal secretion is 7700 U/h. Checking IF is helpful for the diagnosis of atrophic gastritis, gastric atrophy and pernicious anemia. Conducive to the diagnosis of the above three diseases, a small number of patients with pernicious anemia can still detect trace IF in gastric juice, but not enough for vitamin A, B12 absorption, chronic atrophic gastritis IF can also be reduced to 400 ~ 600U, but Can maintain a low level of vitamin B12 absorption, according to Ardeman's study 400 ~ 500U IF can be used to absorb 1g of vitamin B12, food stimulates gastric secretion every 5 ~ 10ml containing IF 400 ~ 500U, so can explain the atrophic gastritis IF Secretion is also low but no pernicious anemia occurs.
4, gastrin
Gastrin is secreted by gastric antrum G cells. The normal serum gastrin content is reported separately (30-140pg/ml). The results of our hospital examination are (130.84±8.34) (SE)pg/ml; superficial gastritis average (219.09±36.04) pg/ml; type A chronic atrophic gastritis averaged (566.22±140.3) pg/ml; type B averaged (246.76±9.52) pg/ml, gastrin can promote gastric juice, especially gastric acid secretion Due to the feedback effect, the secretion of gastrin is low when gastric acid is low, and the secretion of gastrin is low when the stomach acid is high. In addition, the serum gastrin level is closely related to the presence or absence of lesions in the gastric antrum mucosa, and the acid-free patients should have elevated gastrin, but If not high, the gastric sinus mucosal lesions are severely reduced by G cells.
5. Parietal cell antibody (PCA)
The positive rate of PCA in type A gastritis is high. The detection of this antibody is helpful for the classification of chronic gastritis, and it is helpful for the understanding and treatment of the pathological process of chronic gastritis.
6, gastrin secreting cell antibody (GCA)
In 1979, Vandelli examined 106 cases of type B gastritis, 8 cases of GCA-positive, 35 cases of type A were negative, 35 cases of pernicious anemia and 115 cases of blood donors were also negative.
Film degree exam
1, gastroscopy
The Sydney Classification System has a series of provisions for the description of gastroscopy, including descriptions of edema, erythema, fragility, exudation, flat erosion, bulging erosion, nodules, wrinkle hypertrophy, wrinkle atrophy, vascular permeability and bleeding points. Generally speaking, superficial gastritis is seen in the skin of a child with a variegated flush such as measles (or red and white). In the vertical part of the small bend, the line is flushed at the top of the longitudinal fold; followed by mucus Increased secretion, attached to the mucous membrane is not easy to exfoliate, the surface of the mucous membrane often becomes red or erosive after detachment, mucus of swallowing or reflux often contains air bubbles, and flows with creeping, it is not difficult to identify; again is the performance of edema, pale mucous membrane The small concave is obvious and the reflection is strong; the last is erosion, because the exfoliation of the epidermis above the gland is erosive and often accompanied by bleeding, it can be divided into 3 types:
(1) The central depression of the papule-like bulge is covered with dark brown blood or white moss, and the surrounding redness such as the lesion of the smallpox occurs mostly at the top of the antrum of the gastric antrum.
(2) The flat type is almost the same as the mucosal level, and the surface is not smooth and covered with brown or white secretions.
(3) The concave type is the most common, lower than the normal mucosa, the surface is rough or there is secretion or even bleeding, the range is large or small, several millimeters to several centimeters, the shape is often irregular, or limited or diffuse.
There are two outstanding manifestations of atrophic gastritis gastroscopy:
1 color change, mostly gray, gray, grayish yellow or gray-green, the same part of the depth can be inconsistent, the realm is often unclear, the range is large or small, and there may be residual red spots in the shrinkage range.
2 Because the mucous membrane is thin and the gas is inflated, the submucosal blood vessels can often be revealed. The light vascular network is dense, and the branches of the blood vessels such as dendrites can be seen. The dark red microstrips are blue and easy to be mixed with the wrinkles. The long axis of the stomach is vertical and can be identified.
Vascular exposure is closely related to intragastric pressure. According to the test, continuous injection of 2000ml (compressed gas injection button for 2min), if the patient does not have a heating stomach pressure of 20mmHg, the normal gastric mucosa can also reveal small blood vessel network, especially the most stomach It is easy, when the intragastric pressure is 1.3 to 2.0 kPa (10 to 15 mmHg), the medium and heavy type 3 atrophic gastritis can reveal the blood vessels, and when it is 0.66 to 1.33 kPa (5 to 10 mmHg), only the medium and heavy can be exposed and light. It is not revealed that when it is 0 to 0.66 kPa (0 to 5 mmHg), only heavy duty is revealed. According to the above results, the intragastric pressure is 1.3 to 2.0 kPa, and the gas injection amount is about 1000 ml.
The coincidence rate between gastroscopic diagnosis and pathological diagnosis of superficial and atrophic gastritis is 60%-80%. However, there is no consistent rule between gastroscope and pathological findings. It is also difficult to explain the gastroscope-like flushing with pathological changes. Vascular penetration and so on.
2, X-ray inspection
Superficial gastritis was found to be non-positive in X-ray, atrophic gastritis was fine or disappeared, and tension was reduced. Badenoch used X-ray to diagnose gastric atrophy in 88 cases, and 22 cases were correct. Mucosal hyperplasia was easily considered as tumor, antral mucosa The rough disorder is often diagnosed as hypertrophic gastritis but can not be confirmed by biopsy. The double contrast angiography can be used to find the stomach plot (1~1.5mm), thus opening up new avenues for the diagnosis of intestinal metaplasia and papular erosive erosion. .
Diagnosis
Diagnosis and diagnosis of chronic gastritis
diagnosis
According to the patient's symptoms, such as fullness, pain and thick tongue coating after the meal, the existence of suspicious gastritis, but the diagnosis must be confirmed by the endoscopy and biopsy, and must also exclude ulcer disease, stomach cancer, Chronic liver disease and chronic gallbladder disease should not be satisfied with the diagnosis of gastritis.
With reference to the Sydney classification of chronic gastritis, the diagnosis of chronic gastritis should include the cause, location of the lesion, histomorphology (including inflammation, activity, atrophy, intestinal metaplasia, and Hp), and grade the lesion (none, Light, medium, and heavy), parallel to histology, and classified and diagnosed by endoscopic findings.
Differential diagnosis
1, gastric cancer: symptoms of chronic gastritis such as loss of appetite, upper abdominal discomfort, anemia and a small number of gastric sinus gastritis X-ray signs and gastric cancer are quite similar, need to pay special attention to identification, the vast majority of patients with fiber gastroscopy and biopsy can help identify.
2, peptic ulcer: both have chronic upper abdominal pain, but the peptic ulcer above the regularity of the abdomen, periodic pain, while the chronic stomach is less painful and regular dyspepsia, the identification depends on X-ray Barium meal and gastroscope.
3, chronic biliary tract disease: such as chronic cholecystitis, cholelithiasis often have chronic right upper abdomen, abdominal distension, hernia and other dyspepsia, easy to be misdiagnosed as chronic gastritis, but the disease is found without abnormal findings, gallbladder angiography and B-ultrasound An abnormality can be finally diagnosed.
4, other: such as hepatitis, liver cancer and pancreatic diseases can also be due to loss of appetite, indigestion and other symptoms and delay diagnosis and treatment of comprehensive and detailed physical examination and related examinations can prevent misdiagnosis.
