Chronic gastritis

Chronic gastritis is a group of chronic diseases that are morphologically characterized by inflammatory and dystrophic processes, a violation of physiological regeneration and, as a result, atrophy of the glandular epithelium (with progressing course), intestinal metaplasia, and a disorder of the secretory, motor and endocrine functions of the stomach.

[1], [2], [3], [4], [5], [6]

Epidemiology

The disease is widespread, occurs in more than half of the adult population, but only 10-15% of people with chronic gastritis go to the doctor. The share of chronic gastritis accounts for 85% of all diseases of the stomach.

The prevalence of chronic gastritis is estimated as approximately 50-80% of the total adult population; with age, the incidence of chronic gastritis is increasing. The absolute majority of cases of chronic gastritis (85-90%) is associated with Helicobacter pylori infection, the etiological role of which has been proved.

Chronic autoimmune gastritis, characterized by the formation of antibodies to parietal cells and the internal factor of Castle, is 3 times more often observed in women. These patients significantly increased the risk of pernicious anemia.

[7], [8], [9], [10], [11], [12],

Causes of the chronic gastritis

Helicobacter pylori infection is the most frequent cause of chronic gastritis. According to studies, Helicobacteria are the cause of gastritis in 95% of cases.

In 1983 B. Marshall and D. Warren isolated a microorganism called Helicobacter pylori from a biopsy specimen of the gastric mucosa of a patient with an antral gastritis. Helicobacteria are microaerophilic, non-negative bacteria, having a curved S-shaped or slightly spiral shape. The thickness of bacteria is 0.5-1.0 μm, the length is 2.5-3.5 μm. The bacterial cell is covered with a smooth membrane, one of the poles has from 2 to 6 monomeric flagella. Currently, 9 species of Helicobacteria are known. It has been established that Helicobacteria produce a number of enzymes: urease, alkaline phosphatase, glucophosphatase, protease, mucinase, phospholipase, superoxide dismutase, as well as hemolysin, vacuolizing cytotoxin, protein inhibiting the secretion of hydrochloric acid, and adhesion proteins.

Thanks to its structure and the production of the above substances, Helicobacteria can overcome protective barriers in the stomach cavity, attach to the cells of the gastric epithelium, colonize the gastric mucosa, damage it and cause the development of chronic gastritis.

The natural habitat for Helicobacter pylori is mucus of the stomach, in addition, they are often found deep in the gastric fossa, concentrating in the intercellular connections. Helicobacteria also adhere to the cells of the gastric mucosa.

Due to the flagella, the bacteria move with corkscrew movements and contact the gastric epithelium.

The most favorable conditions for the existence of Helicobacter pylori are the temperature of 37-42 ° C and the pH of the gastric contents of 4-6, but bacteria can survive in a medium with a pH of 2.

Two factors contribute to the reduction of colonization of Helicobacter pylori: widespread atrophy of the gastric glands with metaplasia of the gastric epithelium by intestinal type and hypochlorhydria.

Currently, the role of Helicobacter pylori in the development of chronic gastritis is considered proven, chronic gastritis caused by Helicobacter pylori is called Helicobacter pylori or associated with Helicobacter pylori infection. It accounts for about 80% of all types of chronic gastritis.

According to scientific research, H. Pylori causes antral gastritis in 95% of cases, and pangastritis in 56%.

Almost 100% of the relationship between Helicobacter pylori infection, chronic gastritis and peptic ulcers has been established.

Helicobacter pylori infection is very widespread among the population. It is more often detected in the older age group, and at 60 years of age, more than half of the population of developed countries can be infected. In developing countries, the infection spreads to a much greater extent, and the age at which infection begins is much less.

According to the data of the discoverer of Helicobacteria Marshall (1994), in the developed countries H. Pylori is found in 20% of people over 40 years old and in 50% - over 60 years.

It has now been established that the source of the infection is a person - a sick or a bacterial carrier (Mitchell, 1989). Helicobacteria can be found in saliva, feces, plaque. Transmission Helicobacter infection occurs orally-oral, as well as fecal-oral route. Oral-oral contamination is also possible with gastric probing and fibrogastroscopy, if sterilization of endoscopes and probes involves imperfect disinfection methods. Under adverse conditions, Helicobacteria acquire a coccoid form, are at rest and lose the ability to reproduce as a result of a decrease in the activity of enzymes. However, having got into favorable conditions, Helicobacteria again become active.

Chronic Helicobacter gastritis is localized at first in the antral region, then as the disease progresses, the body of the stomach or the entire stomach (pangastritis) is involved in the pathological process.

[13], [14]

Autoimmune factor

Approximately in 15-18% of cases, chronic gastritis is caused by the development of autoimmune processes - the formation of autoantibodies to parietal cells of the gastric mucosa that produces hydrochloric acid and the internal factor of the gastromucoprotein.

Autoimmune gastritis is localized in the fundus of the stomach and its body, in these areas are concentrated parietal cells.

[15], [16], [17], [18], [19], [20]

Duodenogastric reflux

A frequent cause of chronic gastritis is duodenogastric reflux. It is due to the inadequacy of the pyloric closure function, chronic duodenosis and associated with it hypertension in the duodenum.

With duodenogastric reflux, duodenal and pancreatic juice mixed with bile is injected into the stomach, which leads to the destruction of the mucous barrier (primarily in the antrum part of the stomach) and the formation of reflux gastritis. Often such a gastritis develops as a consequence of resection of the stomach and reconstructive operations on the stomach.

[21], [22], [23], [24], [25], [26], [27],

Treatment with gastrointestinal drugs

In some cases, chronic gastritis develops on the background of treatment (especially with prolonged ingestion) with drugs that have a damaging effect on the gastric mucosa and destroy the protective mucous barrier. These drugs include salicylates (primarily acetylsalicylic acid); NSAIDs (indomethacin, butadiene, etc.); potassium chloride; reserpine and preparations containing it; anti-tuberculosis drugs, etc.

Food allergy

Food allergy is often associated with the pathology of the gastrointestinal tract, in particular with chronic gastritis. In patients with food allergies, inflammatory changes in the gastric mucosa are often found, and the number of plasma cells synthesizing immunoglobulins E, G, and M. In biopsy specimens of the gastric mucosa, eosinophilic infiltration and mast cells are found.

Chronic gastritis can develop with food allergies to dairy products, fish, eggs, chocolate, etc. The role of food allergy in the emergence of chronic gastritis is proved by the disappearance of the clinical and histological picture of the disease against the background of elimination of the product - allergen.

[28], [29], [30]

Alment factor

In recent years, after establishing the leading role of Helicobacteria in the development of chronic gastritis, the nutritional factor is not as important as it was before. However, clinical observations suggest that in the development of chronic gastritis, the following factors may have some significance:

• violation of the rhythm of nutrition (irregular, hasty food with insufficient chewing food);
• the use of poor quality food;
• abuse of very spicy food (pepper, mustard, vinegar, adzhika, etc.), especially persons for whom such food is not habitual. It is established that extractive substances significantly increase the production of gastric juice and hydrochloric acid, and with prolonged, long-term use, they deplete the functional capacity of the gastric glands. Marinades, smoked meats, strongly fried dishes with their frequent use can cause chronic gastritis. In experiments on dogs, it was shown that the systematic feeding of red ground pepper caused them first gastritis with increased and then reduced gastric secretion;
• the abuse of very hot or very cold food also contributes to the development of chronic gastritis.

[31], [32], [33], [34]

Alcohol abuse

Alcohol with frequent long-term use causes the development of a superficial, and later - atrophic gastritis. Especially the chances of developing a chronic gastritis with the use of strong drinks and surrogates of alcohol are especially high.

[35], [36]

Smoking

Prolonged long-term smoking contributes to the development of chronic gastritis (the so-called gastritis of smokers). Nicotine and other components of tobacco smoke disrupt the regeneration of the gastric epithelium, first increase, then reduce the secretory function of the stomach, damage the protective mucous barrier.

Influence of occupational hazards

Production factors can cause the development of a professional toxic gastritis. This can occur when ingestion of harmful components contained in the air: coal, metal, cotton and other types of dust, acid vapors, alkalis and other toxic and irritating gastric mucosa.

Effects of endogenous factors

The endogenous factors that cause chronic gastritis include:

• chronic infections (oral cavity, nasopharynx, nonspecific inflammatory diseases of the respiratory system, tuberculosis, etc.);
• diseases of the endocrine system;
• metabolic disorders (obesity, gout);
• deficiency of iron in the body;
• diseases leading to tissue hypoxia (pulmonary and cardiac insufficiency of various origins);
• autointoxication with chronic renal failure (release of toxic products of nitrous metabolism by the gastric mucosa).

Among the endogenous factors, chronic inflammatory diseases of the abdominal cavity are most important due to their considerable prevalence (chronic cholecystitis, pancreatitis, hepatitis, enteritis, colitis). These diseases are accompanied by neural-reflex disorders of the motor-evacuation function of the stomach, reflux of the contents of the duodenum with bile acids and enzymes of the pancreas, damaging the gastric mucosa; reflex disorders of blood circulation in the mucous membrane of the stomach; a direct transition of the inflammatory process to the stomach; intoxication and allergic effects on the gastric mucosa.

The actual cause of chronic gastritis is also endocrine diseases.

With chronic adrenal insufficiency, there is a decrease in gastric secretion and atrophy of the gastric mucosa; with diffuse toxic goiter, gastric secretion first increases, further develops chronic gastritis with a decrease in secretory function; Diabetes mellitus is often accompanied by atrophy of the gastric mucosa; hypothyroidism develops a chronic gastritis with a decreased secretory function; with the disease of Itenko-Cushing and hyperparathyroidism - with increased secretory function.

Probably, with endocrine diseases, at first develop marked dystrophic changes in the mucous membrane, a violation of its secretory function, and in the future - inflammation.

Among all the above-named causes of chronic gastritis, the most significant and reliable are Helicobacter pylori infection and autoimmune factors; accordingly it is allocated Helicobacter and autoimmune gastritis.

[37], [38], [39], [40], [41], [42]

Pathogenesis

Pathogenesis of Helicobacter pylori

Helicobacteria enter the lumen of the stomach with contaminated food, with swallowed saliva or from the surface of an insufficiently disinfected gastroscope, a gastric tube.

In the stomach there is urea, it penetrates from the bloodstream by sweating through the wall of the capillaries. Under the influence of the enzyme urease helikobakterii from urea formed ammonia. Ammonia neutralizes hydrochloric acid of gastric juice and creates around the helicobacteria a local alkaline medium, which is very favorable for its existence.

In addition, under the influence of the mucinase enzyme, released by helicobacteria, the mucin protein contained in the gastric mucus is destroyed. As a result, a zone of local decrease in the viscosity of gastric mucus is formed around the helicobacteria.

Thanks to the environment of ammonia and the local zone of mucus with reduced viscosity, as well as spiral shape and high mobility of Helicobacter pylori from the lumen of the stomach, they easily penetrate into the layer of protective mucus and adhere to the integumentary pit epithelium of the antral part of the stomach. Part of Helicobacter pylori penetrates into lamina propria through interepithelial spaces.

Further helikobakterii pass through a layer of protective mucus and reach the mucous membrane lined with mucus-forming epithelial cells, as well as endocrine cells that produce gastrin and somatostatin.

Only on the surface of the mucus-forming cells of the cylindrical epithelium there are receptors for Helicobacterial adhesins.

There are 5 classes of helicobacterial adhesins (Logan, 1996):

• Class 1 - Fimbrial haemagglutinin; Hemagglutinin, specific for sialic acid (20 kDa);
• Class 2 - Non-fimbrial haemagglutinins: specific for sialic acid (60 kDa), unidentified surface hemagglutinins;
• Class 3 - Lipid-binding gangliotetraosylceram;
• Class 4 - Sulfamucin-binding (sulfatide, heparan sulfate);
• Class 5 - Adhesins interacting with erythrocyte antigens of the blood group O (I) (Lewis).

Helicobacterial adhesins are bound by receptors of the gastric epithelium. Already this relationship and the location of Helicobacter pylori on the surface of the mucous membrane of the stomach have a damaging effect on the epithelial cells, dystrophic changes occur in them, their functional activity decreases. Helicobacteria intensively multiply, completely colonize the mucous membrane of the antral part of the stomach and cause its inflammation and damage due to the following basic mechanisms:

• Helicobacteria secrete enzymes of phospholipase, proteases, mucinase, which destroy the protective mucous barrier of the stomach;
• helikobakterii with the enzyme urease decompose urea to ammonia and CO2, this leads to a sharp alkalization of the membranes of the cells of the gastric epithelium, which disrupts the cell homeostasis, causes their dystrophy and death, and facilitates the penetration of Helicobacter pylori into the mucous membrane;
• ammonia, formed under the influence of Helicobacter, has a dual effect on the endocrine cells of the gastric mucosa: increased secretion of gastrin and suppressed - somatostatin, which leads to increased secretion of hydrochloric acid and, of course, to an increase in the acidity of gastric juice. The latter circumstance should be considered an aggressive factor in the initial stage of Helicobacteriosis;
• Helicobacteria induce the production and release of inflammatory mediators. In response to the penetration of Helicobacter pylori into the mucous membrane of the stomach, macrophages and leukocytes are the first to react. These cells rush into the mucous membrane of the stomach and phagocytize Helicobacteria and, consequently, their antigens. Further, T-lymphocytes are activated (under the influence of interleukin-1 secreted by macrophages), which ensure the blast-transformation of B-lymphocytes into plasma cells. The latter produce antibodies to Helicobacteria. Macchia et al. (1997) found that Helicobacteria produce heat shock proteins that initiate antibody formation. In the process of phagocytosis of Helicobacteria and the formation of antibodies to them, various cytokines are involved that are involved in the development of the inflammatory process in the gastric mucosa. The resulting antibodies to heli-cobacteria come not only into the blood, but also the submucosal layer of the stomach, where they bind to helicobacteria and neutralize their toxins and contribute to their death. In the gastric mucosa, the production of predominantly IgA antibodies is enhanced, which have the ability to prevent the adhesion of helikobacteria, blocking the receptors by which they are fixed to epithelial cells. Thus, it is IgA-antibodies that have a protective role in Helicobacter pylori infection. However, in chronic Helicobacter pylori gastritis, the protective function of anti-Helicobacter pylori antibodies of IgA class is clearly insufficient. Along with IgA, IgG and IgM antibodies are formed that activate complement and initiate the development of a neutrophil reaction;
• in response to the interaction of helicobacteria with gastric epithelium, the latter produces a large amount of interleukin-1 and interleukin-8. This process is stimulated by endotoxin Helicobacteria. Interleukins-1 and 8 cause chemotaxis of neutrophils and stimulate the formation of free radicals by them, causing damage to the gastric epithelium. Cytokines also cause degranulation of mast cells, the release of histamine from them, which sharply increases the permeability of blood vessels and facilitates the entry into the inflammatory focus of neutrophils, lymphocytes, macrophages;
• high-grade S-shaped Helicobacteria produce cytotoxins - the vacuolizing and CaGA-toxin ("associated" protein), under the influence of which the gastric mucosa undergoes pronounced structural changes. The degree of damage to the gastric mucosa can be very significant - up to the formation of erosion or even ulcers. This is facilitated by stimulation of the production of interleukin-8, an intensive mediator of inflammatory reactions, by the vacuolizing toxin and CaGA-toxin. In the ulcer Helicobacteria is absent, since there are no adhesion and epithelial cells in it. If Helicobacteria do not produce a vacuolizing cytotoxin, then erosion and ulceration does not occur and the process of lesions of the gastric mucosa stops at the stage of chronic gastritis.

Thus, Helicobacter pylori infection not only has a local pathogenic effect on the gastric mucosa (an immuno-inflammatory process with the migration and infiltration of immunocompetent cells into the inflammatory focus, their activation, the synthesis of mediators of inflammation and destruction), but also causes a system specific humoral and cellular immune response with development antigelo-dependent and cell-mediated mechanisms of chronic gastritis. Chronic helico-bacterial gastritis is initially localized in the aspiral department (early stage). With prolonged infection and with progression of the disease, the inflammatory process from the antral part extends to the body of the stomach, the atrophic changes in the gastric mucosa begin to predominate, and the diffuse atrophic pangastritis develops (the late stage of the disease).

At this stage, helikobacteria are no longer detected. This is probably due to the fact that atrophy of the mucous membrane of the stomach develops atrophy of the glands and transformation of the gastric epithelium into the intestinal (metaplasia), which is deprived of receptors to the Helicobuber adhesins.

Prolonged infection with Helicobacteria of the gastric mucosa causes permanent damage to the gastric epithelium. As a response to this prolonged damaging factor, the proliferation of cells of the gastric epithelium, which also becomes permanent (permanent), sharply increases. The proliferating epithelium undergoes full maturation, the proliferation processes predominate over the processes of maturation (differentiation) of cells.

Proliferation is enhanced by the weakening of the function of the ceylons (these intracellular hormones inhibit the division of cells), and also due to damage to the helicobacteria of the intercellular contacts. The weakening of intercellular contacts is a well-known cause of stimulation of cell division.

With the localization of Helicobacter pylori gastritis in the antrum (antral gastritis), the secretory function of the stomach is increased or normal. The increase in acid and pspin-excretory function of the stomach is associated with the preservation of the main glands (in the body and the stomach bottom), as well as with the switching off of the regulation mechanism of the acid-forming function by the affected antral section. Normally, when the concentration of hydrogen ions reaches pH <2, the inhibition of gastrin secretion begins in the antrum, which consequently reduces the secretory activity of the main glands of the stomach. With antral gastritis, this regulation process is disturbed, which leads to ongoing hyperfunction of the main glands of the stomach and hyperproduction of hydrochloric acid and pepsin

[43], [44], [45],

Pathogenesis of autoimmune gastritis

Autoimmune gastritis is observed much less frequently than Helicobacter pylori. For this variant of gastritis, a combination with B12 folio-deficient anemia is characteristic, a combination with Adzison's disease (chronic primary adrenocortical insufficiency), hypoparathyroidism, autoimmune thyroiditis is less common. With autoimmune gastritis from the very beginning, the main glands of the stomach, located in the body and the fundus of the stomach, are affected. The most characteristic feature of autoimmune gastritis is the rapid development of diffuse atrophy of the gastric mucosa, which is due to the production of autoantibodies to the lining cells and the internal factor-gastro-coprothein.

Antibodies bind to the microvilli of the intracellular system of tubules of parietal cells.

There are several types of autoantibodies against parietal cells in chronic autoimmune gastritis:

• "Classical" autoantibodies against microsomal antigens of parietal cells;
• cytotoxic antibodies (specific for autoimmune gastritis, Auer, 1990);
• antibodies to kgastrin-binding proteins, block receptors for gastrin;
• Antibody against H + -K + -ATPase, which provides the function of the proton pump in the secretion of hydrochloric acid.

These antibodies are found in 30% of patients with autoimmune gastritis, they block the function of the proton pump and are responsible for the development of hypo- and achilles.

Antibodies against the internal factor (gastromucoprotein) are of two types:

• blocking binding of vitamin B12 with an internal factor;
• forming a complex with vitamin B12.

Circulating antibodies damage the base glands. The mechanism of this damaging action is different.

It has been established that autoantibodies can have a specific cytotoxic effect on parietal cells with complement, while some of the parietal-cell antibodies have the ability to bind complement. Thus they are involved in the destruction of the gastric mucosa. In addition, an antibody-dependent and cell-mediated cytotoxic effect appears.

In the damage of the gastric epithelium in chronic autoimmune gastritis, local humoral and cellular immune mechanisms play an important role. Specific features of cellular infiltration of the mucosa during autoimmune gastritis have been established. Sixfold increase in the content of B-lymphocytes and T-lymphocytes of helpers was detected in the fundus of the stomach. At the same time, the number of IgA-plasmatic cells decreases sharply and the amount of IgG-plasmocytes increases. Local predominance of IgG is currently regarded as a violation of local humoral immunity, which provides a damaging effect on the gastric mucosa.

The causes that cause the appearance of autoantibodies and the development of chronic autoimmune gastritis are not known. Most researchers believe that the development of autoimmune processes in the gastric mucosa requires a hereditary predisposition. In such conditions, any, even insignificant, damage to the gastric mucosa results in the affected parietal cells becoming autoantigens, to which antibodies are formed. At a sufficiently high level of these antibodies (individual for each patient), their interaction with parietal cells occurs, followed by lesion and atrophy of the gastric mucosa.

Autoimmune gastritis is localized primarily and primarily in the bottom and body of the stomach, in these areas mucosal atrophy develops with the progressive loss of specialized glands and replacement of their pseudopiloric glands and intestinal epithelium (intestinal metaplasia of the mucous membrane).

The antral department retains its structure, and it reveals only superficial gastritis, which can undergo reverse development. However, in 36% of patients with B12-deficiency anemia, in addition to atrophic funda- mental gastritis, not only superficial, but also atrophic pyloric gastritis can be observed.

Perhaps this is a feature of the course of chronic autoimmune gastritis. It is possible that autoimmune mechanisms can participate in the lesion of the antral part of the stomach in a chronic autoimmune gastritis, but so far no antibodies against the pyloric glands have been identified.

With chronic autoimmune gastritis Helicobacter pylori infection is very rare, even less often than in healthy people. This is due to the following circumstances:

• with autoimmune gastritis, intestinal metaplasia of the epithelium of the stomach occurs; in the areas of such metaplasia, Helicobacterium does not develop;
• with autoimmune gastritis, the resistance of the mucous membrane of the antrum to Helicobacteria develops.

A characteristic feature of pyloric glands in patients with autoimmune gastritis is hyperplasia of gastrin-producing cells (secondary nature) and, of course, hypergastrinemia.

Autoimmune gastritis in the body and bottom of the stomach is characterized by accelerated progression, especially in individuals over the age of 50, and also in the stage of severe mucosal damage. In the antral section, there is a stabilization or even reverse development of the chronic inflammatory process.

The pathogenesis of chronic gastritis caused by the intake of NSAIDs

Chronic gastritis, caused by the use of non-steroidal anti-inflammatory drugs, is more likely to develop in people who have certain risk factors. This is an old age and the presence in the anamnesis of such diseases of the digestive system as chronic hepatitis, chronic noncalculent and calculous cholecystitis, pancreatitis.

The mechanism of development of chronic gastritis under the influence of NSAIDs is that they block the enzyme cyclooxygenase-1, which participates in the production of arachvdonic acid protective prostaglandins, stabilizing the cell membrane and possessing cytoprotective action in the stomach and kidneys. In the treatment of NSAIDs, the activity of the enzyme cyclooxygenase-1 is disrupted, which disrupts the synthesis of protective prostaglandins and creates all the necessary conditions for the development of chronic gastritis.

The pathogenesis of chronic reflux gastritis

Chronic reflux gastritis occurs as a result of duodenogastric reflux and is observed in patients who underwent gastrectomy (gastritis of the stump of the resected stomach), as well as in patients suffering from chronic impairment of duodenal patency with the development of hypertension and stasis in the duodenum.

In these conditions, a significant amount of bile enters the stomach. Bile acids have a damaging effect on the gastric mucosa. This is also facilitated by an alkaline reaction of the gastric contents, which is usually observed in the stomach stump after resection.

Infection with Helicobacteria in chronic reflux gastritis is not typical. This is due to the presence of bile in the gastric contents, as well as a decrease in the amount of mucus produced by the mucus, which is necessary for the functioning of Helicobacter pylori.

General pathogenetic factors of chronic gastritis

Common for various etiological variants of chronic gastritis are violations of the synthesis of prostaglandins in the gastric mucosa and the function of the gastrointestinal endocrine system.

Violations of the synthesis of mediators of protection

The gastric mucosa synthesizes so-called defense mediators - prostaglandins and growth factors (epidermal growth factor and a-transforming growth factor).

It has been established that the mucous membrane of the stomach and duodenum is able to recover very quickly after the injury (within 15-30 minutes) due to the fact that the cells move from the crypts of the gastric glands along the basal membrane and, thus, the defect is closed in the damaged epithelium site . The main, additional and parietal cells are produced by prostaglandins E2, which protect the gastric mucosa by reducing the activity of parietal cells and, consequently, reducing the production of hydrochloric acid, stimulating the secretion of mucus and bicarbonates, increasing blood flow in the mucosa, reducing the reverse diffusion of H + and speed up cell renewal.

With chronic gastritis, the functioning of these protective mechanisms is reduced, which, naturally, contributes to the progression of the disease.

Violation of the function of the gastrointestinal endocrine system

In the mucous membrane of the stomach and intestine there are endocrine cells that produce hormones and hormone-like substances that have a pronounced effect on the function of the stomach and intestines.

Hormones of the gastrointestinal tract affect some parts of the immune system. Thus, neurotensin stimulates the release of histamine from mast cells, chemotaxis, phagocytosis. VIP stimulates the activity of adenylate cyclase in T-lymphocytes and suppresses mitogenic response, lymphocyte migration, T-cell link of immunity, lymphoblastic transformation. Bombesin activates lymphocyte migration. A-endorphin stimulates the natural killer activity of lymphocytes.

The state of the gastrointestinal system was studied mainly with autoimmune gastritis. The hyperplasia of pyloric G-cells is established, which correlates with a high level of gastrin in the blood, but not in the mucous membrane of the stomach.

Hyperplasia of G cells is associated with the absence of an inverse inhibitory effect of hydrochloric acid (with atrophic autoimmune gastritis, Achilles is observed). The number of pyloric D-cells decreases, which is accompanied by a decrease in the production of somatosgathin and hydrochloric acid.

In connection with the multifaceted influence of the gastrointestinal endocrine system on the functional state of the stomach and the immunity system, it should be considered that it plays a large role in the pathogenesis of chronic gastritis.

Pathomorphology of chronic gastritis

The most characteristic manifestation of chronic gastritis is the infiltration of its own layer of the envelope by mononuclear cells-lymphocytes and plasma cells, as well as by neutrophilic leukocytes and eosinophils.

The higher the activity of inflammation of the gastric mucosa, the more pronounced cellular infiltration.

The following characteristic feature of chronic gastritis is atrophy, a progressive decrease and disappearance of the main (pepsin-forming) and obkladovye (acid-forming) cells. These highly specialized cells are replaced by cells that produce a large amount of mucus (intestinal metaplasia). At the same time, the process of regeneration of the gastric mucosa is disrupted, especially the differentiation, maturation of specialized stomach cells (major and obkladochnoy) is disrupted. In areas of intestinal metaplasia, there is no colonization of helicobacteria.

Symptoms of the chronic gastritis

Chronic gastritis caused by H. Pylori infection has no symptoms. The syndrome of dyspepsia in the background of chronic Helicobacter pylori is to be regarded as a manifestation of functional dyspepsia.

Chronic autoimmune gastritis is observed mainly in middle and old age. It is often combined with pernicious anemia, thyroiditis, thyrotoxicosis, primary hypoparathyroidism. The anamnesis and symptoms found during the examination are mainly due to these diseases.

Usually, autoimmune gastritis is characterized by a feeling of heaviness in the epigastric region after eating, a feeling of overeating, and overfilling of the stomach. Patients are disturbed by burping food and air, an unpleasant aftertaste in the mouth. The appetite is reduced. Possible meteorism, unstable stool.

Symptoms of chronic Helicobacter pylori

Symptoms of chronic Helicobacter pylori depend on the stage of the disease. For the early stage of the disease (it is observed more often in persons of mainly young age), the localization in the antrum part of the stomach is characteristic, with the development of non-atrophic antral gastritis without secretory insufficiency.

It is characterized by an ulcerative symptomatology:

• Periodic pain of veggastria after 1.5-2 hours after eating;
• often hungry pains (early in the morning, on an empty stomach);
• heartburn; belching sour;
• normal appetite;
• propensity to constipation.

As the disease progresses, the inflammatory process spreads to the rest of the stomach and acquires a diffuse character with atrophy of the gastric mucosa and secretory insufficiency. Helicobacteria are not detected so often and not in such a large quantity as in the early antral form of chronic gastritis.

In the late stage, the subjective symptomatology of chronic Helicobacter pylori corresponds to a known clinic of chronic gastritis with secretory insufficiency:

• poor appetite; sometimes nausea;
• sensation of metallic taste and dry mouth;
• belching with air, food, sometimes rotten;
• a feeling of heaviness in the veggie and overcrowding after eating;
• stupid, unintentional epigastric pain after eating;
• rumbling and swelling of the abdomen;
• inclination to rapid and fluid stools.

[46],

Chronic autoimmune gastritis

Chronic autoimmune gastritis is characterized by atrophy of the gastric mucosa and secretory insufficiency.

It is very rare, less than 1% in the population. A characteristic feature of it is the localization in the fundus of the stomach, while the pyloric department remains practically unaffected or changes insignificantly. This leads to a sharp decrease in the secretion of hydrochloric acid, pepsinogen, internal factor (gastromucoprotein). Deficiency of gastromucoprotein leads to impaired absorption of vitamin B12 and the development of B12-deficient anemia.

[47], [48], [49], [50],

Granulomatous gastritis

Granulomatous gastritis develops with Crohn's disease, sarcoidosis, tuberculosis, and mycosis of the stomach. His morphological picture is described above. In the clinical picture, the symptoms of the underlying disease predominate. The manifestations of gastritis itself are expressed in dyspepsia, sometimes there is vomiting, in some patients - bloody.

Eosinophilic gastritis

Eosinophilic gastritis is a rare disease. It is observed most often with systemic vasculitis, sometimes with food allergies, bronchial asthma, eczema.

A characteristic pathological feature of the disease is the infiltration of the gastric mucosa, and sometimes other layers of the stomach wall with a large number of eosinophils. Possible development of eosinophilia. There are no specific gastroenterological manifestations.

The clinic of eosinophilic gastritis corresponds to the clinic of chronic gastritis with the normal secretory function of the stomach.

[51], [52], [53], [54], [55]

Lymphocytic gastritis

Lymphocytic gastritis is characterized by pronounced lymphocytic infiltration of the gastric epithelium, thickened folds, nodules and erosions.

Lymphocytic gastritis has a characteristic localization. In 76% - it is pangastritis, in 18% of cases - the foundation and in 6% - antral gastritis.

According to Whitehead (1990), there are two forms of chronic lymphocytic gastritis - with acute and chronic erosions.

Many gastroenterologists believe that the origin of lymphocytic gastritis is important infection with Helicobacter pylori. However, this is not a generally accepted point of view.

The clinical course of lymphocytic gastritis is similar to the early stage of chronic Helicobacter pylori gastritis (with normal or increased secretory function).

Hypertrophic gastritis (Menetries disease)

The main characteristic morphological sign of hypertrophic gastritis is pronounced hypertrophy of the gastric mucosa in the form of giant folds covered with a large amount of viscous mucus.

Histological examination of the biopsy specimens of the gastric mucosa reveals a sharp thickening, lengthening and widening of the gastric pits. In the epithelial layer, signs of transformation into the intestinal epithelium, as well as cysts, are found. Erosions and hemorrhages can be detected.

The main clinical manifestations of hypertrophic gastritis are:

• pain in the epigastrium, often very intense, occurring soon after eating;
• heartburn;
• belching with air, food;
• often vomiting with an admixture of blood;
• anorexia;
• loss of body weight;
• swelling of the feet and hands;
• diarrhea;
• hypoproteinemia;
• increase or decrease in the secretion of hydrochloric acid;
• possible combination with peptic ulcer of duodenum.

Hypertrophic folds of the mucosa should be differentiated from gastric lymphoma.

Chronic polyposis gastritis

Polyps are a consequence of dysregenerator hyperplasia of the gastric mucosa.

Chronic polyposis gastritis is characterized by the same clinical manifestations as chronic gastritis with secretory insufficiency. Sometimes there are gastric bleeding. At a roentgenoscopy of the stomach, small uniform defects of filling are revealed, the relief of the mucous membrane is not changed; in gastroscopic examination, multiple polyps of small size are found, which are located mainly in the antrum part of the stomach.

[56], [57], [58], [59], [60], [61]

Forms

There are two main forms of chronic gastritis:

1. Chronic autoimmune gastritis (5% of all cases of chronic gastritis) is associated with the formation of antibodies to parietal cells of the stomach and the internal factor of the Castle. Its characteristic feature is the primary development of atrophic changes (inflammation in combination with thinning of the mucosa, loss of glands, metaplasia of the epithelium) of the mucous membrane of the fundus of the stomach.
2. Chronic gastritis caused by Helicobacter pylori infection (95% of all cases of chronic gastritis). Structural changes in the gastric mucosa develop in all infected individuals.

Chronic gastritis can be active (in the inflammatory infiltrate contains mononuclear cells and neutrophils) and inactive (there are only mononuclear cells - lymphocytes, plasma cells and macrophages), and also accompanied by intestinal metaplasia (developing in all parts of the stomach) or pseudopiloric metaplasia, which is a substitution gland of the fundus by the mucus glands of the pyloric department.

In 1990, the Sydney classification of chronic gastritis was proposed. It takes into account the morphological changes in the gastric mucosa (the degree of activity of inflammation, the severity of atrophy and metaplasia of epithelial cells, the presence of the mucous membrane of the stomach by the microorganisms Helicobacter pylori), the topography of the lesion (antral gastritis, gastritis of the stomach, pangastritis), the etiology of the disease (gastritis, associated with Helicobacter pylori, autoimmune gastritis, idiopathic gastritis) and, in addition, involves the isolation of special forms of chronic gastritis (granulomatous, eosinophilic, imfotsitarny and reactive). The Sydney classification of chronic gastritis also contains an endoscopic section that reflects along with other characteristics and the presence of erosions of the gastric mucosa and subepithelial hemorrhages.

The last classification of chronic gastritis was proposed in 1994 and was named Houston. In this classification the following variants of the disease are distinguished:

• Non-atrophic gastritis (synonyms: superficial, diffuse antral, interstitial, hypersecretory, type B);
• Atrophic gastritis:
  • autoimmune (synonyms: type A, diffuse body of the stomach,
  • associated with pernicious anemia),
  • multifocal (found in countries with high incidence of gastric cancer);
• Special forms of chronic gastritis:
  • chemical (synonyms: jet reflux gastritis, type C),
  • radiation,
  • lymphocyte (synonyms: varioloform, associated with celiac disease),
  • Non-infectious granulomatous (synonym - isolated granulomatosis),
  • eosinophilic (synonym - allergic),
  • Other infectious forms caused by various microorganisms, excluding Helicobacter pylori.

Members of the working group indicate that the diagnosis of chronic gastritis should be primarily descriptive, and then, if possible, etiological factors are added to it.

The following morphological variants of changes in the mucosa are distinguished in the classification:

1. Normal mucosa.
2. Acute gastritis.
3. Chronic gastritis - with the allocation of 4 degrees, depending on the severity of infiltration of lymphocytes and plasma cells (minimal, minor, moderate and severe).
4. Intestinal metaplasia of 3 types.
   1. Type 1 - full or intestinal.
   2. Type 2 - incomplete: goblet cells among the superficial epithelium of the stomach.
   3. Type 3 - incomplete metaplasia of the small intestine type with secretion of sulfomucins.

There are also focal and widespread metaplasia.

Morphological manifestations of special forms of chronic gastritis are as follows.

• Granulomatous gastritis - characterized by the presence of epithelium-cell granulomas, sometimes with an admixture of giant multinucleated cells in the lamina propria of the mucosa. Granulomatous gastritis is found in sarkovidosis, Crohn's disease, mycoses, tuberculosis and foreign bodies. Granulomatous gastritis can be isolated, idiopathic (unknown etiology).
• Eosinophilic gastritis - is characterized by severe infiltration of eosinophils not only of the gastric mucosa, but also of other layers of its wall. Infiltration with eosinophils is combined with edema and fullness. The etiology of this variant of gastritis is unknown. According to research data, 25% of patients have history of allergy, bronchial asthma, eczema, hypersensitivity to food proteins. Sometimes the disease is a manifestation of eosinophilic gastroenteritis, which can develop at any age, with the defeat of the mucous membrane of the small intestine accompanied by the development of malabsorption syndrome, muscular layers damage - fibrosis and bowel obstruction - ascites.

With eosinophilic gastritis, the predominantly antral part is affected, along with eosinophils, there are polymorphonuclear leukocytes, lymphocytes, macrophages, IgE, and plasma cells.

• Lymphocytic gastritis - characterized by selective expressed lymphocytic infiltration of the gastric epithelium; in its own plate of lymphocytes and plasma cells is relatively small. About lymphocytic gastritis can be said when the number of lymphocytes exceeds 30: 100 epitheliocytes.

Endoscopic examination reveals nodules, thickened folds, and erosion.

The etiology and pathogenesis of this form of gastritis is unknown.

It is assumed that the main role in the development of chronic lymphocytic gastritis is played by the immune response to local effects on the gastric mucosa of some antigen (the effect of Helicobacter pylori infection is not excluded, gluten intolerance is also assumed). A characteristic feature of chronic lymphocytic gastritis is erosion of the gastric mucosa.

When describing the morphological changes in the gastric mucosa with chronic gastritis, the intensity of inflammation, the activity of the process, atrophy, intestinal metaplasia and the severity of hemobacteria are assessed. These basic morphological changes are assessed semi-quantitatively as weak, moderate and severe. There are also nonspecific and specific non-variable changes (they are simply described, but the degree of expression is not taken into account).

Nonspecific changes include such as mucus, epithelial degeneration, edema, erosion, fibrosis, vascularization. Specific non-variable changes refer to one of the specific (special) types of gastritis (granulomatous, lymphocytic, eosinophilic, reactive).

[62], [63], [64], [65], [66]

Endoscopic classification section

The endoscopic classification section also reflects the localization of changes in the gastric mucosa (gastritis antrum, gastritis of the body of the stomach, pangastritis) and suggests the following terms to describe the changes: edema; hyperemia (erythema); loosening; exudation; erosion (flat, raised); nodularity; hyperplasia of folds; visibility of the vascular reaction; intramural hemorrhages; duodenogastric reflux. All these descriptive signs of chronic gastritis, detected by endoscopy, can have a semiquantitative evaluation (severity - mild, moderate, severe).

Based on these descriptive signs, the following endoscopic categories of gastritis are defined:

• erythematous-exudative (in a widespread view "superficial" gastritis);
• atrophic gastritis;
• hemorrhagic gastritis;
• hyperplastic gastritis.

The authors of the classification cite exemplary formulations of histological conclusions: "autoimmune chronic pangastritis with predominance of severe atrophy in the fundus"; "Associated with Helicobacter pylori infection, antral chronic gastritis of moderate activity", "reactive antral gastritis associated with bile", "reactive antral with erosions, gastritis associated with non-steroidal anti-inflammatory drugs".

In the Sydney and Houston classifications of chronic gastritis there is no section "The state of secretory function of the stomach," which is very important from a practical point of view.

[67], [68], [69], [70]

Diagnostics of the chronic gastritis

With antral helicobacter pylori gastritis (early stage) the following characteristic symptomatology is revealed:

• the tongue is clean or lightly covered at the root;
• local soreness in the pyloroduodenal zone (in the epigastrium, mainly on the right);
• the lower border of the stomach, determined by the noise of the splash, is located normally (3-4 cm above the navel);
• with severe aggravation of antral gastritis, a slight weight loss is possible.

In the diffuse form of chronic Helicobacter pylori gastritis (late stage), objective examination reveals the following symptoms (a picture of chronic gastritis with secretory insufficiency):

• decrease in body weight (usually with prolonged existence of the disease, development of a secondary enteric syndrome and a decrease in the exocrine function of the pancreas);
• the language is heavily laden;
• in the corners of the mouth of the crack ("seizures");
• moderate diffuse soreness in the epigastric region;
• the lower limit of the stomach, determined by the noise of the splash, is below the normal level (at the level of the navel or lower);
• it is often determined by rumbling during palpation of the large intestine, significant meteorism can be detected.

Laboratory diagnostics

As part of a clinical survey: a clinical blood test, a clinical urinalysis, clinical stool analysis, a feces occult blood test, a blood group determination and Rh-accessory. Changes in laboratory parameters are not characteristic for chronic gastritis. In the case of atrophic gastritis, combined with B12-deficiency anemia, it is possible to reduce the content of hemoglobin, increase the color index of erythrocytes, the appearance of megakaryopites.

Biochemical blood tests: the content of total protein, albumin, cholesterol, glucose, bilirubin, transaminases, amylase, serum iron.

Identification of H. Pylori infection is invasive (rapid urease test, morphological methods) or non-invasive [breath test, detection of antibodies (AT) against H. Pylori] by methods.

[71], [72], [73], [74], [75], [76]

Additional laboratory tests

• Investigation of antibodies to parietal cells of the stomach - detection of antibodies is typical of chronic autoimmune gastritis, however, in some patients infected with H. Pylori, antibodies to parietal cells of the stomach are also found in serum.
• Investigation of the level of pepsinogen I - a decrease below the threshold indicates the atrophy of the body of the stomach.

[77], [78], [79], [80]

Instrumental research

• Compulsory instrumental research

FEGDS is the main method of confirming the diagnosis, as it allows to conduct a histological examination of the biopsy specimen. Histological examination of the biopsy specimens of the mucous membrane of the fundal and antral parts of the stomach is performed to determine the type of pathomorphological changes and clarification of the gastritis variant, and if it is not possible to conduct non-invasive tests for H. Pylori detection for the study of biopsies for its presence.

Ultrasound examination (ultrasound) of the liver, pancreas, gall bladder - for the diagnosis of concomitant pathology of the hepatobiliary system and pancreas.

X-ray, gastroscopy and histological examination

Diagnosis of Helicobacter pylori infection

• Cytological examination

For cytological examination, smear-prints of biopsy specimens of the gastric mucosa (anthral section) are used for gastroscopy. A biopsy should be taken from areas with the greatest hyperemia and edema, but not from the bottom of erosions or ulcers. Then the smears are dried and painted according to the method of Romanovsky-Giemsa. Helicobacteria are located in mucus, have a spiral, curved shape, are S-shaped.

There are three degrees of dissemination of Helicobacter pylori:

• weak (+) - up to 20 microbial bodies in the field of view;
• average (++) - up to 50 microbial bodies in the field of view;
• high (+++) - more than 50 microbial bodies in the field of view.

Used magnification of the microscope x 360.

[81], [82], [83], [84]

Urease test

The urease test for the determination of Helicobacter pylori is based on the following principle.

Helicobacteria secrete the enzyme urease, under the influence of which urea, contained in the stomach, decomposes with the release of ammonium:

The ammonium ion formed as a result of the reaction significantly increases the pH of the medium, which can be ascertained with the help of an indicator, and, therefore, also visually by changing its color.

Expressive urease method is used to detect Helicobacter pylori infection. The express kit contains urea, a bacteriostatic agent and a phenol-mouth as a pH indicator (the indicator changes color from yellow to crimson when the reaction is shifted to the alkaline side).

The biopsy of the gastric mucosa obtained by gastroscopy is placed in the express kit environment.

If there is a helicobacterium in the biopsy material, the medium acquires a crimson color. The appearance of crimson coloring indirectly indicates the amount of Helicobacter pylori.

• (+) - insignificant infection (raspberry staining at the end of the day);
• (++) - moderate infection (raspberry staining for 2 hours);
• (+++) - significant infection (raspberry staining appears within the first hour);
• (-) - the result is negative (raspberry staining occurs later than in a day).

Foreign firms produce test systems for the determination of Helicobacteria by the urease method (de-nol-test by Yamanouchi, CLO-test - Australia, etc.).

C-urease respiratory test

The method is based on the fact that ingested urea, labeled with 13C, under the influence of urease, Helicobacteria decomposes to form ammonia and CO2. In exhaled CO2, the content of 13C is determined and, according to its level, a conclusion is made about the infection with Helicobacteria.

The study is conducted on an empty stomach. Initially, two background samples of exhaled air are taken into plastic tubes at intervals of 1 minute. Then the patient takes inside a light test breakfast (milk, juice) and a test substrate (aqueous solution of urea, labeled 13C). Then, for 4 hours, 4 samples of exhaled air are taken at intervals of 15 minutes.

The 13C content in the exhaled air is determined using a mass spectrometer. Depending on the percentage of the isotope 13C in the exhaled air, there are 4 levels of infection with Helicobacter pylori:

• less than 3.5% - easy;
• 3.5-6.4% is the average;
• 6.5-9.4% - heavy;
• more than 9.5% - extremely difficult.

Normally, 13C content in the exhaled air does not exceed 1% of the total amount of CO2.

The method is extremely expensive and is still not widely available.

[85], [86], [87], [88], [89], [90], [91],

Microbiological method

Crops for the determination of helicobacteria are produced from biopsy specimens of the gastric mucosa. Incubation of crops is carried out under microaerophilic conditions with an oxygen content of not more than 5%. To create such an environment, special gas-generator chemical packages are used. To grow Helicobacteria, special blood nutrient media are used. After 3-5 days, small, round, transparent, dewy colonies of Helicobacteria appear on the nutrient medium. Then, the identified culture is identified.

Histological method

The material is biopsy of the gastric mucosa in the places of the most pronounced inflammation.

Thin sections are prepared and the preparations are stained with hematoxylin and eosin or according to the Romanovsky-Giemsa method. Helicobacteria are detected in the form of spiral, S-shaped bacteria.

In recent years, the most accurate methods for identifying Helicobacter pylori have appeared. These include the immunochemical method with monoclonal antibodies. Currently, there are commercial kits that allow the use of conventional biopsy material, fixed in formalin and embedded in paraffin. Monoclonal antibodies included in these kits work at a dilution of 1: 200,000 and selectively stain only Helicobacteria.

Recently, methods have been used to detect Helicobacteria using DNA hybridization in conventional paraffin sections.

Immunological methods

3-4 weeks after infection with helicobacteria of the gastric mucosa and 12 duodenal ulcer, antibodies to Helicobacteria appear in the blood of patients. These antibodies are determined by the method of enzyme immunoassay.

Using this method, antibodies IgG, IgA, IgM classes in the blood and secretory IgA, IgM in saliva and gastric juice are detected.

The test remains positive for a month after the successful elimination of Helicobacter.

Study of the secretory function of the stomach

In chronic helicobacter pylori gastritis secretory function can be changed, but the severity of changes depends on the stage of gastritis. With antral gastritis (early stage of Helicobacter gastritis), acid-forming and pepsin-forming functions are normal or more often elevated, with pangastritis (late stage) reduced, but the state of achlorhydria, as a rule, does not happen.

At present, there are three main methods for determining the acid-forming function of the stomach:

• intragastric pH-metry;
• fractional study of gastric juice using a thin probe with the use of stimulants of gastric secretion;
• bezsonde methods - determination of acidity with the help of ion-exchange resins ("Acidotest"). Bezsonde methods are not very informative and are rarely used at present.

Fractional study of gastric juice

The method allows to study gastric secretion for a long time, as well as to get an idea of its character in the reflex reflex phase (the response to a mechanical stimulus in the stomach - the gastric tube) and the neurohumoral phase (reaction to the enteral or parenteral stimulus). In this connection, two stages of fractional gastric sensing are distinguished:

• determination of basal secretion;
• definition of sequential (stimulated) secretion.

The first stage - the definition of basal secretion - is performed as follows. In the morning on an empty stomach the patient is injected into the stomach with a thin probe, all the contents of the stomach are removed and then gastric juice is aspirated every 15 minutes.

The total volume of these portions in ml and represents the volume of basal secretion of gastric juice. In each portion, the content of total and free hydrochloric acid and pepsin is also determined.

The second stage - sequential stimulated secretion - is the determination of the secretory function of the stomach every 15 minutes after subcutaneous administration of histamine (it stimulates gastric secretion). In order to avoid side effects of histamine, 2 ml of a 2% solution of suprastin (after receiving 3 portions of basal secretion, ie 30 minutes before the start of the second stage of the gastric secretion study) are preliminarily administered to the patient. After administration of histamine, gastric juice is collected every 15 minutes for 1 hour.

There are submaximal and maximum histamine tests. For submaximal stimulation, histamine is administered at a dose of 0.008 mg / kg body weight, for a maximum of 0.025 mg / kg body weight. The maximum histamine test is rarely used due to severe side effects.

Pentagastrin or tetragastrin is widely used as a stimulant for gastric secretion at a dose of 6 mg / kg body weight. The tolerability of gastrin preparations is good, they are more preferable in comparison with histamine. Other stimulants of gastric secretion - so-called prasal breakfasts are rarely used (breakfast according to Leporskiy - 200 ml of cabbage juice, according to Petrova - 300 ml of 7% of cabbage broth, according to Zimnitsky - 300 ml of broth, according to Erman - 300 ml of 5% alcohol solution, Kachu and Kalku - 0.5 g of caffeine per 300 ml of water).

The following indices of gastric secretion are determined:

• the volume of juice on an empty stomach;
• juice volume for an hour before stimulation (basal secretion);
• juice volume within an hour after stimulation with histamine or pentagastrin;
• total acidity, free hydrochloric acid and pepsin content;
• pH of gastric juice.

The production of hydrochloric acid is calculated for 1 hour (flow-hour) and expressed in meq / h or mg / h.

After using histamine, the secretory effect begins after 7-10 minutes, reaches a maximum after 20-30 minutes. And lasts about 1-1.5 hours. Approximately also acts pentagastrin.

Intragastric pH-metry

The basis of the intragastric pH-metry method is the determination of the concentration of free hydrogen ions in the gastric contents, which allows us to conclude that the acid-forming function of the stomach. Intragastric pH-metry has several advantages over the above fractional aspiration-titration method:

• when studying the acidity of gastric juice, test-indicators with low sensitivity are used for testing, so sometimes a condition regarded as an anatomical does not in fact correspond to such. This disadvantage is lacking in the pH-metry method;
• in contrast to the otospiratsionno-titratsionnogo method pH-metry allows you to judge the acid-forming function in patients with a resected stomach, and also allows you to diagnose pellets of acid contents of the stomach in the esophagus (gastroesophageal reflux).

Intragastric pH-metry is performed with the help of the complex "Gastroscan-24" (RF), which allows to determine pH in the esophagus, stomach and duodenum within 24 hours, to study the effect of various drugs on the acid-forming function of the stomach.

According to AS Loginov (1986), the pH of gastric contents in the body of the stomach is 1.3-1.7 (normaciditas); pH within 1.7-3.0 indicates a hypoacid state; pH more than 3.0 indicates an anacidic state; pH <1.3 is characteristic of a hyperacid state.

In the pyloric department with a normal acid-forming function of the stomach pH <2.5.

When revealing an anacadian state, it is of great importance to ascertain his character - is this true achlorhydria (caused by atrophy of the gastric mucosa) or false (caused by inhibition of acid formation). To do this, determine the pH of the gastric contents after maximum stimulation with histamine or pentagastrin. Preservation of the anacidic state after maximum stimulation indicates true achlorhydria.

Bezsonde methods of studying the secretory function of the stomach

Bezsonde methods of studying the secretory function of the stomach are of little informative, allow only an approximate judgment about it. These methods are used in situations where stomach probing is contraindicated: decompensated defects; IHD; hypertonic disease; aortic aneurysm; stenosis of the esophagus; lung diseases with respiratory failure, etc.

Desmoid test. Salt is based on the ability of gastric juice to digest catgut. A sick person on an empty stomach swallows a bag of methylene blue, tightened with catgut. After that, urine is collected after 3, 5, 20 hours. Intensive staining of all three portions indicates a hyperacid state, the second and third - of normal acidity; the staining of only one portion of urine points to achlorhydria.

The method of ion-exchange resins is based on the ability of the indicator ions (low-molecular compound bound to ion-exchange resin) to exchange in the stomach for the same amount of hydrogen ions of hydrochloric acid. At the same time, the indicator is released from the resin, absorbed in the intestine and excreted in the urine, where it is found.

The determination of uropepsin in urine indirectly allows one to judge the enzyme-forming function of the stomach (peptic activity of the gastric juice). Normally, 0.4-1.0 mg of uropepsin is excreted per day in the urine.

General, biochemical, immunological tests of blood

There are no significant changes in the general, biochemical, immunological analyzes of blood in patients with chronic Helicobacter pylori.

Diagnosis of chronic autoimmune gastritis

Chronic gastritis, the morphological substrate of which is inflammation of the gastric mucosa, proceeds without any clinical manifestations. The diagnosis of chronic gastritis should be based not on a clinical picture, but on the results of laboratory and instrumental studies (primarily morphological study of the gastric mucosa).

[92], [93]

Objective study of patients

The general condition is satisfactory, but with severe atrophy of the gastric mucosa and achlorhydria, digestion in the small intestine is significantly impaired and the following characteristic symptoms appear:

• weight loss;
• dry skin, sometimes its darkening due to the development of hypocorticism (skin pigmented in the nipples, face, palmar folds, neck, genitals);
• pallor of the skin (due to anemia);
• signs of multivitaminosis (vitamin A deficiency - dry skin, visual impairment, vitamin C deficiency - bleeding and loosening of the gums, vitamin B2 deficiency - "seizures" in the corners of the mouth, vitamin PP deficiency - dermatitis, diarrhea);
• loss of hair, brittle nails;
• possibly lowering blood pressure (due to hypocorticism), there may be dystrophic changes in the myocardium;
• the language is imposed;
• diffuse soreness in the region of epigastrium;
• with the development of intestinal dyspepsia, soreness and rumbling during palpation of the umbilical and ileocecal region;
• can be determined by the omission of the large curvature of the stomach.

X-ray, gastroscopy and histological examination

With X-rays of the stomach, a decrease in the expression of the folds of the gastric mucosa is found.

Gastroscopy reveals the following characteristic changes:

• folds of the mucosa are much lower than normal, in far-reaching cases of atrophy they may be absent altogether;
• the mucous membrane of the stomach is thinned, atrophic, pale, through it a vascular pattern is clearly visible;
• often you can see an excessive amount of mucus, which is associated with an increase in the number of mucus-forming cells;
• the gatekeeper gaping, the contents of the stomach are discharged into the 12-colon, the peristalsis of the stomach is sluggish, the mucus lingers on the walls of the stomach;
• antrum part of the stomach with autoimmune gastritis is practically unchanged;
• it is extremely rare for autoimmune gastritis to see erosion of the mucous membrane, in this case, it is possible to assume a combination of Helicobacter and autoimmune gastritis and it is necessary to conduct a biopsy study for the presence of helicobacteria.

Histological examination in the fundus of the stomach reveals atrophy of the gastric mucosa with a progressive loss of specialized glands and the replacement of their pseudopiloric glands and intestinal epithelium. Antral department, in contrast to chronic Helicobacter pylori, retains its structure, but a histological picture of superficial gastritis, which tends to reverse development, is determined. According to studies, antral gastritis is combined with atrophic fundus gastritis in 36% of patients with B12-deficient anemia, and it can be atrophic in some patients. Perhaps this is due to the autoimmune nature of the defeat of the pyloric section, since its mucous membrane is highly resistant to colonization of helicobacteria.

A characteristic sign of chronic autoimmune gastritis is hyperplasia of gastrin-producing cells of pyloric glands.

LI Aruin points out specific features of mononuclear infiltration for chronic autoimmune gastritis:

• a sixfold increase in the content of B-lymphocytes and T-helpers;
• a sharp decrease in the number of IgA-plasmocytes and a significant increase in the number of IgG-plasmatic cells.

Local predominance of IgG indicates the predominant involvement of local humoral immune mechanisms.

Autoimmune gastritis in the fundus during severe lesions of the gastric mucosa and in patients over the age of 50 acquires a tendency to rapid progression. In the antrum, on the contrary, there is stabilization and even possible the reverse development of the inflammatory process with the disappearance of the round-cell inflammatory infiltration.

Studies indicate that in the body of the stomach with autoimmune gastritis over time inflammatory infiltration also decreases and the dominant value begins to acquire atrophy of the gastric mucosa.

Status of the secretory function of the stomach

To study the secretory function of the stomach in patients with chronic autoimmune gastritis, the same methods as described above (in the section on chronic Helicobacter pylori gastritis) are used. Chronic autoimmune gastritis is characterized by a sharp decrease in acid and pepsin formation, with the most severe disease of achlorhydria.

Immunological blood test

Patients with autoimmune gastritis are naturally detected in the blood of autoantibodies to parietal cells and to a gastritis-coprotein. Autoantibodies to the microsomal fraction of parietal cells are specific for autoimmune chronic gastritis. Antibodies to gastromukoprotein block the binding of vitamin B12 with gastromucoprotein, in addition, the formation of antibodies to vitamin B12.

Antibodies to gastrin-binding proteins are also detected, they block receptors of gastrin. In 1/3 of patients with autoimmune gastritis, antibodies to H + K-ATP-ase, which provides the function of a proton pump in the secretion of hydrochloric acid, were detected. These antibodies are given a leading role in the development of hypo- and achlorhydria.

In a number of cases with chronic autoimmune gastritis, there is a decrease in the content of T-lymphocyte suppressors in the blood, an increase in T-lymphocytes of helpers and immunoglobulins, and the appearance of circulating immune complexes in the blood.

General and biochemical blood test

With the development of B12-deficiency anemia, a decrease in the content of hemoglobin and erythrocytes in the blood, a rise in the color index, leukopenia, thrombocytopenia is noted.

Biochemical analysis of the blood is characterized by hyperbilirubinemia, moderately expressed (with the development of hemolysis in patients with B12-deficiency anemia), an increase in the content of y-globulin in the blood.

Differential diagnosis

In addition to chronic gastritis, the so-called functional disorders of the stomach are additionally isolated (differential diagnosis is extremely difficult, since multiple biopsies and a whole complex of other laboratory and instrumental studies are required for this).

Chronic atrophic gastritis must be differentiated from gastric ulcer with reduced secretory function, benign and malignant tumors of the stomach. The most important task is a differential diagnosis with stomach cancer. Difficulties occur with endophytic growth of the tumor. For correct diagnosis, a complex X-ray endoscopy study with multiple targeted biopsies from the most altered areas of the mucosa is used. In unclear cases, a dynamic observation is carried out with a repeated FEGDS with a biopsy. In these cases, endoscopic ultrasound is effective.

Indications for specialist consultation

• The oncologist - at revealing of a cancer of a stomach.
• Hematologist - if necessary to clarify the diagnosis of concomitant anemia within the framework of chronic autoimmune gastritis.

Treatment of the chronic gastritis

The goals of treatment of chronic gastritis are to prevent the development of precancerous changes in the gastric mucosa - intestinal metaplasia and mucosal dysplasia.

Criteria for assessing the effectiveness of therapy: eradication of H. Pylori, a decrease in signs of gastritis, the lack of progression of atrophic changes.

Indications for hospitalization

Chronic gastritis does not serve as an indication for hospitalization. Hospitalization is indicated only when it is necessary to conduct a complex examination and difficulties in the differential diagnosis. With autoimmune gastritis, hospitalization is necessary for B12 deficiency anemia.

Mode

It is advisable to quit smoking, as a correlation between smoking and the severity of metaplasia of the gastric mucosa by intestinal type has been revealed. You should stop taking medications that have adverse effects on the gastric mucosa (eg, NSAIDs).

Diet

Does not have independent value as a medical measure for chronic gastritis.

[94], [95], [96]

Drug therapy for chronic gastritis

[97], [98], [99], [100], [101]

Chronic non-atrophic gastritis

Eradication of H. Pylori in its detection. Eradication is indicated for patients with a hereditary predisposition to gastric cancer or those who need NSAIDs. The use of antisecretory drugs, prokinetics and preparations with cytoprotective effect (sucralfate, sub-citrate of colloidal bismuth) is advisable in the syndrome of functional dyspepsia in the background of chronic gastritis.

[102], [103], [104], [105],

Chronic atrophic gastritis

• With the identification of the etiological role of H. Pylori - eradication therapy.
• Treatment of B12-deficiency anemia.

[106], [107], [108],

Further management of the patient

Of fundamental importance is the diagnosis of the result of H. Pylori eradication therapy, in connection with which, after 4-8 weeks after this course of treatment, a check should be conducted for H. Pylori. Patients with atrophy of the body of the stomach or the body of the stomach and antrum, especially with the presence of precancerous changes in the mucous membrane, are subject to follow-up, with 1 time in 1 to 2 years of endoscopic examination with a histological evaluation of mucosal biopsy specimens.

Patient education

Advise patient to avoid taking NSAIDs. The patient should be convinced of the need for strict adherence to the recommended regimen for taking medications, in spite of the fact that in some cases the amount of drugs may seem excessive to the patient.

It is necessary to inform the patient about possible complications of chronic gastritis and their clinical manifestations (peptic ulcer, stomach cancer). If there is a likelihood of pernicious anemia, the patient (or his relatives, especially if the patient is elderly and senile) should know her basic clinical manifestations for a timely referral to the doctor.

Prevention

Prevention of chronic gastritis is not developed.

[109], [110], [111]

Forecast

The prognosis of chronic gastritis is usually favorable. Danger is the precancerous changes in the mucous membrane (intestinal metaplasia and dysplasia) against the background of atrophic gastritis. Timely treatment of pernicious anemia developing in chronic atrophic autoimmune gastritis in the overwhelming majority of cases helps to prevent an unfavorable development of events for the patient.

[112]