home Audience 6 Gastritis: definition, classification, etiology, pathological anatomy, complications. Chronic gastritis - treatment and symptoms But perhaps it is more correct to treat not the effect, but the cause

Gastritis: definition, classification, etiology, pathological anatomy, complications. Chronic gastritis - treatment and symptoms But perhaps it is more correct to treat not the effect, but the cause

Acute gastritis as a pathological change in the mucous membrane of the stomach and its wall is primarily an inflammation of the mucous membrane, which can be widespread throughout the entire organ or involve any of its parts.

The most common cause of gastritis is the side effects of drugs and poisons (non-steroidal anti-inflammatory drugs, alcohol), which, by reducing the protective function of the mucous membrane, lead to the reverse flow of pepsin and protons from the gastric contents into the gastric mucosa and its wall.

The entry into the stomach of strong acids (sulfuric, hydrochloric) and alkalis, as well as solutions of substances such as formaldehyde and trinitrophenol through necrobiotic changes in the stomach wall lead to its inflammation, which also occurs in the mucous membrane (corrosive gastritis).

Pathological centralization of blood circulation in the acute period after severe wounds, injuries, burns, which is enhanced and maintained by prolonged pathogenic pain, through juxtacapillary shunting (the passage of blood past the exchange capillaries) in the stomach reduces the protective function of the mucous membrane, which can also be the cause of acute gastritis.

A rare cause of acute gastritis is bacterial invasion of the stomach wall (phlegmonous gastritis). Most often, the stomach wall is infected by streptococcus, less often by staphylococci, Escherichia coli and some Proteus species.

Only in 30% of patients acute gastritis manifests itself with symptoms such as a burning sensation and pain in the epigastric region, nausea and vomiting. In a small proportion of patients, acute gastritis leads to bleeding from the vessels of the stomach wall damaged by primary alteration and inflammation itself (hemorrhagic erosive gastritis).

Endoscopic examination in patients with acute gastritis reveals petechial hemorrhages in the mucous membrane, its swelling, as well as various degrees of destruction up to superficial ulcerations. Endoscopy is the final stage in identifying acute gastritis in patients.

Pathogenetic principles of treatment of acute gastritis include:

♦ elimination of effects that reduce the protective function of the mucous membrane (stop taking or administering non-steroidal anti-inflammatory drugs, giving up alcohol) or directly damaging the stomach wall (gastric lavage with alkaline solutions in case of poisoning with strong acids, etc.);

♦ the use of antacids, and in particular histamine H2 receptor blockers, to reduce the destructive properties of gastric contents regarding the gastric mucosa and its entire wall.

With hemorrhagic gastritis, due to hypovolemia and pathological reactions to blood loss, the need for infusions and transfusions may arise. At the same time, to stop bleeding from the stomach wall into its lumen, the pH of the gastric contents must be maintained at a level higher than 3.5. Bleeding due to hemorrhagic gastritis can sometimes be an indication for surgery with high postoperative mortality.

Chronic gastritis in morphopathogenetic terms is characterized by lymphocytic infiltration of the muscular layer of the gastric mucosa. In this case, lymphocytes mainly infect the part of the muscle layer that is in direct contact with the gastric mucosa.

The most common causes of chronic gastritis are the constant inhibition by alcohol of the protective function of the gastric mucosa, its damage by ionizing radiation, as well as autoimmune damage through the formation of autoantibodies to the surface antigens of gastric epithelial cells.

In chronic gastritis type A, autoantibodies are formed to antigens on the surface of parietal cells of the mucous membrane. This type of gastritis is characterized by a high level of gastrin secretion and its concentration in the circulating blood as a result of the constant action of such a stimulus for secretion by O-cells as achlorhydria, which occurs as a result of autoimmune damage to parietal cells.

In chronic gastritis type A, lesions of the gastric mucosa are mainly localized in the fundus and body of the stomach. Pernicious anemia in this type of chronic gastritis is associated with insufficient formation of internal Castle factor in the gastric mucosa, which decreases due to its autoimmune damage.

Pathological changes in the gastric mucosa in chronic gastritis type B occur predominantly in the antrum, that is, to a lesser extent they affect the hydrochloric acid-secreting cells of the gastric mucosa. In some patients with this type of chronic gastritis, autoantibodies to O cells are detected in the blood. Damage to gastrin-secreting cells of the mucous membrane in chronic gastritis type B reduces the level of its secretion. Therefore, in patients with this type of gastritis, the level of release of hydrochloric acid into the lumen of the stomach is usually not increased, and is often at a normal level.

Chronic gastritis of both types is often asymptomatic. Like many autoimmune diseases, chronic gastritis type A is combined with other diseases of an autoimmune nature, hypothyroidism associated with autoimmune damage to the thyroid gland, insulin-dependent diabetes mellitus, etc.

Over the course of 10-20 years, both types of gastritis lead to severe atrophy of the gastric mucosa and pernicious anemia. Both types of gastritis are risk factors for stomach and duodenal ulcers, polyps, and stomach cancer, but cancer occurs more often in patients with type B gastritis.

Eosinophilic gastroenteritis refers to the infiltration of eosinophils into the antrum of the stomach and (or) small intestine. Such infiltration, which is considered a consequence of unclear immunopathological changes, leads to thickening of the walls of the stomach in the antrum, which leads to obstruction of the entry of food into the stomach from the esophagus. In patients with this rare type of gastritis, an increase in the content of eosinophils in the circulating blood is often detected. Under the influence of corticosteroid therapy, eosinophilic gastroenteritis may undergo reversal through eosinophil apoptosis.

Gastric hyperplasia in morphopathogenetic terms is characterized, first of all, by a significant increase in the folds of the gastric mucosa. A study of the biopsy reveals hyperplasia (an increase in the number of cells to a value greater than normal) of the cells of the gastric mucosa, as well as (in some patients) its infiltration by activated cellular effectors of inflammation with the properties of phagocytes and lymphocytes. Gastric hyperplasia is caused by:

♦ Ménétrier's disease;

♦ hypersecretory gastropathy;

♦ gastrinoma (Zollinger-Ellison syndrome).

Ménétrier's disease is characterized by rough, convoluted folds of the mucous membrane with hyperplasia of mucous cells and a decrease in the number of parietal and chief cells (zymogenic cells that secrete pepsin). Hyperplasia of gastric epithelial cells is accompanied by the formation of gaps between them, which causes loss of albumin through the pathologically altered mucous membrane into the lumen of the stomach. A decrease in the proteolytic activity of gastric juice as a cause of insufficient partial digestion of food in the stomach, as well as an increase in the colloid-osmotic pressure of the stomach contents entering the duodenum due to the migration of albumin into the gastric lumen cause osmotic diarrhea in patients with Ménétrier's disease. Often the only symptom of the disease is pain localized in the epigastric region. Hypoalbuminemia as a consequence of the disease can cause interstitial edema.

Gastritis is a long-term disease that manifests itself in changes in the mucous membrane of an inflammatory and often dystrophic nature. It causes disruption of regeneration and atrophy of epithelial cells, as well as the replacement of healthy glands with fibrous tissue.

But what is atrophic gastritis? What are its symptoms, reasons for its appearance, how to treat it, what consequences can it have? This is exactly what we will talk about now.

Characteristics of the disease and etiology

Before moving on to considering the symptoms of atrophic gastritis, it is worth talking about what it actually is.

So, this is one of the most dangerous forms of the disease in question. It is diagnosed if a person experiences inflammatory processes in the pancreas and mucous membrane. Also, during the course of this disease, the cells that are responsible for the production of gastric juice stop functioning normally. Because of this, the glands that produce hydrochloric acid and enzymes subsequently die.

Atrophic gastritis often spreads to the entire stomach, and not just to part of the organ. Also, this disease often becomes the cause of a precancerous condition.

The reasons why this disease occurs include the following:

Lack of balanced and rationed nutrition.
Addiction to alcoholic beverages.
Mental and nervous stress.
Smoking.
Disturbances of the endocrine system.
Hereditary predisposition.

Any of the above first leads to a violation of the integrity of the mucous membrane, and the consequence of this is its inflammation. Then the disease begins to develop rapidly.

Signs

The main symptom of focal atrophic gastritis is the formation of local inflammation in the wall of the stomach, accompanied by increased function of its healthy areas (compensation mechanism).

But these changes cannot be noticed. More obvious symptoms of atrophic gastritis include:

Discomfort in the epigastric region (upper, middle area under the ribs).
Pain and burning after eating.
Feeling of heaviness and nausea. They appear even after a light snack.

These signs characterize the initial form of the disease. If you ignore them and do not go to the doctor for treatment, the symptoms of atrophic gastritis of the stomach will not only intensify, but will also be supplemented by the following manifestations:

Loss of appetite.
Heartburn.
Increased pain syndrome.
Weight loss.
Constant weakness.
Low-grade fever.
Increased secretion of hydrochloric acid and its entry into the lumen of the stomach.
Increase in the level of general acidity.

Moreover, during this period, a person is especially susceptible to the influence of Helicobacter pylori, an opportunistic bacterium. For this microorganism, increased acidity is an ideal habitat.

In small quantities, bacteria cannot harm, but in such good conditions they multiply quickly, which leads to negative consequences. After all, bacterial waste products are cytotoxins that increase inflammation of the mucous membrane.

In addition, against the background of weakened defenses of the body, Helicobacter pylori penetrates deeper, as a result of which the cells of the tissues of the stomach and its glands are poisoned. Because of this, ulcers often occur.

Other warning signs

It is important to note that the above symptoms of atrophic gastritis are not observed in all patients. But each of them experiences disturbances associated with the process of absorption of various substances (vitamins, iron, etc.), as a result of which anemic syndrome begins to develop.

This causes the appearance of symptoms caused by a lack of the mentioned elements in the body. They appear as follows:

Burning in the mouth.
Dyspnea.
Drowsiness.
Fatigue.
Apathy.
Paleness of mucous membranes and skin.
Impaired sensitivity of the limbs.
Pain in the tongue, accompanied by a change in its color.
Brittle nails and dry hair.
Chest pain.
"Air" belching.
Stool instability (constipation may be replaced by diarrhea).

After an external examination, it is possible to detect plaque. Also, bad breath, a similar taste, and hypersalivation (increased salivation) are often observed.

The symptoms of atrophic gastritis of the stomach cannot be ignored. This is fraught with serious consequences. Some patients consult a doctor already when their acidity is reduced to alchemy (that is, there is no acid in the stomach completely).

Consequences

Before moving on to the principles of eliminating symptoms and treating atrophic gastritis with folk and medical remedies, it is necessary to list the consequences that arise as a result of ignoring the disease. These include:

Disturbance of digestive processes. A neglected condition leads to the development of dysbiosis.
Anemia, vitamin deficiency, asthenia.
The occurrence of fermentation and putrefaction processes in the stomach.
Frequent vomiting, blood in saliva.
Constant dehydration.
Formation of ulcerative lesions.
Decreased secretory function, loss of interest in food, development of exhaustion, which turns into cachexia.
Formation of multiple follicles from lymphoid tissue in the gastric walls.
Attachment of a secondary infection. Possible phlegmonous gastritis.

It should be mentioned that with this disease there is a risk of internal gastric bleeding. This complication poses a serious threat to life.

Antibiotics

It is very important to choose the right treatment for atrophic gastritis of the stomach, the symptoms and causes of which were listed above. This, of course, is done by the doctor - he prescribes drugs that are suitable for the patient in his particular case, and always those that are gentle on the stomach.

As a rule, the choice is made in favor of the following drugs:

"Flemoxin Solutab". Penicillin antibiotic with bactericidal action. It can be used from 6 months (but for babies - only in the form of a suspension). The daily dosage for an adult is 1000 - 1500 mg. The specified volume should be divided into morning and evening doses. As a rule, this antibiotic is combined in combination therapy. It must be taken for at least 10 days.
"Panclave". Penicillin antibiotic with a broad spectrum effect. It can be taken only from 12 years of age, the minimum patient weight is 40 kg. For patients with moderate health conditions, the norm is 750 mg. The dosage is divided into three doses. If the lesion is severe, you need to take 500 mg 3 times a day. Therapy usually lasts from 5 to 14 days.
"Ospamox". It is approximately the same as the first antibiotic listed. The dosage is similar, 1000-1500 mg/day. In severe cases, it should be increased to 3 g. Ospamox is taken with meals to reduce the negative effects of the medication on the stomach. The duration of therapy is determined individually, but it is at least 7 days.

These drugs are the most effective in eliminating symptoms and treating focal atrophic gastritis. And reviews allow you to verify this. There are also drugs “Gonoform”, “Amosin”, “Amoxikar”, “Grunamox”, “Amoxicillin”, “Ecobol” and other antibiotics, but the gastroenterologist will determine which one will have to be treated.

Proton pump inhibitors

They are also prescribed to eliminate unpleasant symptoms and treat focal atrophic gastritis. Reviews make it clear that these drugs help quickly get rid of pathologies of the mucous membrane that arise due to impaired acidity. They reduce the production of hydrochloric acid by blocking the proton pump in the parietal cells.

The best drugs in this group are considered to be the following antisecretory drugs:

"Omeprazole." Typically, the daily dose is 20 mg. In severe cases and during exacerbations, it is doubled. It is best to take the product at night. Be sure to take the tablets with plenty of water. Therapy lasts from 14 to 30 days.
"Bioprazole". One capsule per day is enough, which contains just 20 mg of the active substance. It is worth noting that this drug is very quickly absorbed in the stomach.
"Omezol". A mildly acting drug that is prescribed even for duodenal ulcers. One tablet contains 40 mg of active ingredient, so the doctor will prescribe the dosage individually. As a rule, one piece per day is enough.
"Control". An inhibitor whose main active ingredient is pantoprazole. Its particular purpose is to have a gentle effect on the gastric mucosa. Therefore, the course of treatment is usually long. This is necessary to prevent relapses.
"Nolpaza". The action of the drug is similar to Controloc. But it is prohibited for people under 18 years of age to take it. An analogue is a medicine called “Ulthera”. Any of the drugs is taken in the morning, the dosage is determined by the doctor.

In addition to the listed remedies, there are also tablets based on rabeprazole and esomeprazole. They are also prescribed to relieve symptoms and treat atrophic gastritis in adults. Preparations with esomeprazole are special in that their components remain in the human body for a long time (this is the reason for the minimum dosages). And rabeprazole drugs are usually indicated for ulcers.

Other drugs

In addition to the above, there are many other medications that help eliminate symptoms and treat atrophic gastritis.

Gastritis -inflammation of the gastric mucosa.

According to the nature of the flow there are acute and chronic gastritis.

There are several morphological forms of acute gastritis:

· catarrhal,

· fibrinous,

· purulent,

· necrotic.

Catarrhal gastritis.Macroscopically, the gastric mucosa is thickened, with high hyperemic folds covered with thick viscous mucus. Sometimes, at the height of the folds, pinpoint hemorrhages and erosions are visible. On histological examination, the mucous membrane is covered with serous-mucosal exudate with an admixture of neutrophils and desquamated integumentary epithelium. In the lamina propria of the mucous membrane there is edema, vascular congestion, diapedetic hemorrhages and slight neutrophil infiltration.

Fibrinous gastritis. There is a yellow-gray or yellow-brown film on the surface of the gastric mucosa. This film is either easily torn away (lobar gastritis) or is firmly attached; when you try to separate it, ulcerative defects are exposed (diphtheritic gastritis).

Purulent (phlegmonous) gastritis It is rare and complicates injuries, tumors or ulcers. Macroscopically, the wall of the stomach is thickened, the folds are smoothed, and covered with a purulent greenish-yellow film. Microscopically, diffuse infiltration of all layers of the wall by neutrophils, sometimes with colonies of microorganisms, is pronounced. The process can spread to the peritoneum with the development of perigastritis and peritonitis.

Necrotizing gastritis usually develops when acids, alkalis and other drugs that destroy the mucous membrane enter the stomach. Necrosis involves the superficial sections of the mucous membrane or the entire wall of the stomach and can be coagulative and colliquating in nature. When necrosis is rejected, erosions or ulcers are exposed. In acute ulcers, perforation of the stomach wall often occurs.

Outcomes and complications of acute gastritis With catarrhal gastritis, complete recovery and restoration of the mucous membrane usually occurs. Less often the process becomes chronic. With fibrinous gastritis, deformation of the stomach wall is possible. With purulent gastritis, perigastritis, mediastinitis, purulent pleurisy, subphrenic abscess, and liver abscess occur. Necrotizing gastritis is complicated by gastric bleeding and perforation of the stomach wall.

Chronic gastritis is a widespread disease. It is believed that half of the world's population suffers from chronic gastritis. The diagnosis of chronic gastritis is established only on the basis of a morphological study of biopsy material from the gastric mucosa. To obtain optimal information, it is recommended that multiple biopsies be performed. When morphologically diagnosing chronic gastritis, take into account:

degree of contamination H.pylori;

· degree of infiltration of the mucous membrane by neutrophils and mononuclear cells;

· severity of atrophy;

Etiology. Exogenous and endogenous factors are important in the development of gastritis.

Of the exogenous factors, the greatest role is played by Helicobacter pylori(H.pylori).

Helicobacter pylori– a gram-negative bacterium with five motile flagella at one end. Usually H.pylori located in the pyloric part of the stomach under a layer of mucus.

H.pylori affects both the proliferation and apoptosis of epithelial cells of the gastric mucosa, disrupting the normal regeneration processes of the gastric epithelium. Disruption of cellular renewal processes in the gastric mucosa underlies the morphogenesis of atrophy in gastritis.

Except H.pylori There are other etiological factors of chronic gastritis.

Exogenous causes:

· chronic violation of the diet and rhythm;

· exposure to chemical, thermal, mechanical agents, radiation;

· long-term use of non-steroidal anti-inflammatory and other medications;

long-term drinking of alcohol.

Endogenous factors:

autointoxication (uremia);

Hypoxia (chronic cardiovascular failure);

· operations on the stomach (gastroenteroanastomosis);

· autoimmunization, etc.

It is currently generally accepted classification of chronic gastritis, called the Modified Sydney System (1996).

In accordance with it, they distinguish:

non-atrophic gastritis;

· atrophic (autoimmune, multifocal) gastritis;

· special forms of gastritis (chemical, radiation, lymphocytic, granulomatous, eosinophilic, giant hypertrophic, etc.)

Chronic non-atrophic (superficial) gastritis. The gastric mucosa is of normal thickness. Covering epithelium with dystrophic changes. The lamina propria is infiltrated with lymphocytes and plasma cells. The infiltrate is usually located in the superficial sections at the level of the ridges. The prognosis for superficial gastritis is favorable. The disease lasts for many years, and reverse development is possible.

Chronic atrophic gastritis differs from superficial by the appearance of atrophy. The mucous membrane is thinned, its relief is smoothed. The ridges are shortened and flat, the pits are deepened. The integumentary pit epithelium is flattened. The glands are shortened, their number is reduced. In the lamina propria there are fields of sclerosis and a polymorphic cellular infiltrate in place of the former glands. Foci of complete or incomplete intestinal metaplasia, as well as epithelial dysplasia, often occur. Chronic atrophic gastritis is a long-term disease, a precancerous disease of the stomach, since cancer can develop against the background of severe epithelial dysplasia.

Varieties of chronic atrophic gastritis are autoimmune and multifocal gastritis.

Autoimmune gastritis – a rare genetic disease in which antibodies to parietal cells and intrinsic factor are detected in the blood and gastric juice. Given the localization of parietal cells, autoimmune gastritis always affects the body of the stomach (fundic gastritis). Diffuse atrophic changes with elements of inflammation develop here, while the antrum remains unaffected.

Multifocal atrophic gastritis characterized by damage to the mucous membrane in the form of multiple foci, involving the body and antrum of the stomach. Irreversible atrophic changes in the mucous membrane develop with a decrease in the number of glands and their partial replacement by intestinal epithelium (intestinal metaplasia). Multifocal atrophic gastritis serves as a background for the development of stomach cancer.

From the group of special forms of chronic gastritis, chemical and lymphocytic gastritis should be distinguished.

1. Pathophysiology of chronic Helicobacter gastritis and the natural course of H. Pylori infection

H. pylori infection is characterized by long-term persistence on the gastric mucosa with the development of infiltration of its lamina propria with inflammatory cells. Infection with H. pylori always leads to the development of an immune response, which almost never ends, however, in the complete elimination of the pathogen. This is primarily due to the fact that, unlike other extracellular pathogens, H. pylori causes a predominantly type 1 immune response, accompanied by activation of the cellular component of immunity.

The development of neutrophil infiltration of the lamina propria is associated with two different mechanisms. The direct mechanism is realized through the release of neutrophil-activating protein by H. pylori, and the indirect mechanism is through stimulation of the expression of IL-8 by epithelial cells, followed by the launch of a complex inflammatory cascade.

Granulocytes migrating into the gastric mucosa damage epithelial cells by releasing reactive oxygen species and intensively produce pro-inflammatory cytokines. Under such conditions, against the background of progression of inflammation, in some cases there is damage and death of epithelial cells with the formation of erosive and ulcerative defects, while in others atrophy, metaplasia and neoplasia of the gastric mucosa gradually form.

Another significant feature of the pathogenesis of H. pylori infection is the failure of humoral immunity and the lack of eradication under the influence of anti-Helicobacter antibodies. This fact is usually explained by the “inaccessibility” of the bacterium to antibodies in the layer of gastric mucus, the inability to release IgG into the lumen of the stomach with a relative deficiency of secretory IgA, as well as “antigenic mimicry” of the bacterium.

Despite the fact that chronic gastritis develops in all people infected with H. pylori, not every case has any clinical manifestations. In general, for H. pylori-positive patients, the lifetime risk of developing peptic ulcers and gastric cancer is 10-20% and 1-2%, respectively.

Duodenal ulcers (DU) and gastric cancer are commonly associated with different types of chronic gastritis. With antral gastritis with the absence or minimal severity of atrophy, normal or increased secretion of hydrochloric acid, duodenal ulcers often develop. In pangastritis with severe atrophy of the mucous membrane, hypo- or achlorhydria, gastric cancer is recorded much more often.

This fact was explained after the discovery of H. pylori, when it became clear that in most cases, antral gastritis and pangastritis represent different directions of the natural course of this infection.

After infection, which usually occurs in childhood or adolescence, H. pylori causes acute gastritis with nonspecific transient symptoms of dyspepsia (epigastric pain and heaviness, nausea, vomiting) and hypochlorhydria.

Subsequently, acute Helicobacter pylori gastritis becomes chronic. Either superficial antral gastritis or atrophic multifocal pangastritis gradually forms. The key factor determining the topography of gastritis, and therefore the likelihood of developing duodenal ulcer or gastric cancer, is the level of hydrochloric acid secretion.

In individuals with normal or high secretory activity of parietal cells, hydrochloric acid inhibits the growth of H. pylori in the body of the stomach, and the bacterium intensively colonizes only the antrum, causing, accordingly, limited antral gastritis. Chronic inflammation in the antrum leads to hypergastrinemia and hyperchlorhydria, acidification of the duodenal cavity and ulcer formation. In patients with reduced levels of hydrochloric acid secretion, H. pylori freely colonizes the mucous membrane of the gastric body, causing pangastritis. Chronic active inflammation, through the effects of a number of cytokines, further inhibits the function of parietal cells, and subsequently causes the development of atrophy and metaplasia of the main glands. As a result, this category of patients has a significantly increased risk of developing stomach cancer.

According to modern concepts, the decisive role in the determination of these processes belongs to the genetic factors of the human body. They are directly related to the characteristics of the immune response, in particular, the level of production of the proinflammatory cytokine IL-1b, which has pronounced antisecretory properties. Genetically determined overexpression of this substance causes persistent suppression of hydrochloric acid secretion already at the stage of acute Helicobacter gastritis. In such a situation, favorable conditions are created for the colonization of H. pylori in the body of the stomach.

The close relationship between gastric cancer and H. pylori has also been confirmed by large epidemiological studies. The presence of infection increases the risk of developing this malignant tumor by 4-6 times. In patients with chronic atrophic pangastritis associated with H. pylori, the likelihood of neoplasia increases even more. The International Agency for Research on Cancer has classified H. pylori as a Class I human carcinogen for non-cardiac gastric cancer.

Thus, chronic Helicobacter gastritis is the background against which gastric cancer develops in most cases. An important condition for its occurrence is the presence of disturbances in cellular renewal in the gastric mucosa in the form of its atrophy and intestinal metaplasia.

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Introduction

Literature

Introduction

At the present stage of development of gastroenterology, the term “chronic gastritis”; unites a whole group of diseases characterized by inflammation of the gastric mucosa.

The main cause of chronic gastritis is H. pylori infection. Only less than 10% of cases occur due to autoimmune gastritis, rare forms of gastritis (lymphocytic, eosinophilic, granulomatous), other infectious agents and chemicals. The prevalence of chronic gastritis in the world population is very high and ranges from 50 to 80%. In Russia this figure is at the same level.

Classification of chronic gastritis: The modified Sydney classification involves the division of chronic gastritis according to the etiology and topography of morphological changes. There are three types of gastritis:

* non-atrophic (superficial) gastritis;

* atrophic gastritis;

* special forms of chronic gastritis (lymphocytic, eosinophilic, granulomatous, chemical, radiation).

Non-atrophic antral gastritis and multifocal atrophic gastritis involving the body and antrum of the stomach are associated with H. pylori infection. Atrophic gastritis of the body of the stomach is of an autoimmune nature.

The basic principles of diagnosis and rational pharmacotherapy of chronic gastritis associated with H. pylori are discussed below.

chronic gastritis Helicobacter pylori infection

1. Pathophysiology of chronic Helicobacter gastritis and the natural course of H. Pylori infection

2. Diagnosis of chronic gastritis

A reliable diagnosis of chronic gastritis can be established only after a morphological examination of biopsy samples of the gastric mucosa by a morphologist. To adequately assess histological changes and determine the topography of chronic gastritis in accordance with the requirements of the Sydney system, it is necessary to take at least five biopsies (2 from the antrum, 2 from the body and 1 from the angle of the stomach). The conclusion should contain information about the activity and severity of inflammation, the degree of atrophy and metaplasia, and the presence of H. pylori.

Non-invasive diagnosis of atrophic gastritis can be carried out using a number of serum markers. Severe atrophy of the mucous membrane of the gastric body is characterized by a decrease in the level of pepsinogen I, and atrophy of the antrum is manifested by low levels of basal and postprandial gastrin-17.

Determining antibodies to gastric parietal cells and identifying signs of B12-deficiency anemia helps to exclude autoimmune chronic gastritis.

The fundamental point in the diagnosis of chronic gastritis is the identification of H. pylori. In practice, the choice of a specific method in most cases is determined by the clinical characteristics of the patient and the availability of certain tests.

All methods for diagnosing H. pylori, depending on the need for endoscopic examination and collection of biopsy material, are divided into invasive and non-invasive. Initial anti-Helicobacter therapy can be prescribed if a positive result of any of them is obtained.

Chronic gastritis always requires morphological confirmation. In this case, preference should be given to invasive methods for diagnosing helicobacteriosis, which include a rapid urease test, histological examination of biopsy specimens of the gastric mucosa for the presence of H. pylori, and polymerase chain reaction in the biopsy specimen.

Primary diagnosis of helicobacteriosis using these tests can give false negative results when the density of bacterial contamination of the mucous membrane is low, which often occurs when taking proton pump inhibitors (PPIs), antibiotics and bismuth preparations, as well as with severe atrophic gastritis. In such cases, a mandatory combination of invasive methods with the determination of antibodies to H. pylori in blood serum is recommended.

Eradication monitoring, regardless of the tests used, should be carried out no earlier than 4-6 weeks after the end of the course of eradication therapy. Preference should be given to a urease breath test and determination of the H. pylori antigen in stool using an enzyme-linked immunosorbent assay (ELISA). If these non-invasive methods are not available, histological examination and rapid urease test should be repeated.

3. Treatment of chronic Helicobacter gastritis

Treatment of chronic Helicobacter pylori gastritis involves eradication therapy, the goal of which is the complete destruction of H. pylori in the stomach and duodenum. The need for treatment of helicobacteriosis in such patients is associated with the prevention of non-cardiac gastric cancer and peptic ulcer, since most patients with gastritis do not present any complaints. Only eradication of H. pylori allows one to achieve regression of inflammatory phenomena, as well as prevent the development or progression of precancerous changes in the mucous membrane.

It should be noted that long-term monotherapy with PPIs for chronic Helicobacter gastritis is unacceptable. Persistent suppression of acid production promotes the movement of H. pylori from the antrum to the body of the stomach and the development of severe inflammation there. The prerequisites are created for changes in the topography of gastritis. Predominantly antral gastritis turns into pangastritis. In such patients, the likelihood of developing atrophy of the mucous membrane of the body of the stomach increases, in fact, iatrogenic atrophic gastritis.

In the recommendations of the III Maastricht Consensus, only atrophic gastritis appears among the absolute indications for prescribing anti-Helicobacter therapy. At the same time, the compilers of authoritative international guidelines emphasize that it is still optimal to carry out therapy before the development of atrophy and intestinal metaplasia of the mucous membrane, still at the stage of non-atrophic (superficial) gastritis. Eradication in close blood relatives of patients with gastric cancer is strongly recommended.

Modern anti-Helicobacter therapy is based on standard regimens based on PPIs and bismuth tripotassium dicitrate (De-Nol). The Third Maastricht Consensus recommendations for the treatment of H. pylori infection distinguish between first- and second-line treatment regimens. Options for third-line regimens (rescue therapy), which can be used after two unsuccessful eradication attempts, are being actively discussed.

Treatment begins with a triple first-line regimen: PPI at a standard dose 2 times a day, clarithromycin 500 mg 2 times a day and amoxicillin 1000 mg 2 times a day. It is recommended to extend the duration of therapy from 7 to 14 days, which significantly increases the effectiveness of eradication. The use of triple regimens including metronidazole is absolutely unjustified, since the critical threshold of H. pylori resistance to this antibiotic (40%) in Russia has long been overcome.

The prospects for first-line triple therapy are significantly limited by the rapid increase in Helicobacter pyloric resistance to clarithromycin.

The main reasons for the increase in the number of antibiotic-resistant strains of H. pylori are an increase in the number of patients receiving inadequate anti-Helicobacter therapy, low doses of antibiotics in eradication regimens, short courses of treatment, incorrect combination of drugs and uncontrolled independent use of antibacterial drugs by patients for other indications.

Multicenter studies to determine the resistance of H. pylori to clarithromycin, conducted in countries of the European Region, revealed its presence in 21-28% of cases in adults and in 24% of cases in children. The same unfavorable situation is gradually emerging in Russia. In 2006, in Moscow among adults and in St. Petersburg among children, resistant strains were detected in 19.3 and 28% of those examined. By 2009, in St. Petersburg, their share in adult patients increased to 40-66%.

Increasing resistance of H. pylori to clarithromycin is leading to a steady decline in the effectiveness of standard first-line clarithromycin-based triple therapy. According to both Russian and foreign clinical studies, this figure is already 55-61%.

As an effective alternative to triple therapy, the Third Maastricht Consensus recommends a standard four-component regimen based on bismuth as the first line of eradication: bismuth tripotassium dicitrate (De-Nol) 120 mg 4 times a day, PPI at a standard dose 2 times a day, tetracycline 500 mg four times a day and metronidazole 500 mg 3 times a day for 10 days. It should be emphasized that the use of bismuth makes it possible to overcome the resistance of Helicobacter pyloricus to metronidazole.

This eradication option is preferable if there is a high level of H. pylori resistance to clarithromycin in the region (above 20%), if the patient has a history of allergic reactions to clarithromycin, amoxicillin or other antibiotics from their groups, as well as with previous use of macrolides for other indications.

In our country, a three-component regimen is used as first-line therapy with the inclusion of bismuth tripotassium dicitrate at a dose of 120 mg 4 times a day, amoxicillin at a dose of 1000 mg 2 times a day and clarithromycin at a dose of 500 mg 2 times a day. This combination is especially suitable for patients with chronic atrophic gastritis in the absence of any clinical symptoms. In such patients, there is no need for rapid suppression of hydrochloric acid production, and these regimens may be optimal in terms of cost/effectiveness ratio.

If, after triple anti-Helicobacter therapy of the first stage, treatment turned out to be ineffective (no eradication of H. pylori 6 weeks after complete withdrawal of antibiotics and antisecretory drugs), in accordance with the Maastricht recommendations, quadruple therapy based on bismuth tripotassium dicitrate is prescribed as a second-line regimen for a period of 10 days . Replacing metronidazole with furazolidone in this regimen does not reduce the effectiveness of treatment.

If quadruple therapy was used at the first stage, alternative second-line triple regimens can be used, including PPI at a standard dose and amoxicillin 1000 mg 2 times a day in combination with tetracycline (500 mg four times a day) or furazolidone (200 mg 2 times a day). once a day).

In general, with the increasing resistance of H. pylori to the main antibacterial drugs, bismuth tripotassium dicitrate (De-Nol) begins to play a leading role in the first and second line eradication schemes, which is due to the presence of a number of unique properties.

Bismuth tripotassium dicitrate has the most pronounced antibacterial properties against H. pylori infection among all bismuth preparations. De-Nol is highly soluble in the aqueous environment of gastric juice and is able to maintain high activity at any level of gastric secretion. It easily penetrates the gastric pits and is captured by epithelial cells, which makes it possible to destroy bacteria located inside the cells. An important point is the complete absence of H. pylori strains resistant to bismuth salts.

The anti-Helicobacter effect of De-Nol is complex and is due to a number of mechanisms:

* precipitation on the membrane of H. pylori with subsequent disruption of its permeability and death of the microorganism;

* suppression of H. pylori adhesion to epithelial cells;

* suppression of H. pylori motility;

* effect on vegetative and coccal forms of H. pylori;

* synergism against H. pylori with other antibiotics (metronidazole, clarithromycin, tetracycline, furazolidone).

The latest data on the use of bismuth tripotassium dicitrate as an anti-Helicobacter therapy were obtained in a recent study aimed at assessing the effectiveness of a modified 7- and 14-day triple regimen in the first line. Tripotassium bismuth dicitrate was added to the standard combination, which included omeprazole, clarithromycin and amoxicillin, at a dose of 240 mg 2 times a day. Before starting treatment, the sensitivity of H. pylori to antibiotics was determined.

The results of the study showed extremely promising results. The 14-day treatment regimen demonstrated significantly greater effectiveness than the 7-day regimen. In the first case, eradication was achieved in 93.7% of patients, while in the second only in 80% of patients. In the presence of clarithromycin-resistant strains of H. pylori, treatment was successful in 84.6% of individuals who underwent a two-week course of treatment, and only in 36.3% of cases when using a 7-day regimen, which indicates the possibility of overcoming bacterial resistance to clarithromycin against the background use of bismuth preparation.

The indicated four-component regimen consisting of bismuth tripotassium dicitrate, PPI, amoxicillin and clarithromycin has already been recommended by leading Russian experts as one of the first-line treatment options for the treatment of helicobacteriosis.

Thus, the widespread use of bismuth tripotassium dicitrate provides in the future a real chance to compensate for the lack of new highly active antibacterial agents against H. pylori. A modified 14-day regimen containing this drug appears to be able to be used successfully as first-line therapy even in areas with a high prevalence of clarithromycin-resistant strains of the bacterium. This strategy will significantly reduce the level of Helicobacter pyloric resistance to currently used antibiotics and maintain high rates of effectiveness of eradication therapy.

In addition to the antibacterial effect, bismuth tripotassium dicitrate has a pronounced cytoprotective effect. The drug creates a film on the surface of the mucous membrane of the stomach and duodenum that protects epithelial cells from the effects of the acid-peptic factor and potentiates repair processes in the area of erosive and ulcerative defects. Moreover, bismuth ions have the ability to directly stimulate the proliferation of epithelial cells.

De-Nol has almost no effect on the basal and stimulated secretion of hydrochloric acid and does not seriously disrupt the physiology of the stomach. This is especially important for patients with mucosal atrophy due to severe inflammation. Additional suppression of acid production when taking PPIs in such a situation can trigger intestinal epithelial differentiation and the development of intestinal metaplasia.

Bismuth tripotassium dicitrate stimulates the synthesis of prostaglandin E2 and improves the quality of the hydrophobic layer of gastric mucus produced by the surface epithelium. An increase in the production of prostaglandin E2 potentiates the secretion of bicarbonates, improves microcirculation, stimulates angiogenesis, supports the reconstruction of the extracellular matrix, and has an anti-inflammatory effect. The drug prevents degradation of the mucous layer, protects against destruction and fixes epidermal growth factor in the area of damage, which is necessary for complete physiological and reparative regeneration of epithelial cells.

The pronounced antioxidant effect of bismuth salts has been proven, suppressing lipid peroxidation and protecting DNA from the effects of reactive oxygen species. Against this background, the risk of mutations in epithelial cells, which serve as the basis for the onset of tumor growth, is reduced.

The positive side of using De-Nol is its low bioavailability. When taking this drug as a course for 1 month, its concentration in the blood is 50 mcg/l, and in gastric juice - 100 mg/l, which practically eliminates the manifestation of systemic effects of bismuth.

If second-line therapy fails, there are two options:

* Conducting empirical “rescue” therapy (third line);

* Selection of drugs depending on the results of determining the sensitivity of H. pylori to all antibiotics used in eradication regimens.

Currently in Russia, the use of two potential options for ten-day “rescue” therapy is most justified. To PPI (standard dosage 2 times a day) and amoxicillin (1000 mg 2 times a day), levofloxacin (250 mg 2 times a day) or furazolidone (200 mg 2 times a day) is added.

The effectiveness of individual selection of antibiotics depending on the sensitivity of H. pylori to them is illustrated by the results of using a seven-day third-line regimen consisting of bismuth tripotassium dicitrate, esomeprazole, doxycycline and amoxicillin. Even when strains with resistance to several antibacterial drugs were identified, eradication was achieved in 91% of cases. The general algorithm for anti-Helicobacter therapy is presented in Figure 1.

Despite the fact that the elimination of H. pylori leads to a gradual reduction of inflammation and normalization of epithelial cell renewal processes, a significant proportion of patients retain exhelicobacter gastritis, the morphological basis of which is mononuclear infiltration of the lamina propria of the mucous membrane. Its long-term persistence creates conditions for the progression of structural changes in the post-eradication period, even in the absence of an infectious factor.

In such a situation, it is pathogenetically justified to prolong the course of treatment for H. pylori with the prescription of monotherapy with De-Nol 240 mg 2 times a day for 6 weeks. Due to its cytoprotective and antioxidant properties, bismuth tripotassium dicitrate prevents damage to epithelial cells, and stimulation of cellular turnover potentially contributes to the reversal of atrophy.

In general, in patients with chronic gastritis, successful eradication of H. pylori allows for regression of inflammatory infiltration and restoration of the normal morphological structure of the gastric mucosa. In the presence of atrophy and metaplasia, elimination of the infectious agent makes it possible to stop the further progression of these precancerous changes, and in some cases, achieve the reverse development of atrophy. Considering that Helicobacter gastritis, especially in the presence of atrophic changes, significantly increases the risk of developing stomach cancer, treatment of H. pylori infection followed by a course of bismuth tripotassium dicitrate is the most important measure for the prevention of this widespread cancer.

Literature

1. Baryshnikova N.V., Denisova E.V., Kornienko E.A., et al. Epidemiological study of Helicobacter pylori resistance to clarithromycin in residents of St. Petersburg with peptic ulcer // Experimental and clinical gastroenterology. - 2009. - No. 5 - P. 73-76.

2. Baryshnikova N.V., Uspensky Yu.P., Tkachenko E.I. Optimization of treatment of patients with diseases associated with Helicobacter pylori: justification for the need to use bismuth preparations // Experimental and clinical gastroenterology. - 2010. - No. 6. - P. 116-121.

3. Ivashkin V.T., Sheptulin A.A., Lapina T.L. Chronic gastritis caused by Helicobacter pylori infection: diagnosis, clinical significance, prognosis. A manual for doctors. - Moscow. - 2011. - 24 p.

4. Livzan M.A., Kononov A.V., Mozgovoy S.I. Post-eradication period of chronic gastritis associated with Helicobacter pylori infection // Consilium medicum. - 2010. - No. 8. - pp. 15-20.

5. Maev I.V., Kucheryavyi Yu.A., Oganesyan T.S. Allelic polymorphism of interleukin-1 in Helicobacteriosis // Ross. magazine gastroenterol., hepatol., coloproctol. - 2008. - No. 5. - P. 4-11.

6. Standards for diagnosis and treatment of acid-dependent and Helicobacter pylori-associated diseases (Fourth Moscow Agreement) // Experimental and clinical gastroenterology. - 2011. - No. 5. - P. 113-118.

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