Chronic gastritis and gastroduodenitis in children

Chronic gastritis is a chronic recurrent focal or diffuse inflammation of the mucosa (submucous) of the gastric membrane with a violation of physiological regeneration, prone to progression, development of atrophy and secretory insufficiency, underlying the digestive and metabolic disorders.

Chronic gastroduodenitis is a chronic inflammation with structural (focal or diffuse) restructuring of the mucous membrane of the stomach and duodenum, as well as the formation of secretory, motor and evacuation disorders.

ICD-10 code

K29. Gastritis and duodenitis.

Epidemiology of chronic gastritis and gastroduodenitis in children

Chronic gastritis and chronic gastroduodenitis are the most common gastroenterological diseases of childhood, occurring with a frequency of 300-400 per 1,000 children, and isolated lesions do not exceed 10-15%.

In the structure of diseases of the upper gastrointestinal tract, chronic gastroduodenitis is 53.1%, chronic gastritis - 29.7%, chronic duodenitis - 16.2%. Non-ulcer gastroduodenal pathology affects children of all age groups, but most often the disease is diagnosed at the age of 10-15 years. At the younger school age, there are no sex differences in the frequency of chronic gastritis and chronic gastroduodenitis, and boys are more likely to suffer in older school age.

The frequency of chronic gastritis associated with H. Pylori infection varies depending on the child's age and is 20% in children 4-9 years old, 10-14 years old - 40%, over 15 years old and in adults - 52-70%.

[1]

Causes and pathogenesis of chronic gastritis and gastroduodenitis

Chronic gastritis and chronic gastroduodenitis are multifactorial diseases. They matter:

• hereditary-constitutional predisposition to diseases of the digestive system - the indicator of family burden is 35-40%;
• Infection with Helicobacter pylori;
• nutritional errors (irregular, inferior in composition, poor chewing, abuse of spicy food);
• chemical, including medicamentous, effects;
• physical and psycho-emotional overload;
• food allergy;
• foci of infection, parasitosis and diseases of other digestive organs.

Against the background of the continued relevance of alimentary, acid-peptic, allergic, autoimmune, hereditary factors in the development of chronic gastritis and chronic gastroduodenitis, the infectious factor is considered decisive and determining. H. Pylori - the main etiological factor in the development of chronic inflammatory diseases of the gastroduodenal zone, which significantly increases the risk of developing peptic ulcer and stomach cancer.

Prolonged H. Pylori stay in the gastric mucosa results in neutrophilic and lymphocytic infiltration with stimulation of pro-inflammatory and immunoregulatory cytokines, which forms a specific T- and B-cell response and provokes an atrophic process, interstitial metaplasia and neoplasia.

In children, the association of gastroduodenal pathology with H. Pylori infection in erosive lesions of the mucous membrane of the stomach and duodenum varies from 58 to 85%, and in gastritis or gastroduodenitis without destructive changes it varies from 43 to 74%.

The main ways of transfer of H. Pylori - oral-oral through personal hygiene, as well as fecal-oral.

Aggressive environment of the stomach is critically unfit for living microorganisms. Due to the ability to produce urease, H. Pylori can convert urea, penetrating into the lumen of the stomach by sweating through the capillary walls, into ammonia and CO ₂. The latter neutralize the hydrochloric acid of the gastric juice and create local alkalinization around each H. Pylori cell . Under these conditions, bacteria actively migrate through the layer of protective mucus, attach to epithelial cells, penetrate into the crypts and glands of the mucous membrane. Antigens of microorganisms stimulate the migration of neutrophils and contribute to the development of acute inflammation.

These conditions are based on regulatory disorders affecting cortical and subcortical centers, the autonomic nervous system, the receptor apparatus of the stomach, a system of neurotransmitters and biologically active substances. In this process, neurotransmitters (catecholamines, serotonin, histamine, bradykinin, etc.) play a complex role, as evidenced by the discovery of an increasing number of these substances common to brain and stomach tissue. Circulating in the blood. They have not only a direct effect on the receptors of organs and tissues, but also regulate the activity of the pituitary gland, the structures of the reticular formation, form a long-term stress state.

In addition to chronic gastritis associated with H. Pylori, 5% of children suffer from autoimmune gastritis caused by the formation of antibodies to the gastric mucosa (atrophic gastritis in the Sydney classification system). The true frequency of autoimmune gastritis in children is unknown. A correlation of autoimmune chronic gastritis with other autoimmune diseases (pernicious anemia, autoimmune thyroiditis, polyendocrine autoimmune syndrome, type I diabetes, chronic autoimmune hepatitis, primary biliary cirrhosis, ulcerative colitis, idiopathic fibrosing alveolitis, hypogammaglobulinemia, Addison's disease, vitiligo). The frequency of autoimmune chronic gastritis in these diseases is much higher than in the population (12-20%).

Classification of chronic gastritis, duodenitis, gastroduodenitis in children

By origin	Etiological factors	Topography	Forms of lesions of the stomach and duodenum
			Endoscopic	Morphological
Primary (exogenous)	Infection: H . Pylori; other bacteria, viruses, fungi.   Toxic reactive (chemical, radiation, medicinal, stress, alimentary)	Gastritis: antral; foundation; pagastrit.   Duodenitis: bulbitis; postbulbar; panduodenitis.   Gastroduodenitis	Erythematous / exudative. Nodular. Erosive (with flat or raised defects). Hemorrhagic. Atrophic. Mixed	According to the depth of the lesion: - superficial Diffusive. By the nature of the lesion: - with an assessment of the degree of inflammation, activity, atrophy, intestinal metaplasia - without grading (subatrophy, specific, nonspecific)
Secondary (endogenous)	Autoimmune (with Crohn's disease, granulomatoea, celiac disease, systemic diseases, sarcoidosis, etc.)

The main antigen for autoantibodies on the gastric mucosa was previously thought to be the secretory tubules and microsomes of parietal cells. Modern biochemical and molecular studies identified as the main antigen of parietal cells of the a and beta subunits of H +, K + -ATPase, as well as the internal factor and gastrin-binding proteins.

An important role in the pathogenesis of autoimmune organ-specific diseases, including autoimmune chronic gastritis, is played by the HLA system necessary for processing and presentation of antigens. Such a presentation initiates a complex interaction between antigens of target cells, antigen presenting cells. CD4 helper T lymphocytes, effector T cells and CD8 + suppressor T lymphocytes. As a result of the activation of T-lymphocytes, the production of gamma-interferon, some cytokines and additional molecules (ICAM-1 molecules, heat shock proteins, CD4 + and others needed to coordinate immune responses) is triggered. At the same time, the synthesis of certain antibodies by B lymphocytes is induced. All these substances lead to the expression of target cells of HLA class II antigens, ICAM-1, various cytokines and autoantigens that further modulate immune responses.

It is suggested that H. Pylori infection can not only cause classical antral gastritis B, but also play the role of a trigger mechanism in triggering autoimmune reactions in the gastric mucosa. In experiments on mice, it was shown that the production of antiparietal autoantibodies depends on the antigenic status. These phenomena are associated with molecular mimicry and high homology between H. Pylori antigens and H + \ K + -ATPase parietal cells.

Currently, the trigger role in immunopathological lesions of the upper gastrointestinal tract is assigned to the virus of herpesvirus type IV, the Epstein-Barr virus, cytomegalovirus, and a combination of the above-listed viruses with H. Pylori.

Special forms of gastritis, attributed to chemical, radiation, medicinal and other lesions, diagnose in 5% of children; other types of gastritis are even less common. It is not uncommon for cases when one and the same patient combines several etiological factors.

What causes chronic gastritis and gastroduodenitis?

[2], [3], [4], [5], [6], [7], [8]

Symptoms of chronic gastritis and gastroduodenitis in children

Symptoms of chronic gastritis and gastroduodenitis in children consist of 2 main syndromes: pain and dyspeptic.

Pain in the abdomen varies in intensity, may be early (occurs during or 10-20 minutes after eating), late (worries patient on an empty stomach or 1-1.5 hours after eating). Localized pain, as a rule, in the epigastric and pyloroduodenal areas. It is possible to irradiate pain in the left hypochondrium, the left half of the thorax and the arm.

Among the dyspeptic symptoms, most often there are eructations, nausea, vomiting, and a violation of appetite. There are no characteristic clinical symptoms of H. Pylori infection, possibly an asymptomatic course.

The clinical variant of autoimmune gastritis, accompanied by atrophy of the gastric mucosa, anacidity, hypergastrinemia and pernicious anemia, in children is practically not found. In childhood, the disease is asymptomatic, has no morphological features and is diagnosed when examining patients with other autoimmune conditions for the content of antiparietal autoantibodies.

With antral gastritis and anthroduodenitis, the disease proceeds according to the ulcerative type. The leading symptom is abdominal pain:

• occur on an empty stomach or 1.5-2 hours after a meal, sometimes at night;
• decrease after eating;
• often accompanied by heartburn, sometimes acidic eructations, occasionally vomiting, bringing relief.

Also typical are:

• morbidity during palpation in epigastrium or pyloroduodenal zone;
• propensity to constipation;
• appetite is usually good;
• the secretory function of the stomach is normal or increased;
• when endoscopy - inflammatory-dystrophic lesion of the antral part of the stomach and duodenal bulb (anthroduodenitis);
• an association with HP is typical.

With a base pain gastritis :

• arise after eating, especially after plentiful, fried and fatty foods;
• localized in epigastrium and navel region;
• have noel character;
• pass independently through 1 - 1,5 hours;
• accompanied by a feeling of heaviness, overflow in the epigastrium, belching with air, nausea, occasionally vomiting eaten food, bringing relief.

Of the other symptoms:

• stool is unstable;
• appetite reduced and selective;
• with palpation diffuse tenderness in epigastrium and navel region;
• the secretory function of the stomach is retained or lowered;
• when endoscopy - the defeat of the fundus and the body of the stomach, histologically, atrophic changes in the mucous membrane of the stomach can be detected;
• this type of chronic gastroduodenitis can be both autoimmune and associated with HP under the condition of its prolonged course.

Along with the main clinical forms of chronic gastroduodenitis, many atypical and asymptomatic cases are possible. Almost 40% of chronic gastroduodenitis is latent, the degree of morphological changes and clinical signs may not coincide.

Symptoms of chronic gastritis and gastroduodenitis

Classification of chronic gastritis and gastroduodenitis

In pediatric practice, the classification of chronic gastritis, chronic duodenitis and chronic gastroduodenitis, proposed in 1994 by A.V. Mazurin et al. In 1990, at the 9th International Congress on Gastroenterology, a modern classification of gastritis was developed, called the Sydney system, supplemented in 1994. On its basis, the classification adopted in Russia at the IV Congress of the Union of Pediatricians of Russia in 2002 was revised and supplemented.

[9], [10], [11], [12],

Diagnosis of gastroduodenitis in children

Verification of the diagnosis of chronic gastroduodenitis is carried out on the basis of a certain diagnostic algorithm, including a gastroduodenoscopy with a targeted biopsy of the mucous membrane, the determination of HP, the level of acid production, motor disorders of the duodenum. The diagnosis should include the type of gastritis, duodenitis, localization and activity of the inflammatory process, the nature of the acid-forming function and the phase of the disease.

Progress in gastroenterology is associated with the introduction (1973) of the practice of a new diagnostic method - endoscopy, which allowed to review many aspects of gastroduodenal diseases in children. Far ahead was the development of endoscopic technique. The use of devices with two planes of freedom (instead of the first Japanese endoscopes of type P «Olympus»), having different diameters of the working part (5-13 mm), allows to carry out studies in children of different ages, beginning with birth. To replace the examination of the mucous membranes through the eyepiece of the endoscope under the conditions of the monocular intensively illuminated field of vision came video endoscopy. Camcorders transmit the image of the mucous membrane to the television screen, thereby increasing image quality (it became possible to record changes in various departments of the digestive organs not only with static photographs or slides, but also in the form of dynamic video films). Recently, there are systems that allow you to receive and store high-quality digital images using a computer.

Esophagogastroduodenoscopy is a diagnostic test for gastroduodenitis and peptic ulcer disease in children.

Since 1980, the indications for out-of-hospital endoscopy have been extended. Currently, more than 70% of all endoscopic procedures are performed on an outpatient basis. Gastroduodenofibroscopy allows to determine the localization of the inflammatory process, to conduct an aspiration biopsy of the gastroduodenal mucosa to clarify the nature and severity of pathomorphological changes. The endoscopic picture helps to establish the degree of activity of gastritis and duodenitis due to the presence of focal or diffuse nature of hyperemia, edema, the area of vascular branching, the level of thickness of the mucous membrane, changes in the structure of villi and crypts (width, elongation, folding, dystrophy), as well as the density of cellular infiltration neutrophils, lymphocytes, histiocytes, MEL, plasma cells) and the number of sclerosis sites - atrophy, erosion (complete, incomplete, intermediate, hemorrhagic). Determination of erosions from the edematous and hyperemic mucous membrane protruding above the surface to the petechial (from point forms to 0.5 cm) corresponds to the 3-4 levels of activity and severity of the inflammatory process. In peptic ulcer disease, ulcerative defects of the oval form are diagnosed against the background of inflammatory changes in the mucosa in the pyloric ventral part of the stomach (78%) and in the bulb of the duodenum in the anterior wall in 35% of patients, 22% in the posterior wall, in the bulboduodenal transition zone - in 32 %, at the base of the bulb - 7%, in the area of its apex - 5% (size from 0.4 to 1.8 cm). Multiple localization of ulcers is determined in 36% of patients. Of these, superficial ulcers (59%) are observed 1.5 times more often than deep ulcers (41%). The healing of defects with the formation of scar deformation of the duodenal bulb is noted in 34% of patients, in the stomach - in 12%.

Endoscopic signs of pyloric helicobacteriosis have been developed. These include erosions and ulcers, multiple different-caliber "bulging" on the walls of the mucous membrane of the antrum of the stomach (a picture of "cobblestone pavement" - nodular gastritis), edema and thickening of the folds of the antrum and the body of the stomach. Diagnosis of Helicobacteriosis includes both invasive and non-invasive methods. It is based on the complex clinical and immunological, histomorphological examination of the mucous membrane of the digestive organs, the rapid urease test, the determination of specific antihelicobacterial antibodies of classes M, A, B, E and the polymerase chain reaction (PCR) in feces. A significant advantage of PCR is that it allows not only to diagnose the infection, but also in earlier periods to effectively evaluate eradication - only 2 weeks after treatment. An immunoenzymatic method for determining the concentration of HP antigen in stool has been developed. Morphocytological examination of smears-prints from the biopsy specimen of the gastric mucosa obtained at endoscopy is considered to be the "gold standard" of diagnosis of HP, with an estimate of the degree of contamination: weak (+) - 20 microbial bodies in the field of view, moderate (++) - 20-40 microbial bodies in the field of vision and, with a larger number, high (+++). In dried and stained by Panenheim smears, HP is detected in mucus; bacteria have a curved, spiral shape, can be 8-shaped or in the form of "wings of a flying gull". However, the cytological method does not provide information on the structure of the mucosa. According to the speed of detection of persistent HP, cytological research is not inferior to the express method, based on urease activity of HP, called the campi-test (clo-test, de-nol-test). The method is based on the ability of a living microorganism to carry out biochemical reactions: the produced HP urease metabolizes urea (carrier gel) to form ammonia, shifting the pH of the medium to the alkaline side (phenol-mouth as a pH indicator), which is fixed by a change in the color of the medium. Raspberry staining of the dough testifies to the presence in the biopsy of HP. The time of staining allows you to indirectly judge the number of viable bacteria: significant infection - the appearance of crimson staining for the first hour (+++), for the next two hours - moderate infection (++), by the end of the day - insignificant (+); when the staining occurs at a later date, the result is considered negative. A noninvasive urease respiratory test is based on the effect of urease HP on labeled urea, resulting in the release of carbon dioxide, recorded in the exhaled air. The study is carried out on an empty stomach - two background samples of exhaled air are taken to the plastic bags, then the test person takes a test breakfast (milk or juice) and a test substrate (urea water, labeled C). For an hour every four minutes, four samples of exhaled air are taken and the content of the stabilized isotope is determined. The cytological method in addition to the density level of HP colonization makes it possible to determine the presence and severity of proliferative processes and thereby diagnose the shape and activity of gastroduodenitis. A characteristic feature of such tests is the high accuracy of the results and the possibility to correct the therapy in time to prevent recurrence of the disease. X-ray examination in patients with chronic gastroduodenitis is performed in complicated conditions (penetration, perforation of ulcerative defects) and with constant abdominal pain, despite adequate therapy, as well as in patients with frequent relapses of the disease.

To study the motor function of the stomach, external electrogastrography is used, which allows recording the biocurrents of the stomach from the surface of the body: 70% of sick children of school age have a hypokinetic type of motor function.

Blood, urine and other instrumental examination methods do not contain specific diagnostic signs of gastroduodenitis, they are performed for the diagnosis of concomitant diseases and for the development of complications.

Chronic gastroduodenitis should be differentiated with peptic ulcer, pancreatitis, cholepathies, acute appendicitis, colitis.

Abdominal syndrome is also possible with hemorrhagic vasculitis, nodular polyarteritis, rheumatism, diabetes, pyelonephritis. The main differential diagnostic criteria are endoscopic and morphocytological signs of gastroduodenitis, as well as the absence of specific symptoms characterizing the diseases with which differential diagnosis is performed.

Diagnosis of chronic gastritis and gastroduodenitis

[13], [14]

Treatment of chronic gastroduodenitis in children

Treatment of patients with chronic gastroduodenitis and peptic ulcer reduces to the effect on the body of a number of therapeutic factors: regimen, therapeutic nutrition, drug and non-pharmacological therapy.

Dietotherapy is based on the principles of antacid properties of food; mechanical, chemical, thermal shielding of the gastroduodenal mucosa. The food should be exercised 4-5 times a day. Use therapeutic diets 1a, 16, 1: steamed food, boiled (meat, fish, soft-boiled eggs, vegetables), mashed (mashed), jelly, mucous porridge, stale bread, alkaline mineral water (Essentuki № 4, 17), compotes of sweet varieties of berries and fruits, baked apples; exclude rich meat, fish, mushroom soups, cabbage soup, fresh and rye bread, fresh pastries, pancakes, coffee, carbonated drinks, juices, raw vegetables, garlic, beans, fried and smoked products, marinades, spicy seasonings, mayonnaise, ketchup; limiting the use of table salt and foods rich in cholesterol. The duration of each therapeutic diet (table) is from 7 to 15 days, maintained for 6-12 months. Products that have a high antisecretory effect include cream, meat, cottage cheese. You can use the products of therapeutic nutrition: antacid bifilact, enriched with vitamins C and E; lactic acid lactobacterin, enriched with physiological doses of zinc sulfate.

Phytotherapy - the therapeutic effect of infusions and decoctions from plants is based on their anti-inflammatory, sedative, bactericidal, spasmolytic effects on the gastroduodenal mucosa. Depending on the phase of the disease, they are prescribed: with exacerbation, infusions and broths of chamomile, valerian, peppermint, blood-grouse, yarrow, dog rose; in remission - marsh fever, marshmallow medicinal, St. John's wort, swine swine, big plantain, nettle nettle.

Physiotherapy in the form of sparing procedures in small doses is used from 2 and 3 weeks (thermal procedures) of basic therapy: paraffin, ozocerite; electrosleep (patients with increased excitability); bromoelectrophoresis on the collar area and coniferous baths (for children with severe autonomic dysfunction); ultrasound and magnetotherapy (intensification of metabolic processes and healing of erosive-ulcerative mucosal defects); electrophoresis of medicinal substances (novocaine, papaverine, platyfilin, zinc sulfate, lidase, terrylitin), which have analgesic, reparative and resolving effects; sinusoidal-modulated currents affect the motor function and have a good analgesic effect, improve trophism of tissues. With a low effectiveness of conservative therapy, patients with frequent relapses are treated with laser and acupuncture, as well as sessions (8-10) of hyperbaric oxygenation.

Drug therapy is based on the pathogenetic principle: simultaneous or sequential impact on the main pathogenetic mechanisms:

• eradication therapy for HP infection.
• suppression of gastric acid production.

Treatment of gastroduodenitis in children associated with H. Pylori

Purpose of treatment:

• eliminate Helicobacter pylori infection;
• to suppress active inflammation in the mucosa;
• to ensure the healing of erosions and ulcers;
• reduce the risk of relapse.

The algorithm of eradication therapy was approved by the European Consensus (2000, Maastricht), as well as by the Russian group on the study of HP (Prof. Morozov IA, Prof. Shcherbakov PL, Prof. Ivanikov Ivan, Prof. Korsunsky AA) and WHO experts developed treatment regimens for children.

The list of drugs with anti-Helicobacterial activity includes: metronidazole (trichopolum, clion, tyberal), tinidazole, clarithromycin (klatsid, klabaks, fromelid), amoxicillin, tetracycline, bismuth colloidal subcitrate. Given the reduced sensitivity of HP strains to metronidazole, it is replaced with furazolidone. Treatment is based on the use of highly effective antibacterial drugs in combination with anti-acid drugs - triple therapy and quadrotherapy: the use of acid-fast groups of antibiotics, the absorption of which in the presence of bismuth subcitrate and antisecretory drugs slows down, which ensures their deposition in the stomach. The appointment of treatment regimens with minimum multiplicity during the day (2 times) and duration of no more than 7-10 days, taking into account the family character of Helicobacter pylori infection (compliance with sanitary and hygienic standards and anti-Helicobacter therapy for all cohabiting relatives) is considered the most radical and rational highly effective method of therapy .

Schemes providing eradication of HP more than 80% of cases

One-week triple therapy with a bismuth drug.

1. Bismuth tricalcium dicitrate-de-nol - 4 mg / kg.
2. Amoxicillin - 25-50 mg / kg or clarithromycin - 7.5 mg / kg.
3. Furazolidone - 20 mg / kg.

One-week triple therapy with H +

1. K + -ATPase.
2. Omeprazole (lossek, omez, gastrozole) - 0.5 mg / kg.
3. Amoxicillin or clarithromycin or roxithromycin (rulid) - 5-8 mg / kg and furazolidone.

One-week quadrotherapy.

1. Bismuth tricalcium bismuth dicitrate + amoxicillin / clarithromycin / roxithromycin.
2. Furazolidone + omeprazole.

The results of the course treatment of chronic gastroduodenal diseases associated with HP showed complete (100%) clinical dynamics and eradication of bacteria to 94.6% with the following combination of drugs:

1. de-nol + metronidazole + furazolidone;
2. pyloride (ranitidine + bismuth citrate) + rovamycin - 1.5 million units / 10 kg of body weight;
3. pyloride - 400 mg twice a day + clarithromycin or tetracycline or amoxicillin;
4. 10-day regimens include ranitidine (zantac, famotidine) 300 mg twice daily, or gastrosidine (quamatel) 40 mg twice daily, or a proton pump inhibitor (lobe, omez, pariet, romesec) + potassium salt of disubstituted bismuth citrate 108 mg 5 times a day), or de-nol - 120 mg 4 times a day + metronidazole - 250 mg 4 times a day + tetracycline hydrochloride 500 mg 4 times a day, or klatsid - 2 times a day.

For eradication of HP it is possible to use registered complex sets of medicines - pilobact (romesque, tinidazole, clarithromycin) and gastrostat (tetracycline, metronidazole, colloidal bismuth) in children of senior school age.

Significantly increases the effect of eradication therapy the inclusion of immunomodulators (derinat, viferon), enterosorbents (SUMS, algisorb), reception of complex probiotics containing bifido- and lactobacilli. After successful eradication therapy, signs of a specific inflammation of the mucous membrane (cell infiltration of the interepithelial space and its own plate), the balance between protective and aggressive factors is restored, the persistence of HP is eliminated.

Treatment of gastroduodenitis in children not associated with H. Pylori

The goal of the treatment is to stop the symptoms of the disease and provide epithelization of erosions, cicatrization of ulcers, the occurrence of which is caused by the fact that peptic and acid activity is the cause of peptic ulceration, increasing the likelihood of peptic ulcer. Elimination of erosive and ulcerative defects in the mucous membrane is facilitated by the appointment of antisecretory drugs capable of "keeping" intragastric pH above 3 during the day (a condition for scarring of the duodenal ulcer in 4 weeks).

To drugs with antisecretory action include: blockers of H2 receptors - ranitidine, zantac, quamate, famotidine, famosan, ulfamid, gastrosidin; inhibitors of the proton pump (pump N K-ATPase) - rabeprazole (pariet), omeprazole (losek, omez, gastrozole, romesec), lansoprazole (laxophed, lanzap); antacid preparations - Almagel Ar, Geluside, Talcid, Thysacide, Phosphalugel, Remagel, Topalcane, Gastalum, Maalox, Megalac, Gasterin, Gelosil. The most effective blocker of H2 receptors is ranitidine - its antisecretory effect is associated with suppression of basal and stimulated pepsin production, increased production of gastric mucus and bicarbonate secretion, improvement of microcirculation in the gastroduodenal mucosa and normalization of gastroduodenal motility. Proton pump inhibitors are parietal cell H +, K + -ATPase inhibitors, their antisecretory activity is higher than that of other agents with the same effect; accumulation occurs in the secretory canals of the parietal cell, where they are converted into sulfenamide derivatives, which form covalent bonds with the molecules of cysteine H +, K + -ATPase and, therefore, inhibit the activity of this enzyme. When administered once a day, gastric acid release during the day is inhibited by 80-90% and the pH is maintained above 3.0 more than 18 hours per day. The most effective drug in this group is pariet (rabeprazole), the mechanism of its action is associated with blocking the activity of the enzyme H +, K + -ATPase (provides synthesis of hydrochloric acid) - a proton pump of the membrane of the parietal cell of the stomach. A high level of selectivity of the drug is provided by the accumulation of its active sulfanilamide form in the apical part of the parietal cell. By binding to the sulfhydryl groups of the enzyme and inhibiting K + -dependent phosphorylation, it suppresses the enzyme activity and, as a result, prevents the release of free hydrogen ions into the lumen of the stomach as early as the first day of treatment. Antacid preparations contain in their composition aluminum and magnesium compounds, which determines their antacid and enveloping action; they reduce the increased acidity of gastric juice, eliminate epigastric pain and heartburn. Form release - tableted, suspensions, gels. The greatest use in practice was Maalox. Antacids are not prescribed simultaneously with tetracycline and H2-histamin blockers, since they reduce the absorption of the latter.

Schemes of drug therapy include an antisecretory drug in combination with a cytoprotector - sucralfate (venter) - 4 g per day and sucrat gel - 2 grams a day for 4 weeks; further - in a half dose for a month.

1. Ranitidine 300 mg a day once - at 19-20 hours + antacid preparation maalox 1 tablet or 1 tablespoon or 1 packet for reception 3 times a day 40 minutes before meals and overnight.
2. Famotidine - 40 mg a day once in the evening (at 20 hours) + antacid Gastal - 1/2 tablets (dissolve) 1 hour after eating 4-6 times a day.
3. Omeprazole or pariet (20 mg per day), or lansoprazole - 30 mg per day at 14-15 hours.

In gastroduodenitis with dyspepsia of a dyskinetic type, symptomatic treatment includes: domperidone (motilium) inside or metoclopramide 10 mg for 15-3O min before meals 3-4 times a day + antacid for 2 weeks and further - reception by "requirement".

With reflux gastritis, the drug of choice is megalphil-800 and antacid, which adsorb bile acids and other mucosal damaging components of duodenal reflux. Drugs are prescribed for 2-3 weeks.

Requirements for the results of the treatment: relief of clinical and endoscopic manifestations of the disease with two negative HP tests (complete remission). Endoscopic control - after 4 weeks, with peptic ulcer - after 8 weeks. Incomplete remission - cessation of pain and dyspeptic disorders, a decrease in histological signs of activity of the process without eradication of HP.

How is chronic gastritis and gastroduodenitis treated?

How to prevent chronic gastritis and gastroduodenitis in children?

The duration of inpatient treatment, depending on the etiology and clinical and morphological manifestations of the disease, can vary from 10 days or more with possible therapy in outpatient settings. Clinical follow-up should be carried out throughout the life course, and treatment and examination are performed "on demand" in the event of non-disabling symptoms.

Patients with peptic ulcer disease with no complete remission are subject to preventive treatment:

• continuous therapy for months with antisecretory medications in a half dose every evening;
• "on demand" therapy - with the appearance of characteristic symptoms, taking one of the antisecretory drugs for 3 days in a full daily dose, and then in half for 3 weeks.

In case of recurrence of symptoms, it is necessary to conduct EGDS. The progressive course of erosive gastroduodenitis and peptic ulcer disease is more often associated with the ineffectiveness of eradication therapy and, more rarely, with reinfection. A system of medical and ecological rehabilitation for children with chronic gastroduodenitis has been developed. Sanatorium treatment (36-45 days) is carried out in local institutions located in resorts, in sanatorium-type sanatoriums, in the sanatorium of the hospital in order to prevent exacerbations and prolongation of remissions. The sanatorium department of the hospital is intended for treatment of the most severe contingent of puberty patients with peptic ulcer, as well as patients with hereditary complications, with frequent relapses and complications of the disease. Sanatorium treatment (direction in the first 3 months after exacerbation) includes the following factors: therapeutic regimen of motor activity, dietary nutrition, internal and external use of mineral waters, mud applications, physiotherapeutic procedures, exercise therapy, psycho- and acupuncture, according to indications - medications . Treatment is carried out annually for 3 years.

Primary prevention: the identification of risk factors that contribute to the formation of the disease, the elimination of which reduces the likelihood of adverse events.

Secondary prevention: a complex of rehabilitation measures of the group system of medical examination. As the main criterion determining their volume, the stage of the disease is taken, depending on which the registration groups are identified: the stage of persistent remission, remission, reconvalescence, exacerbation of the disease.

Clinical supervision can be carried out in the conditions of a polyclinic, a rehabilitation center, a boarding school of the gastroenterological profile. Using the system of dispensary observation at the outpatient and outpatient stage in the current economic conditions has made it possible to improve the quality of specialized medical care, to reduce the number of relapses of the disease by 1.5-3.6 times and to alleviate the severity of the pathological process.

Forecast

Effective eradication treatment guarantees a favorable prognosis. Repeated reinfection of H. Pylori occurs in no more than 1-1.5% (provided that in the environment of the child there are no carriers of the microorganism, in this case, reinfection occurs in 15-30%).

After eradication of H. Pylori, the inflammatory reaction of the gastric mucosa disappears within 2-6 months; without clinical symptoms, the disease does not require additional treatment. 

[15], [16], [17],