Chronic gastritis and gastroduodenitis in children

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

Chronic gastroduodenitis is a chronic inflammation with structural (focal or diffuse) reorganization 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 gastrointestinal diseases in childhood, occurring at a frequency of 300-400 per 1000 children, with isolated lesions not exceeding 10-15%.

In the structure of diseases of the upper gastrointestinal tract, chronic gastroduodenitis accounts for 53.1%, chronic gastritis - 29.7%, chronic duodenitis - 16.2%. Non-ulcer gastroduodenal pathology affects children of all age groups, but the disease is most often diagnosed at the age of 10-15 years. In primary school age, there are no gender differences in the frequency of chronic gastritis and chronic gastroduodenitis, and in senior school age, boys are more often affected.

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

[ 1 ]

Causes and pathogenesis of chronic gastritis and gastroduodenitis

Chronic gastritis and chronic gastroduodenitis are multifactorial diseases. The following are important:

• hereditary constitutional predisposition to diseases of the digestive organs - the family history rate is 35-40%;
• Helicobacter pylori infection;
• nutritional errors (irregular, poor in composition, poor chewing, abuse of spicy foods);
• chemical, including medicinal, 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 is the main etiological factor in the development of chronic inflammatory diseases of the organs of the gastroduodenal zone, which significantly increases the risk of developing peptic ulcer disease and stomach cancer.

Long-term presence of H. pylori in the gastric mucosa leads to neutrophilic and lymphocytic infiltration with stimulation of proinflammatory 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 gastric and duodenal mucosa ranges from 58 to 85%, and in gastritis or gastroduodenitis without destructive changes - from 43 to 74%.

The main routes of transmission of H. pylori are oral-oral through personal hygiene items, as well as feco-oral.

The aggressive environment of the stomach is critically unsuitable for microorganisms. Due to its ability to produce urease, H. pylori can convert urea, which penetrates the lumen of the stomach by sweating through the walls of the capillaries, into ammonia and CO ₂. The latter neutralize the hydrochloric acid of the gastric juice and create local alkalization around each H. pylori cell. Under these conditions, bacteria actively migrate through the layer of protective mucus, attach to epithelial cells, and penetrate the crypts and glands of the mucous membrane. Microorganism antigens stimulate the migration of neutrophils and contribute to the development of acute inflammation.

These conditions are based on regulatory disorders affecting the cortical and subcortical centers, the autonomic nervous system, the receptor apparatus of the stomach, the system of neurotransmitters and biologically active substances. Neurotransmitters (catecholamines, serotonin, histamine, bradykinin, etc.) play a complex role in this process, as evidenced by the discovery of an increasing number of these substances common to brain and stomach tissue. Circulating in the blood, they not only have a direct effect on the receptors of organs and tissues, but also regulate the activity of the pituitary gland, structures of the reticular formation, and 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 relationship has been found between autoimmune chronic gastritis and other autoimmune diseases (pernicious anemia, autoimmune thyroiditis, polyendocrine autoimmune syndrome, type 1 diabetes mellitus, chronic autoimmune hepatitis, primary biliary cirrhosis, nonspecific ulcerative colitis, idiopathic fibrosing alveolitis, hypogammaglobulinemia, Addison's disease, vitiligo). The frequency of autoimmune chronic gastritis in these diseases significantly exceeds the same indicator in the population (12-20%).

Classification of chronic gastritis, duodenitis, gastroduodenitis in children

By origin	Etiological factors	Topography	Forms of damage to the stomach and duodenum
			Endoscopic	Morphological
Primary (exogenous)	Infectious: H. pylori; other bacteria, viruses, fungi. Toxic reactive (chemical, radiation, drug, stress, alimentary)	Gastritis: antral; fundal; paugastritis. Duodenitis: bulbitis; postbulbar; panduodenitis. Gastroduodenitis	Erythematous/ exudative. Nodular. Erosive (with flat or raised defects). Hemorrhagic. Atrophic. Mixed	By depth of damage: - superficial - diffuse. By the nature of the lesion: - with assessment of the degree of inflammation, activity, atrophy, intestinal metaplasia - without assessment of the degree (subatrophy, specific, non-specific)
Secondary (endogenous)	Autoimmune (in Crohn's disease, granulomatosis, celiac disease, systemic diseases, sarcoidosis, etc.)

The secretory canals and microsomes of parietal cells were previously considered the main antigen for autoantibodies on the gastric mucosa. Modern biochemical and molecular studies have identified the a- and beta-subunits of H+, K+-ATPase, as well as intrinsic factor and gastrin-binding proteins as the main antigen of parietal cells.

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

It is suggested that H. pylori infection may not only cause classical antral gastritis B, but also act as a trigger mechanism in the initiation of autoimmune reactions in the gastric mucosa. Experiments on mice have shown that the production of antiparietal autoantibodies depends on the antigen status. These phenomena are associated with molecular mimicry and high homology between H. pylori antigens and H+ K+-ATPase of parietal cells.

Currently, the trigger role in immunopathological lesions of the upper gastrointestinal tract is attributed to the herpes virus type IV, the Epstein-Barr virus, cytomegalovirus, as well as a combination of the above viruses with H. pylori.

Special forms of gastritis, attributed to chemical, radiation, medicinal and other lesions, are diagnosed in 5% of children; other types of gastritis are even rarer. There are frequent cases when several etiological factors are combined in one and the same patient.

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.

Abdominal pain varies in intensity and can be early (occurs during or 10-20 minutes after eating) or late (worries the patient on an empty stomach or 1-1.5 hours after eating). The pain is usually localized in the epigastric and pyloroduodenal regions. Pain may radiate to the left hypochondrium, left half of the chest, and arm.

Among dyspeptic symptoms, the most common are belching, nausea, vomiting, and loss of appetite. H. pylori infection has no characteristic clinical symptoms; it may be asymptomatic.

The clinical variant of autoimmune gastritis, accompanied by atrophy of the gastric mucosa, anacidity, hypergastrinemia and pernicious anemia, is almost never encountered in children. In childhood, the disease is asymptomatic, has no morphological features and is diagnosed during examination of patients with other autoimmune conditions by the content of antiparietal autoantibodies.

In antral gastritis and antroduodenitis, the disease proceeds in an ulcer-like manner. The leading symptom is abdominal pain:

• occur on an empty stomach or 1.5-2 hours after eating, sometimes at night;
• decrease after eating;
• often accompanied by heartburn, sometimes sour belching, and occasionally vomiting, which brings relief.

Also typical:

• pain on palpation in the epigastrium or pyloroduodenal zone;
• tendency to constipation;
• appetite is usually good;
• gastric secretory function is normal or increased;
• during endoscopy - inflammatory-dystrophic lesion of the antral part of the stomach and the duodenal bulb (antroduodenitis);
• characteristic association with HP.

With fundal gastritis, pain:

• occur after eating, especially after heavy, fried and fatty foods;
• localized in the epigastrium and umbilical region;
• have a nagging character;
• pass on their own within 1 - 1.5 hours;
• accompanied by a feeling of heaviness, fullness in the epigastrium, belching, nausea, and occasionally vomiting of eaten food that brings relief.

Other symptoms include:

• the chair is unstable;
• appetite is reduced and selective;
• on palpation, diffuse pain in the epigastrium and umbilical region;
• the secretory function of the stomach is preserved or decreased;
• during endoscopy - damage to the fundus and body of the stomach, histologically atrophic changes in the gastric mucosa can be detected;
• This type of chronic gastroduodenitis can be either autoimmune or associated with HP, provided that it has a long course.

Along with the main clinical forms of chronic gastroduodenitis, there are many atypical and asymptomatic ones. In almost 40% of cases, 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. was adopted as a basis. In 1990, at the IX 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 somewhat 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 specific diagnostic algorithm, including a gastroduodenal copy with targeted biopsy of the mucous membrane, 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 a new diagnostic method into practice - endoscopy, which allowed us to reconsider many aspects of gastroduodenal diseases in children. The development of endoscopic technology has made great strides. The use of devices with two planes of freedom (instead of the first Japanese endoscopes of the P type "Olympus"), having different diameters of the working part (5-13 mm), allows us to carry out examinations in children of different ages, starting from birth. Video endoscopy has replaced the examination of the mucous membranes through the eyepiece of the endoscope in conditions of a monocular, intensely illuminated field of vision. Video cameras transmit an image of the mucous membrane to a TV screen, thereby improving the quality of the image (it has become possible to record changes in various parts of the digestive organs not only with static photographs or slides, but also in the form of dynamic videos). Recently, systems have appeared that allow us to receive and store high-quality digital images using a computer.

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

Since 1980, the indications for out-of-hospital endoscopic examinations have been expanded. Currently, more than 70% of all endoscopic procedures are performed on an outpatient basis. Gastroduodenofibroscopy helps to determine the localization of the inflammatory process, conduct a targeted 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 by the presence of focal or diffuse hyperemia, edema, the area of vascular branches, the level of mucosal thickness, changes in the structure of villi and crypts (width, elongation, folding, dystrophy), as well as by the density of cellular infiltration (neutrophils, lymphocytes, histiocytes, MEL, plasma cells) and the number of sclerosis areas - atrophy, erosions (complete, incomplete, intermediate, hemorrhagic). Definition of erosions from protruding above the surface of the edematous and hyperemic mucous membrane to petechial (from point forms to 0.5 cm) corresponds to 3-4 degrees of activity and severity of the inflammatory process. In peptic ulcer disease, oval-shaped ulcerative defects are diagnosed against the background of inflammatory changes in the mucous membrane in the pyloroantral part of the stomach (78%) and in the duodenal bulb along the anterior wall in 35% of patients, on the posterior wall - in 22%, in the zone of the bulboduodenal junction - in 32%, at the base of the bulb - in 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 ones (41%). Healing of defects with the formation of cicatricial deformation of the duodenal bulb is observed in 34% of patients, in the stomach - in 12%.

Endoscopic signs of pyloric helicobacteriosis have been developed. These include erosions and ulcers, multiple different-sized "bulges" on the walls of the mucous membrane of the antrum of the stomach ("cobblestone pavement" picture - nodular gastritis), edema and thickening of the folds of the antrum and body of the stomach. Diagnostics of helicobacteriosis includes both invasive and non-invasive methods. It is based on a comprehensive clinical, immunological, histomorphological study of the mucous membrane of the digestive organs, express urease test, determination of specific anti-helicobacterial antibodies of classes M, A, B, E and polymerase chain reaction (PCR) in feces. A significant advantage of PCR is that it allows not only to diagnose the infection, but also to effectively assess eradication at an earlier stage - already 2 weeks after treatment. An enzyme immunoassay has been developed to determine the concentration of HP antigen in feces. The "gold standard" for diagnosing HP is morphocytological examination of smears-prints from a biopsy of the gastric mucosa obtained during endoscopy, with an assessment of the degree of contamination: weak (+) - 20 microbial bodies in the field of vision, moderate (++) - 20-40 microbial bodies in the field of vision and, with a higher number, high (+++). In dried and Panenheim stained smears, HP is determined in mucus; the bacteria have a curved, spiral shape, can be 8-shaped or in the form of "wings of a flying seagull". However, the cytological method does not provide information on the structure of the mucous membrane. In terms of the speed of detection of persistent HP, an express method based on the urease activity of HP, called the campi-test (clo-test, de-nol-test) is not inferior to a cytological study. The method is based on the ability of a living microorganism to carry out biochemical reactions: the developed HP urease metabolizes urea (gel carrier) with the formation of ammonia, which shifts the pH of the medium to the alkaline side (phenol-rot as a pH indicator), which is recorded by a change in the color of the medium. Crimson coloring of the test indicates the presence of HP in the biopsy. The staining time allows indirectly judging the number of viable bacteria: significant infection - the appearance of crimson coloring during the first hour (+++), during the next two hours - moderate infection (++), by the end of the day - insignificant (+); if coloring occurs at a later date, the result is considered negative. The non-invasive urease breath test is based on the effect of HP urease on labeled urea, as a result of which carbon dioxide is released, recorded in the exhaled air. The study is conducted on an empty stomach - two background samples of exhaled air are collected in plastic bags, then the subject takes a test breakfast (milk or juice) and a test substrate (an aqueous solution of urea labeled with C). Four samples of exhaled air are collected every 15 minutes for an hour and the content of the stabilized isotope is determined.The cytological method, in addition to the level of HP colonization density, allows determining the presence and severity of proliferative processes and thereby diagnosing the form and activity of gastroduodenitis. A characteristic feature of such tests is the high accuracy of the results and the ability to promptly adjust therapy to prevent relapses of the disease. X-ray examination of patients with chronic gastroduodenitis is carried out 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 gastric biocurrents from the surface of the body: 70% of sick school-age children have a hypokinetic type of motility.

Blood and urine tests and other instrumental examination methods do not contain specific diagnostic signs of gastroduodenitis; they are used to diagnose concomitant diseases and in the development of complications.

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

Abdominal syndrome is also possible with hemorrhagic vasculitis, nodular polyarteritis, rheumatism, diabetes mellitus, 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 diagnostics are carried out.

Diagnosis of chronic gastritis and gastroduodenitis

[ 13 ], [ 14 ]

Treatment of chronic gastroduodenitis in children

Treatment of patients with chronic gastroduodenitis and peptic ulcer disease is reduced to the impact on the body of a number of therapeutic factors: regimen, therapeutic nutrition, drug and non-drug therapy.

Diet therapy is based on the principles of antacid properties of food; mechanical, chemical, thermal sparing of the gastroduodenal mucosa. Meals should be taken 4-5 times a day. Therapeutic diets 1a, 16, 1 are used: steamed food, boiled (meat, fish, soft-boiled eggs, vegetables), mashed (in the form of puree), jelly, slimy porridge, stale bread, alkaline mineral water (Essentuki No. 4, 17), compotes from sweet berries and fruits, baked apples; Rich meat, fish, mushroom soups, cabbage soup, fresh and rye bread, fresh pastries, pancakes, coffee, carbonated drinks, juices, raw vegetables, garlic, legumes, fried and smoked foods, marinades, hot spices, mayonnaise, ketchup are excluded; the consumption of table salt and foods rich in cholesterol is limited. The duration of each therapeutic diet (table) is from 7 to 15 days, maintained for 6-12 months. Products with a high antisecretory effect include cream, meat, cottage cheese. You can use therapeutic nutrition products: 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 of plants is based on their anti-inflammatory, sedative, bactericidal, antispasmodic effect on the gastroduodenal mucosa. Depending on the phase of the disease, the following are prescribed: during an exacerbation - infusions and decoctions of chamomile, valerian, peppermint, burnet, yarrow, rose hips; in remission - calamus, marshmallow, St. John's wort, marsh cudweed, plantain, stinging nettle.

Physiotherapy in the form of gentle procedures in small doses is used from the 2nd and 3rd weeks (thermal procedures) of basic therapy: paraffin, ozokerite; electrosleep (for patients with increased excitability); bromoelectrophoresis on the collar area and pine baths (for children with severe vegetative dysfunction); ultrasound and magnetotherapy (enhancement of metabolic processes and healing of erosive and ulcerative defects of the mucous membrane); electrophoresis of drugs (novocaine, papaverine, platifillin, zinc sulfate, lidase, terrilitin), which have analgesic, reparative and resorptive effects; sinusoidally modulated currents affect the motor function and have a good analgesic effect, improve tissue trophism. If conservative therapy is ineffective, patients with frequent relapses undergo laser and acupuncture therapy, 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 of HP infection.
• suppression of gastric acid production.

Treatment of gastroduodenitis in children associated with H. pylori

Treatment goal:

• eliminate Helicobacter infection;
• stop (suppress) active inflammation in the mucous membrane;
• ensure healing of erosions and ulcers;
• reduce the risk of relapse.

The algorithm of eradication therapy was approved by the European Consensus (2000, Maastricht), and the Russian group for the study of HP (Prof. Morozov I.A., Prof. Shcherbakov P.L., Prof. Ivanikov I.O., Prof. Korsunsky A.A.) and WHO experts developed treatment regimens for children.

The list of drugs with anti-Helicobacter activity includes: metronidazole (Trichopolum, Klion, Tiberal), tinidazole, clarithromycin (Klacid, Klabax, Fromelid), amoxicillin, tetracycline, colloidal bismuth subcitrate. Given the reduced sensitivity of HP strains to metronidazole, it is replaced by furazolidone. Treatment is based on the use of highly effective antibacterial drugs in combination with agents that suppress acid production - triple therapy and quadruple therapy: the use of acid-resistant groups of antibiotics, the absorption of which is slowed down in the presence of bismuth subcitrate and antisecretory drugs, which ensures their deposition in the stomach. Prescribing treatment regimens with a minimum frequency during the day (2 times) and a duration of no more than 7-10 days, taking into account the familial nature of Helicobacter infection (compliance with sanitary and hygienic standards and anti-Helicobacter therapy for all relatives living together) is considered the most radical and rational highly effective method of therapy.

Regimens that ensure eradication of HP in more than 80% of cases

One-week triple therapy with a bismuth preparation.

1. Tripotassium bismuth 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+ blockers

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

One-week quadruple therapy.

1. Bismuth tripotassium 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 up to 94.6% when using the following combination of drugs:

1. de-nol + metronidazole + furazolidone;
2. pylori (ranitidine + bismuth citrate) + rovamycin - 1.5 million IU/10 kg of body weight;
3. pylori - 400 mg 2 times a day + clarithromycin or tetracycline or amoxicillin;
4. Ten-day regimens include ranitidine (Zantac, famotidine) - 300 mg 2 times a day, or gastrosidine (quamatel) - 40 mg 2 times a day, or a proton pump inhibitor (Losec, Omez, Pariet, Romesec) + potassium salt of dibasic 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 Klacid - 2 times a day.

For the eradication of HP, registered complex sets of drugs can be used - pilobact (romesec, tinidazole, clarithromycin) and gastrostat (tetracycline, metronidazole, colloidal bismuth) in older school-age children.

The effect of eradication therapy is significantly increased by including immunomodulators (Derinat, Viferon), enterosorbents (SUMS, Algisorb), and taking complex probiotics containing bifido- and lactobacilli. After successful eradication therapy, signs of specific inflammation of the mucous membrane (cellular infiltration of the interepithelial space and lamina propria) are relieved, the balance between protective and aggressive factors is restored, and the persistence of HP is eliminated.

Treatment of gastroduodenitis in children not associated with H. pylori

The goal of treatment is to relieve symptoms of the disease and ensure epithelialization of erosions, scarring of ulcers, the occurrence of which is due to the fact that peptic and acid activity is the cause of peptic ulcers, increasing the likelihood of peptic ulcer disease. The elimination of erosive and ulcerative defects of the mucous membrane is facilitated by the administration of antisecretory drugs that can "maintain" intragastric pH above 3 for 24 hours (a condition for scarring of the duodenal ulcer in 4 weeks).

Drugs with antisecretory action include: H2-receptor blockers - ranitidine, zantac, quamatel, famotidine, famosan, ulfamid, gastrosidin; proton pump inhibitors (HK-ATPase pump) - rabeprazole (pariet), omeprazole (losec, omez, gastrozole, romesec), lansoprazole (laxofed, lanzap); antacid drugs - almagel Ar, gelusid, talcid, tisacid, phosphalugel, remagel, topalkan, gastal, maalox, megalac, gasterin, gelosil. Ranitidine is recognized as the most effective H2-receptor blocker - its antisecretory effect is associated with the suppression of basal and stimulated pepsin production, increased production of gastric mucus and bicarbonate secretion, improved microcirculation in the gastroduodenal mucosa and normalization of gastroduodenal motility. Proton pump inhibitors are inhibitors of H+, K+-ATPase of the parietal cell, 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 that form covalent bonds with cysteine molecules of H+, K+-ATPase and thereby inhibit the activity of this enzyme. When taken once a day, gastric acid secretion is suppressed by 80-90% during the day and the pH is maintained above 3.0 for more than 18 hours per day. The most effective drug in this group is considered to be Pariet (rabeprazole), the mechanism of its action is associated with blocking the activity of the enzyme H+, K+-ATPase (provides synthesis of hydrochloric acid) - the proton pump of the membrane of the parietal cell of the stomach. The high level of selectivity of the drug is ensured by the accumulation of its active sulfanilamide form at the apical part of the parietal cell. By binding to the sulfhydryl groups of the enzyme and inhibiting K+-dependent phosphorylation, it suppresses the activity of the enzyme and, as a result, prevents the release of free hydrogen ions into the lumen of the stomach already on the first day of treatment. Antacid drugs contain aluminum and magnesium compounds, which determines their antacid and enveloping effect; they reduce the increased acidity of gastric juice, eliminate pain in the epigastrium and heartburn. Release forms - tablets, suspensions, gels. Maalox has found the greatest application in practice. Antacids are not prescribed simultaneously with tetracycline and H2-histamine blockers, as they reduce the absorption of the latter.

Drug therapy regimens include an antisecretory drug in combination with a cytoprotector - sucralfate (Venter) - 4 g per day and sucrat gelr - 2 g per day for 4 weeks; then - at half the dose for a month.

1. Ranitidine - 300 mg per day once - at 19-20 hours + antacid drug Maalox 1 tablet or 1 tablespoon or 1 sachet per dose 3 times a day 40 minutes before meals and at night.
2. Famotidine - 40 mg per day once in the evening (at 8 p.m.) + antacid Gastal - 1/2 tablet (dissolve) 1 hour after meals 4-6 times a day.
3. Omeprazole or Pariet (20 mg per day), or lansoprazole - 30 mg per day at 2-3 pm.

In case of gastroduodenitis with dyskinetic dyspepsia syndrome, symptomatic treatment includes: domperidone (motilium) orally or metoclopramide 10 mg 15-30 minutes before meals 3-4 times a day + antacid for 2 weeks and then taken on demand.

In case of reflux gastritis, the drug of choice is considered to be megalfil-800 and antacid, which adsorb bile acids and other components of duodenal refluxate that damage the mucous membrane. The drugs are prescribed for 2-3 weeks.

Requirements for treatment results: relief of clinical and endoscopic manifestations of the disease with two negative tests for HP (complete remission). Endoscopic control - after 4 weeks, in case of peptic ulcer - after 8 weeks. Incomplete remission - cessation of pain and dyspeptic disorders, reduction of histological signs of process activity 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, may vary from 10 days or more with possible therapy in outpatient settings. Dispensary observation must be carried out throughout life, and treatment and examination are carried out "on demand" when intractable symptoms appear.

Preventive treatment is required for patients with peptic ulcer disease without complete remission:

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

In case of recurrence of symptoms, EGDS should be performed. Progressive course of erosive gastroduodenitis and peptic ulcer disease is more often associated with ineffective eradication therapy and less often with reinfection. A system of medical and ecological rehabilitation for children with chronic gastroduodenitis has been developed. Sanatorium and spa treatment (36-45 days) is carried out in local institutions located in resorts, in health camps of a sanatorium type, in the sanatorium department of the hospital in order to prevent exacerbations and prolong remissions. The sanatorium department of the hospital is intended for the treatment of the most severe contingent of pubertal patients with peptic ulcer disease, as well as patients with a hereditary burden, with frequent relapses and complications of the disease. Sanatorium and resort treatment (referral in the first 3 months after exacerbation) includes the following factors: therapeutic regimen of physical activity, dietary nutrition, internal and external use of mineral waters, mud applications, physiotherapy procedures, exercise therapy, psycho- and acupuncture, and, if indicated, medications. Treatment is carried out annually for 3 years.

Primary prevention: identification of risk factors that contribute to the development of the disease, the elimination of which reduces the likelihood of its unfavorable course.

Secondary prevention: a set of rehabilitation measures of the group medical examination system. The main criterion determining their volume is the stage of the disease, depending on which the groups of registration are distinguished: the stage of stable remission, remission, convalescence, exacerbation of the disease.

Dispensary observation can be carried out in the conditions of a polyclinic, rehabilitation center, boarding school of gastroenterological profile. The use of the dispensary observation system at the outpatient-polyclinic stage in modern economic conditions has improved the quality of specialized medical care, reduced the number of relapses of the disease by 1.5-3.6 times and alleviated the severity of the pathological process.

Forecast

Effective eradication treatment guarantees a favorable prognosis. Repeated reinfection with H. pylori occurs in no more than 1-1.5% (provided that there are no carriers of the microorganism in the child's environment, in which 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 ]