Gastritis is a group of diseases of different genesis with acute or chronic inflammation of the gastric mucosa. It is manifested by epigastric pain, dyspepsia, intoxication, asthenia. It is diagnosed using EFGDS, gastric radiography, urease test, intragastric pH-metry, gastric juice examination, and other laboratory and instrumental methods. For treatment, antibacterial, antisecretory, gastroprotective drugs, components of gastric juice are used in combination with drugs that affect individual links of pathogenesis. In some forms of the disease, surgical treatment is indicated.

Gastritis is one of the most common diseases of the digestive organs, accounting for up to 80% of stomach diseases. The frequency of the disorder increases with age. According to observations in the field of gastroenterology, up to 70-90% of elderly patients suffer from various variants of pathology. In recent years, cases of diagnosis of gastritis in children have become more frequent, the role of the bacterial factor in the development of inflammation has increased — up to 90% of cases are associated with helicobacter infection. There is a tendency to a predominantly chronic course of the process, the prevalence of acute variants of the disease does not exceed 20%.

Gastritis is a polyetiological disease that occurs when the stomach is exposed to various damaging factors. Its development is promoted by pathological processes in which the local resistance of the mucous layer, the general reactivity of the body, the regulation of the secretory and motor functions of the organ are disrupted. The main causes and prerequisites of gastritis are:

  • Infectious agents. In 90% of patients with chronic inflammation, helicobacter is seeded. Acute gastritis can be caused by E. coli, staphylococci, streptococci, and other opportunistic microflora. Less often, the disease has a viral origin or develops against the background of syphilis, tuberculosis, candidiasis, worm infestations.
  • Chemical effects. Most acute processes occur due to ingestion of aggressive substances into the stomach. When poisoning with sulema, acids, fibrinous inflammation is observed, alkalis, salts of heavy metals — necrotic. When taking NSAIDs, glucocorticoids, a number of antibiotics, cardiac glycosides, cocaine, alcohol abuse, erosive gastritis is possible.
  • Altered reactivity. Inflammation caused by the formation of antibodies to the lining cells and the internal Castle factor is observed in Addison-Biermer disease. Less often, the disease is associated with autoimmune thyroiditis, insulin-dependent diabetes mellitus, autoimmune polyglandular syndrome type I. Hyperreactivity caused by sensitization of the body causes allergic gastritis.
  • Other diseases of the digestive organs. The gastric mucosa becomes inflamed when irritated due to the abandonment of intestinal contents. Biliary reflux gastritis develops due to the functional failure of the pyloric sphincter in chronic duodenitis, biliary dyskinesia. Prerequisites for bile reflux are noted in diseases of the operated stomach, duodenal tumors.
  • Chronic stress. Neurohumoral imbalance often serves as a predisposing factor, although ischemia in an acute stress reaction can provoke the formation of erosions and even hemorrhagic gastritis. Chronic stress is accompanied by prolonged vascular spasm, insufficient blood supply to the mucosa. The situation is aggravated by depletion of reserve capacities and gastrointestinal dyskinesia.
  • Food errors. Eating disorders are one of the main prerequisites for the development of chronic superficial gastritis. The constant intake of fatty, spicy, hot food, dishes with extractive substances, carbonated drinks causes irritation of the mucous membrane and enhances the effect of other factors. Less often, chemical damage or mechanical injury provokes an acute process.

In old age, the main provoking factor is involutive thinning of the mucosa, leading to a decrease in local resistance. In sepsis, severe somatic diseases, oncopathology, chronic ischemia of the gastric wall is a prerequisite for inflammation. Iatrogenic genesis of the disease is possible due to radiation therapy of stomach cancer, esophagus, other malignant neoplasms of the gastrointestinal tract or mechanical damage to the organ during gastroscopy, esophagogastroduodenoscopy, nasointestinal intubation. In some cases (for example, with hyperplastic gastritis), the etiology remains unknown. It is possible that a number of forms of pathology have hereditary origin.

The mechanism of stomach inflammation is associated with an imbalance of damaging and protective factors. The action of toxins, chemicals, autoantibodies, allergens, solid foods, instruments and X-rays provokes local reactions. The more massive the damaging effect, the more acute the inflammatory process. After a short phase of alteration, microcirculation is disrupted, edema, exudation of intravascular fluid and blood components with the development of classical catarrhal gastritis is noted. In more severe cases, acute dystrophy and tissue necrosis are observed.

Chronization of acute inflammation is accompanied by atrophic, hyperplastic, metaplastic, and other dystrophic-regenerative changes in the glandular apparatus. With a low intensity of damaging loads, a key role is played by a decrease in local resistance caused by both local and general impacts. Constant irritation of the epithelium with food, alcohol, bile, endotoxins, violation of the regulation of secretory-motor function contributes to the emergence of chronic inflammation with a gradual increase in pathomorphological changes.

A separate link in the pathogenesis of chronic gastritis is a violation of the acid-producing function. Under the action of ammonia released by helicobacteria, gastrin production increases, the content of somatostatin decreases, which leads to hyperproduction of hydrochloric acid. As a result, the patient develops gastritis with increased acidity. Atrophy of the fundal gastric mucosa and autoimmune damage to the lining cells inhibit the secretion of hydrochloric acid with moderate inflammation. This mechanism underlies gastritis with low acidity.

When systematizing clinical forms of gastritis, the peculiarities of the course of the pathological process, morphological changes in the mucosa, the leading etiological factor, the localization of inflammation, the state of secretory function, the stage of the disease, the presence of complications are taken into account. The most complete is the Houston classification of the disease, taking into account the clinical and morphological criteria proposed by R. Strickland and I. McKay (1973).:

  • Type of inflammation. According to the nature of the course, acute and chronic gastritis variants are distinguished. Special forms of the disease are considered separately - allergic, hypertrophic, lymphocytic, granulomatous, and other atypical inflammations.
  • Localization of the lesion. Often the disease affects one of the departments of the organ (fundal, antral gastritis). When the whole stomach is involved in the pathological process, which is more characteristic of acute forms of pathology, they talk about pangastritis.
  • Etiology. Taking into account the most significant causes, chronic autoimmune gastritis (type A), helicobacter inflammation (type B), chemical-toxic lesion (type C) are isolated. When several factors are combined, the disease is considered as a mixed process.
  • The nature of morphological changes. According to the depth of the spread and the features of the pathological process, inflammation can be catarrhal, fibrinous, corrosive, phlegmonous, erosive. In chronic gastritis, atrophic processes often prevail.
  • Features of gastric secretion. During the systematization, the acid-forming function of the stomach is evaluated. Depending on the content of hydrochloric acid in the gastric juice, gastritis with reduced, increased, normal acidity is distinguished.

Signs of acute gastritis usually appear suddenly against the background of errors in the diet, taking NSAIDs, poisoning. Patients are concerned about epigastric pain of varying intensity, nausea, vomiting, belching, loss of appetite, increased stool. Disorders of the general condition in acute inflammation are represented by weakness, dizziness, decreased ability to work. With the infectious genesis of the disorder, fever, chills, runny nose, cough, myalgia, arthralgia are possible. The peculiarity of the erosive variant of the disease is the presence of bleeding from the gastrointestinal tract, which manifests itself in the form of bloody vomiting or melena.

The symptoms of chronic gastritis depend on the secretory activity of the stomach. Inflammation accompanied by increased acidity is characterized by intense pain in the epigastric zone, occurring 20-30 minutes after eating, chronic constipation, heartburn, acid belching. With a prolonged course, the patient is concerned about increased fatigue, emotional lability, insomnia. In patients suffering from chronic gastritis with reduced acidity, the pain syndrome is expressed slightly or absent. There is morning nausea, a feeling of rapid satiety, heaviness in the stomach, diarrhea, flatulence, belching air, bitter taste in the mouth, gray plaque on the tongue. Due to the violation of digestion and absorption of food, there is a loss of body weight, muscle weakness, swelling on the shins.

Gastritis can be complicated by peptic ulcer of the stomach and duodenum. In the case of erosive damage to the organ wall, profuse bleeding and hemorrhagic shock may occur. With the phlegmonous form of gastritis, perforation of the gastric wall, cicatricial deformation of the organ is often observed, fistulas are formed. Due to the lack of internal Castle factor, some patients develop megaloblastic anemia. With atrophic gastritis, protein-energy starvation with cachexia, hypoproteinemic edema, muscular dystrophy, encephalopathy is noted. Prolonged course of the disease increases the risk of gastric adenocarcinoma.

Usually, in the presence of typical clinical signs, the diagnosis of gastritis is not difficult. The main task of the diagnostic stage is a comprehensive examination of the patient to identify the root cause and determine the clinical variant of the disease. The following instrumental and laboratory methods are considered the most informative:

  • Esophagogastroduodenoscopy. Examination of the mucosa with EGDS reveals pathognomonic morphological signs of the disease. Gastritis is characterized by swelling, hyperemia, erosion, thinning and atrophy of the epithelium, areas of metaplasia, increased vascular pattern.
  • Stomach radiography. A contrast study with a barium mixture is shown. The presence of gastritis is indicated by thickening of the folds (more than 5 mm), the presence of nodes of the mucous membrane, an increase in gastric fields, multiple erosions.
  • Intragastric pH-metry. With the help of a daily measurement of acidity in the stomach, the secretory function of the organ is evaluated and the clinical form of gastritis is determined. The method can also be used to evaluate the effectiveness of antisecretory therapy.
  • A breath test for Helicobacter. To detect H. pylori, the carbon concentration in the exhaled air is measured. The results are positive when the indicator is more than 4%. In doubtful cases, PCR diagnostics, determination of antibodies to helicobacter in the blood is recommended.
  • Examination of gastric juice. The method is aimed at studying the secretory function of the stomach. During the analysis, the total acidity, the content of enzymes, mucus, and other substances are evaluated. Microscopy of the sediment reveals epithelial cells, muscle fibers, etc.
  • In the general blood test, signs of B12-deficiency anemia are possible: a decrease in red blood cells and hemoglobin, the appearance of megaloblasts. If the autoimmune nature of the disease is suspected, serological reactions are carried out to search for antiparietal antibodies. Diagnostically significant is the determination of serum levels of pepsinogens 1 and 2, gastrin. A large number of undigested muscle fibers, starch grains, and fiber are found in the coprogram, and the Gregersen reaction may be positive. In difficult cases, MSCT of the abdominal cavity, ultrasound of the gallbladder, liver, pancreas, antroduodenal manometry are recommended. The most accurate method of establishing a morphological diagnosis is histological examination of the biopsy.

Differential diagnosis is carried out with functional dyspepsia, other gastrointestinal diseases (peptic ulcer, chronic pancreatitis, cholecystitis), intestinal pathology (celiac disease, Crohn's disease), vitamin deficiency (pernicious anemia, pellagra), intestinal infections (salmonellosis, escherichiosis, sprue). In addition to consulting a gastroenterologist, the patient is recommended to be examined by an infectious disease specialist, a hematologist, and a hepatologist. To exclude myocardial infarction, a cardiologist's consultation is prescribed, with possible stomach cancer - an oncologist.

Therapeutic tactics are determined by the factors that provoked the development of gastritis and the clinical form of the disease. The patient is recommended complex differentiated therapy, supplemented by diet correction, smoking cessation, alcohol consumption. The basic scheme of conservative treatment usually includes the following groups of drugs:

  • Antibacterial agents. To destroy helicobacteria, standard eradication schemes are used using macrolides, β-lactam penicillins, nitroimidazoles, tetracyclines, which are necessarily combined with proton pump inhibitors, bismuth preparations. When identifying other pathogens of infectious gastritis, antimicrobial, antifungal, antiparasitic agents of various groups are prescribed.
  • Secretory function correctors. Proton pump inhibitors and H2-histaminoreceptor blockers are used to enhance hydrochloric acid production. To correct secretory insufficiency, replacement therapy with pepsin-containing drugs is carried out. To stimulate the production of gastric juice, drug therapy is supplemented with phytopreparations based on plantain, pyridoxine, ascorbic, nicotinic, weak organic acids.
  • Gastroprotectors. There are several groups of means to protect the epithelium from damaging effects. The principle of action of enveloping drugs is based on the deposition of a thin film that mechanically protects the mucosa from damage. Colloidal suspensions also coagulate helicobacter proteins. Antacids neutralize hydrochloric acid of gastric juice. Prostaglandins of group E make up for the deficiency of natural protective factors.

In acute gastritis, the treatment plan includes gastric lavage, taking sorbents, antidotes, infusion therapy. Sedative phytopreparations and tranquilizers are recommended for patients with severe neurovegetative disorders. Corticosteroids are used for autoimmune inflammation. Patients with severe pain syndrome are prescribed myotropic antispasmodics, with caution - analgesics. To stop bleeding and replenish blood loss in hemorrhagic gastritis, hemostatics are used, whole blood, erythrocyte mass, plasma are transfused. In duodenal-gastric reflux, ursodeoxycholic acid derivatives and dopamine receptor inhibitors are effective. Prokinetics are shown to improve motor skills. Surgical operations are performed with massive destruction of the gastric wall in patients with phlegmonous gastritis, the occurrence of profuse bleeding.

The outcome of the disease in the acute process is more often favorable, chronic inflammation usually has a recurrent course with periods of exacerbations and remissions. The most unfavorable in prognostic terms is chronic atrophic gastritis, which leads to an irreversible decrease in acid formation in the stomach, malignancy. Preventive measures include limiting spicy and fatty foods, quitting smoking and alcohol consumption, taking medications only as prescribed by a doctor, timely detection and treatment of diseases that can cause an inflammatory process in the stomach.

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