The article presents a morphological study of the composition of cells of the lymphoid infiltrate in autoimmune and focal thyroiditis, and their comparative characteristics are carried out. The study was carried out on the basis of a study of medical histories and surgical material obtained from 72 patients with a histologically verified diagnosis of autoimmune thyroiditis and 54 patients with focal thyroiditis due to various pathologies thyroid gland. It has been revealed that in autoimmune thyroiditis, the lymphoplasmacytic infiltrate can form lymphoid follicles with reproduction centers, is located both in the stroma and in the parenchyma of the thyroid tissue and consists of T-helpers and B-lymphocytes, and is to a lesser extent represented by T-suppressors. Focal thyroiditis is characterized by the formation of a lymphoid infiltrate, occupying less than 10% of the area of ​​the microspecimen, located mainly in the stroma of the organ, without forming large lymphoid follicles with reproduction centers. In this case, the composition of the infiltrate includes equal parts of T-helpers, T-suppressors and a small amount of B-lymphocytes.

autoimmune thyroiditis

focal thyroiditis

B lymphocytes

T lymphocytes

immunohistochemical study

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Chronic autoimmune thyroiditis (AIT) is a classic organ-specific autoimmune disease with the formation of autoantibodies, the main morphological manifestation of which is lymphoid infiltration of thyroid tissue. About a hundred years have passed since the first description of autoimmune thyroiditis, however, even today morphological diagnosis autoimmune diseases thyroid disease, in particular Hashimoto's thyroiditis, is still challenging task due to the variety of histological forms. Many authors identify focal thyroiditis as a form of autoimmune thyroiditis, attributing it to the early stage of the disease; other authors identify focal thyroiditis as the body’s immune response to various pathological processes of the thyroid gland that have no connection with autoimmune thyroiditis. There are conflicting data regarding hyperplasia of the thyroid epithelium into B cells. According to some authors, with focal thyroiditis in the area of ​​lymphoplasmacytic infiltration, the thyroid epithelium has characteristic appearance and consists of B cells, and according to others, focal thyroiditis is characterized by the absence of B cells. Due to conflicting data, the importance of studying the nature of cellular infiltration has increased (2). Today there is a large number of scientific articles devoted to the morphological study of the thyroid gland in AIT, however, information about the cellular composition of lymphoid infiltration is very scarce.

Purpose of the study- study of the composition of cells of the lymphoid infiltrate in autoimmune and focal thyroiditis.

Material and research methods

The study was carried out on the basis of a study of medical histories and surgical material obtained from 72 patients with a histologically verified diagnosis of AIT and 54 patients with focal thyroiditis against the background of various pathologies of the thyroid gland, operated on in city hospitals of Stavropol in the period from 2009 to 2011.

For histological and histochemical studies, the material was fixed in 10% neutral formalin, embedded in paraffin, and sections 5-6 μm thick were prepared. Histological sections with hematoxylin and eosin for general review purposes, according to Van Gieson, according to Mallory, modified by Heidenhain. The results of the severity of a particular trait were assessed using a semi-quantitative method proposed by O.K. Khmelnitsky, according to the following criteria: 0 - absent, (+) - weak degree, (++) - moderate degree, (+++) - severe reaction. Immunohistochemical staining of all sections was also performed using antibodies to CD4 (T helper cells), CD8 (T suppressor cells) and CD19 B lymphocytes. For this purpose, paraffin sections 5 µm thick were prepared and glued onto glasses treated with egg albumin. Then the sections were dried for at least 24 hours at a temperature of 37 °C, subjected to deparaffinization and dehydration, unmasking of antigens (by heating in a water bath to 95-99 °C) and directly staining with antibodies. To interpret the results, we took into account the localization of immunoreactants and the intensity of their staining, which was assessed using a semi-quantitative method according to the following criteria: 0 - absent, (+) - weak reaction, (++) - moderate reaction, (+++) - pronounced reaction. Morphometric analysis was carried out on a Nicon Eclipse E200 microscope with a Nicon DS-Fil digital camera, a personal computer with NIS-Elements F 3.2 software installed.

Research results and discussion

Macroscopically, the thyroid gland in autoimmune thyroiditis is often cream-colored, dense, lumpy, unevenly lobulated, often fused to surrounding tissues, and difficult to cut. The cut surface is whitish-yellow, opaque; many whitish retracted cords divide the tissue into small unequal lobules protruding above the surface. The weight of the thyroid gland varied from 15 to 38 grams.

In focal thyroiditis, the thyroid gland had a cream color, lobular structure, elastic consistency, not fused with the surrounding tissues, the weight of the thyroid gland varied from 23 to 29 grams.

Histological examination of the thyroid glands with autoimmune thyroiditis revealed varying degrees of infiltration. In 18 cases, the area of ​​lymphoplasmacytic infiltration occupied 20 to 40%, while the infiltrate formed lymphoid follicles without clear boundaries and reproduction centers. From 40 to 60% in 41 cases, large follicles with reproduction centers in them were identified in the infiltrate. In the tissues of the thyroid glands containing more than 60% lymphoplasmacytic infiltration (13 cases), in addition to large follicles with reproduction centers, more pronounced stromal fibrosis was observed.

Lymphoplasmacytic infiltrates were located both in the stroma and in the parenchyma of the thyroid gland. Near the infiltrates, destruction of the thyroid epithelium and more pronounced B-cell hyperplasia were detected. In two cases (3%) of the gland, isolated areas of epidermoid metaplasia of the follicular epithelium were observed among the lymphoplasmacytic infiltration.

Immunohistochemical study determined weak (+) or moderate expression (++) of CD4 on T helper cells. The number of immunopositive cells in the lymphoid infiltrate varied from 8 to 15% in one field of view. CD8 staining in all cases revealed their pronounced expression on T helper cells (+++), and the number of immunopositive cells in the infiltrate varied from 31 to 47%. CD19 was expressed in the cytoplasm of B lymphocytes, with a pronounced (+++) degree of expression, and the number of immunopositive cells in the infiltrate varied from 38 to 53%.

During histological examination of material with the presence of focal thyroiditis, areas of lymphoid infiltration were determined predominantly in the stroma of the thyroid gland. Moreover, in none of the 54 cases of accumulation lymphoid tissue did not form follicles with reproductive centers. In all cases, the area occupied by the infiltrate did not exceed 10%. An immunohistochemical study revealed equally pronounced (+++) expression of CD4 on T-helper cells and CD8 on T-suppressor cells. When counting CD4 immunopositive cells, 35 to 57% of cells in the field of view were detected. The number of CD8 immunopositive cells varied from 44 to 56%. There was no expression or weak (+) expression of CD19 on B-lymphocytes, respectively, the number of immunopositive cells in the infiltrate was from 0 to 5% in the field of view. Among the lymphoplasmacytic infiltration in focal thyroiditis, areas of epidermoid metaplasia of the thyroid epithelium were not observed.

conclusions

Lymphoplasmacytic infiltration in autoimmune thyroiditis occupies a significant area of ​​the thyroid epithelium and is located both in the stroma and in the parenchyma of the thyroid tissue. The lymphoid infiltrate includes equally B and T lymphocytes, however, among T lymphocytes there is an increase in the number of T helper cells over T suppressor cells.

Unlike autoimmune thyroiditis, focal thyroiditis has the following features.

1. The lymphoid infiltrate is located predominantly in the stroma of the thyroid tissue.
2. Lymphoid infiltrate occupies no more than 10% of the area of ​​the preparation.
3. The lymphoid infiltrate did not form large lymphoid follicles with light centers of reproduction.
4. The infiltrate predominantly consisted of T lymphocytes and a small amount of B lymphocytes.

Based on the above features, there is no reason to consider focal thyroiditis as an early stage of autoimmune thyroiditis.

Reviewers:

Korobkeev A.A., Doctor of Medical Sciences, Professor, Head of the Department of Normal Anatomy, State Budgetary Educational Institution of Higher Professional Education "Stavropol State medical University» Ministry of Health of the Russian Federation, Stavropol;

Chukov S.Z., Doctor of Medical Sciences, Professor of the Department of Pathological Anatomy, Stavropol State Medical University, Ministry of Health of the Russian Federation, Stavropol.

The work was received by the editor on September 25, 2014.

Bibliographic link

What is Inflammatory infiltrate

To designate such forms of inflammatory diseases, many authors use the terms “incipient phlegmon”, “phlegmon in the infiltration stage”, which are contradictory in meaning, or generally omit the description of these forms of the disease. At the same time, it is noted that forms of odontogenic infection with signs of serous inflammation of the perimaxillary soft tissues are common and in most cases respond well to treatment.

With timely initiation of rational therapy, it is possible to prevent the development of phlegmon and abscesses. And this is justified from a biological point of view. The vast majority of inflammatory processes should end and undergo involution at the stage of swelling or inflammatory infiltrate. The option with their further development and the formation of abscesses, phlegmon is a disaster, tissue death, i.e. parts of the body, and when the purulent process spreads to several areas, sepsis often leads to death. Therefore, in our opinion, inflammatory infiltrate is the most common, most “expedient” and biologically based form of inflammation. In fact, we often see inflammatory infiltrates in the perimaxillary tissues, especially in children, with pulpitis and periodontitis, regarding them as reactive manifestations of these processes. Variants of the inflammatory infiltrate are periadenitis and serous periostitis. The most important thing for a doctor in assessing and classifying these processes (making a diagnosis) is recognizing the non-purulent stage of inflammation and the appropriate treatment tactics.

What causes Inflammatory infiltrate

Inflammatory infiltrates constitute a group diverse in etiological factors. Studies have shown that 37% of patients had traumatic genesis diseases, in 23% the cause was an odontogenic infection; in other cases, infiltrates occurred after various infectious processes. This form of inflammation is observed with equal frequency in all age groups.

Symptoms of Inflammatory Infiltrate

Inflammatory infiltrates occur both due to contact spread of infection (per continuitatum) and the lymphogenous route when a lymph node is damaged with further tissue infiltration. The infiltrate usually develops over several days. The temperature of patients can be normal or low-grade. In the affected area, swelling and compaction of tissues occur with relatively clear contours and spread to one or more anatomical areas. Palpation is painless or slightly painful. Fluctuation is not detected. The skin in the area of ​​the lesion is of normal color or slightly hyperemic, somewhat tense. There is damage to all soft tissues of this area - skin, mucous membrane, subcutaneous fat and muscle tissue, often several fascia with inclusion in the infiltrate lymph nodes. That is why we prefer the term “inflammatory infiltrate” over the term “cellulite,” which also refers to such lesions. Infiltration may resolve in purulent forms inflammation - abscesses and phlegmons and in these cases it should be considered as a prestage purulent inflammation, which could not be stopped.

Inflammatory infiltrates may have a traumatic origin. They are localized in almost all anatomical regions maxillofacial area, somewhat more often in the buccal and floor of the mouth. Inflammatory infiltrates of post-infectious etiology are localized in the submandibular, buccal, parotid-masticatory, submental areas. The seasonality of the occurrence of the disease is clearly visible (autumn-winter period). Children with an inflammatory infiltrate are often admitted to the clinic after the 5th day of illness.

Diagnosis of Inflammatory infiltrate

Differential diagnosis of inflammatory infiltrate carried out taking into account the identified etiological factor and duration of the disease. The diagnosis is confirmed by normal or low-grade fever body, relatively clear contours of the infiltrate, absence of signs of purulent melting of tissues and sharp pain on palpation. Other, less pronounced, distinctive features serve: absence of significant intoxication, moderate hyperemia of the skin without revealing tense and shiny skin. Thus, the inflammatory infiltrate may be characterized by a predominance proliferative phase inflammation of the soft tissues of the maxillofacial area. This, on the one hand, indicates a change in the reactivity of the child’s body, on the other, serves as a manifestation of natural and therapeutic pathomorphosis.

The greatest difficulties for differential diagnosis are purulent foci localized in spaces delimited externally by muscle groups, for example in the infratemporal region, under m. masseter, etc. In these cases, an increase in symptoms acute inflammation determines the process forecast. In doubtful cases, the usual diagnostic puncture of the lesion helps.

A morphological examination of a biopsy sample from the inflammatory infiltrate reveals cells typical of the proliferative phase of inflammation in the absence or a small number of segmented neutrophilic leukocytes, the abundance of which characterizes purulent inflammation.

Infiltrates almost always contain accumulations of yeast and filamentous fungi of the genus Candida, Aspergillus, Mucor, and Nocardia. Epithelioid cell granulomas form around them. Fungal mycelium is characterized dystrophic changes. It can be assumed that the long phase of the productive tissue reaction is supported by fungal associations, reflecting possible phenomena of dysbiosis.

Treatment of Inflammatory Infiltrate

Treatment of patients with inflammatory infiltrates- conservative. Anti-inflammatory therapy is carried out using physiotherapeutic agents. A pronounced effect is achieved by laser irradiation, bandages with Vishnevsky ointment and alcohol. In cases of suppuration of the inflammatory infiltrate, phlegmon occurs. Then spend surgery.

Which doctors should you contact if you have Inflammatory infiltrate?

Infectious disease specialist

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Lymphocytic infiltration is a rare chronic dermatosis, which is characterized by benign infiltration of the skin with lymphocytes. The pathology has an undulating course and a tendency to resolve itself. Clinically, it manifests itself as rashes on unaltered skin of smooth, flat, bluish-pink papules or plaques that merge with each other into lesions approximately the size of a palm.

The primary elements have clear boundaries and may peel off. Plaques are usually single, localized on the face, trunk, neck, and limbs. This disease is diagnosed with histological confirmation, and in some cases molecular biological examinations are performed. Treatment of the pathology consists of the use of hormonal therapy, NSAIDs, and topical medications.

Description of this pathology

Lymphocytic infiltration is a benign pseudolymphoma of the skin with a chronic recurrent undulating course. It is very rare and occurs most often in men after 20 years of age. The disease has no racial or seasonal differences and is not endemic. Sometimes the patient's condition may improve during the summer.

First mention of the disease

This disease was first described in medical literature in 1953, when N. Kanof and M. Jessner considered it as an independent pathological process with end-to-end infiltration of all skin structures by lymphocytes. The name “pseudolymphoma” was introduced by K. Mach, who combined the Jessner-Kanof infiltration into a single group with other types of lymphocytic infiltration.

In 1975, O. Brown differentiated the type of pathological process and classified such infiltration as B-cell pseudolymphoma, but somewhat later clinicians began to consider this disease as T-pseudolymphoma, since it is T-lymphocytes that ensure the benign course of the pathology and the possibility of involuntary involution of the original elements. Subsequent studies showed that in development lymphocytic infiltration Immunity plays a significant role, which may be due to the fact that immune cells are located in the gastrointestinal tract, and its damage is observed in 70% of cases. The study of pathology continues to this day. Understanding the reasons for the development of the T-lymphoid process is important in the development of pathogenetic therapy for pseudolymphomas.

Stages of this disease

This disease has several stages of development, which are characterized by the severity of the pathological process. Thus, the following stand out:

• Scattered lymphoplasmacytic infiltration. With it, the symptoms of the disease are insignificant and mild.
• Moderate lymphoplasmacytic infiltration. The formation of a single focus of rash is observed.
• Severe lymphoplasmacytic infiltration. What is this? It is characterized by the formation of multiple foci and lesions.

Causes of the disease

The most possible reasons for the development of focal lymphoplasmacytic infiltration are considered to be tick bites, hyperinsolation, various infections, pathologies of the digestive system, the use of dermatogenous cosmetics and the irrational use of medications that provoke systemic immune changes, externally represented by infiltrative disorders in the skin.

The mechanism of development of lymphocytic infiltration consists of the following process: the intact epidermis provides T-lymphocytes with the opportunity to infiltrate the deep layers of the skin, located around the choroid plexuses and in the papillary processes throughout the thickness of the skin. Pathology triggers trigger an inflammatory process, to which skin and immune cells react directly. In the process of eliminating such inflammation, T-lymphocytes are included, which provide a benign immune response in the form of proliferation of epithelial skin cells.

Stages of the inflammatory process

At the same time, inflammation develops, which goes through three stages: alteration, exudation and proliferation with the participation of cells (histiocytes). These cells cluster and form islets that resemble lymphoid follicles. At the last stage of stopping the inflammatory reaction, two simultaneous proliferation processes enhance and complement each other. Thus, foci of pathology arise.

Since lymphocytes are heterogeneous, the assessment of their histochemical properties using monoclonal antibodies and immunological markers formed the basis for immunophenotyping. This analysis has significant diagnostic value in dermatology.

Many people are wondering what it is - lymphoplasmacytic infiltration of the stomach and intestines?

Disorders in the gastrointestinal tract

The disease can be expressed to varying degrees. At the same time, the glands are shortened, their density significantly decreases. With lymphoplasmacytic infiltration in the stroma, a pronounced increase in reticulin fibers and hyperplasia of smooth muscle walls is observed. Chronic gastritis can be considered reversible if, after therapy, the infiltration disappears, restoration of atrophied glands and cellular renewal are noted.

The exact mechanisms of the onset of type B gastritis with lymphomaplasmacytic infiltration of the stomach still remain unclear. Etiological factors that contribute to the development of chronic gastritis are usually divided into endogenous and exogenous.

Intestinal infiltration

With this disease, there are infiltrates in the connective tissue and disturbances in the functioning of not only the stomach, but also other digestive organs. These also include lymphocytic colitis, which is an inflammatory disease of the colon with lymphoplasmacytic infiltration of the mucous membranes. This type of colitis is characterized by the occurrence of recurrent diarrhea with a prolonged course. Treatment of the disease is specific, based on the use of medications to combat the root cause of its development, as well as symptomatic, to eliminate diarrhea and normalize the intestinal microflora.

Symptoms

The original element skin rashes with lymphocytic infiltration there is a flat, large pink-bluish plaque or papule with clear outlines and a smooth surface, which tends to grow peripherally. Merging with each other, the primary elements form arched or ring-shaped islands with areas of peeling. The resolution of such pathological elements begins, as a rule, from the center, as a result of which confluent lesions may have recesses in the central parts. Typical locations are the face, neck, parotid spaces, back of the head, cheeks, forehead and cheekbones. In some cases, rashes may appear on the skin of the limbs and torso. Usually primary element It can be single; somewhat less often, there is a tendency to spread the pathological process.

Stroma

Often, thick stromas are formed in the stomach area, which represent reticular connective tissue (interstitium), a three-dimensional finely looped network. Lymphatic and blood vessels pass through the stroma.

Lymphocytic infiltration is characterized by a recurrent wave-like course. This disease is resistant to treatment and can spontaneously heal. Relapses usually occur in places of previous localization, but can also involve new areas of the epidermis. Despite the prolonged chronic course, internal organs are not involved in the pathological process.

Diagnosis of the disease

This disease Diagnosed by dermatologists based on clinical symptoms, medical history, fluorescent microscopy (the characteristic glow at the border of the dermoepidermal junctions is not detected) and histology with mandatory consultation with an oncologist and immunologist. Histologically, lymphocytic infiltration reveals unchanged superficial skin. In the thickness of all dermal layers, a grouping of connective tissue cells and lymphocytes around the vessels is observed.

Other diagnostic methods

In more complex cases, tumor immunotyping, molecular and histochemical testing are performed. K. Fan and co-authors recommend diagnostics based on the results of DNA cytofluorimetry with a study of the amount normal cells(for this pathological process - more than 97%). Differential diagnosis is carried out with sarcoidosis, granuloma annulare, centrifugal erythema of Biette, toxicoderma, a group of lymphocytic tumors and syphilis.

Treatment

Treatment of this disease is aimed at eliminating the acute stage of lymphocytic infiltration and lengthening the duration of remission intervals. Therapy for this pathology is nonspecific. High therapeutic effectiveness is observed when prescribing antimalarial medications (Hydroxychloroquine, Chloroquine) and anti-inflammatory non-steroidal drugs (Diclofenac, Indomethacin) after preliminary treatment of concomitant pathologies of the digestive tract. If the state of the gastrointestinal system allows, enterosorbents are used. Locally, the use of hormonal corticosteroid ointments and creams, as well as injection blockade of skin rashes with Betamethasone and Triamcinolone, is indicated.

If there is resistance to the treatment, plasmapheresis is added (up to 10 sessions). Therapy of the digestive system with lymphoplasmacytic infiltration of the intestines and stomach is closely related to diseases of the gastrointestinal tract - gastritis, inflammatory process in the large intestine, etc., which can be characterized by damage to the mucous membranes. To identify them, the patient must undergo appropriate diagnostics and therapy, which consists of taking antidiarrheal, antibacterial and anti-inflammatory medications, as well as following a diet (small meals, avoidance of foods that provoke fermentation, smoked, spicy and fatty foods).

INFILTRATION(lat. in + filtratio filtering) - penetration into tissues and accumulation of cellular elements, liquids and various chemicals in them. I. can be active (cellular I. during inflammation, tumor growth) or passive in nature (impregnation of tissues with anesthetic solutions).

The accumulation of cellular elements in tissues and organs is called infiltrate; in its formation during inflammation along with shaped elements blood plasma and lymph leaving the vessels take part. Impregnation of tissues with biol, liquids without admixture of cellular elements, for example, blood plasma, bile, is designated by the terms edema (see), imbibition (see).

And. as a normal physiol, the process takes place during the differentiation of certain tissues and organs, for example. I. lymphoid cells of the reticular base of the organ during the formation of the thymus gland, lymph nodes.

With pathol. I. cells of inflammatory origin - inflammatory I. (see Inflammation) - there are infiltrates from polymorphonuclear leukocytes, lymphoid (round cell), macrophage, eosinophilic, hemorrhagic, etc. Often tissues are infiltrated with neoplasm cells (cancer, sarcoma) ; in such cases, they speak of tissue inflammation as a tumor, or infiltrative tumor growth. Patol. I. is characterized by an increase in the volume of tissues, their increased density, sometimes pain (inflammatory I.), as well as a change in the color of the tissues themselves: I. polymorphonuclear leukocytes gives the tissues a gray-green tint, lymphocytes - pale gray, erythrocytes - red, etc. d.

The outcome of cellular infiltrates is different and depends on the nature of the process and the cellular composition of the infiltrate. For example, in leukocyte inflammatory infiltrates, proteolytic substances that appear during the release of lysosomal enzymes of polymorphonuclear leukocytes often cause melting of the infiltrated tissues and the development abscess(see) or phlegmon (see); infiltrated cells from polymorphonuclear leukocytes partially migrate from the bloodstream, partially disintegrate, and partially go to build new tissue elements. I. tumor cells entails atrophy or destruction of pre-existing tissue. I. with significant destructive changes in tissues in the future most often gives persistent patol. changes in the form of sclerosis (see), decrease or loss of function of tissues or organs. Loose, transient (eg, acute inflammatory) infiltrates usually resolve and do not leave noticeable marks.

Lymphoid (round cell), lymphocytic-plasma cell and macrophage infiltrates in most cases are an expression of hron, inflammatory processes in tissues. Against the background of such infiltrates, sclerotic changes often occur. They can also be observed in some disorders of tissue metabolism, for example, in the stroma of the thyroid gland with diffuse toxic goiter(see Diffuse toxic goiter), Addison's disease (see), with atrophic changes in the parenchyma of various organs as the initial regenerative act of the elements of the connective tissue of the organ. The same infiltrates can serve as an expression of extramedullary hematopoietic processes, for example, lymphocytic infiltrates and lymphomas in various organs with lymphadenosis (see Leukemia), in the initial stages of reticulosis. In some cases, round cell infiltrates cannot be considered as patol. process: the infiltrate cells themselves, which outwardly resemble lymphocytes, are young forms of the developing sympathetic nervous system. These are, for example, groups of sympathogonia in the medullary substance of the adrenal glands. Lymphocytic plasma cell and macrophage infiltrates can be observed in organs and tissues with various immunol, changes in the body (artificial and natural immunization, allergic immunopathol. processes and allergic diseases). The appearance of lymphocytic plasma infiltrates is a reflection of the process of antibody production carried out by plasma cells, the precursors of which are B lymphocytes, with the participation of macrophages.

From I. chem. the most common substances are glycogen and lipids. I. glycogen of the epithelium of nephron loops (loops of Henle), hepatocytes, and skin epidermis is observed in diabetes and the so-called. glycogen disease (see Glycogenosis), in which there are abundant deposits of glycogen in the liver, striated muscles, myocardium, and the epithelium of the convoluted tubules of the kidneys, sometimes amounting to up to 10% of the weight of the organ. I. lipids can concern neutral fats, for example, fatty I. liver (with an increase in the amount of fat up to 30% of the weight of the organ). However, the appearance of visible fat in the cells of parenchymal organs does not always indicate infiltration. Decomposition of amino- and protein-lipid complexes of the cytoplasm may take place, but the composition of lipids will be different: a mixture of phospholipids, cholesterol and its esters, neutral fats. I. intima of arteries with cholesterol is observed in atherosclerosis (see). I. lipids of the reticuloendothelial system arises as a manifestation of fermentopathy.

In pulmonary tuberculosis, gelatinous I. (gelatinous, or smooth, pneumonia) is observed, which is one of the manifestations of the exudative reaction in pulmonary tuberculosis, tuberculous pneumonia of a lobular, less often lobar nature and is often a prestage of caseous pneumonia; sometimes it occurs as a perifocal process around productive tuberculosis foci (see Respiratory tuberculosis).

Bibliography: Davydovsky I.V. General human pathology, M., 1969; In ii with h n e g F. Allgemeine Pathologie und Atiologie, Miinchen u. a., 1975.

I. V. Davydovsky.

It is very difficult to diagnose chronic gastritis, the symptoms of which cannot always be recognized immediately. Many patients do not pay attention to the unpleasant sensations, thereby missing an important point. But according to statistics, every 5 inhabitants of the planet suffer from a chronic form of this insidious disease. The worst thing is that peptic ulcers or stomach cancer often develop against the background of gastritis.

Difficulty of diagnosis

Gastritis is divided into several types and forms of the inflammatory process of the inner lining of the stomach walls. Gastric juice plays an important role in diagnosing the problem. The course of the disease, therapy and symptoms depend on the level of acidity. There is gastritis with high or low acidity.

The disease develops into a chronic form during prolonged inflammatory processes that affect the deeper layers of the stomach. At risk are patients with an acute form of the disease, as well as those who do not adhere to the rules of healthy and good nutrition. Often chronic gastritis occurs after prolonged use of certain medications or after suffering infectious diseases. The hereditary factor is also taken into account.

Disease provocateur

All causes of the disease are divided into 2 groups: endogenous and exogenous. The first category of irritants includes diseases of internal organs, which give impetus to the development of a chronic form of the disease. With a sharp level of production of hydrochloric acid secretion, atrophic changes in the gastric mucosa occur, and this process is provoked by adrenal insufficiency. If the patient has hypovitaminosis or iron deficiency anemia, chronic gastritis will be endogenous.

The exogenous group includes the following reasons:

• eating rough and dry food;
• excessive passion for marinades, spicy, fried and smoked dishes;
• irregular and quick eating;
• a person is in a hurry and does not chew food properly;
• drinking very hot food or liquid;
• food that irritates the stomach cavity increases the production of hydrochloric acid.

Alcohol and tobacco addiction play a particularly negative role in the development of inflammatory processes. Smoking constantly affects the secretion of hydrochloric acid, stimulating its production. In addition, tobacco leads to disruption of the process of mucus formation, gastroduodenal motility, hyperfunction and hyperplasia of the lining cells of the gastric cavity, so even advanced bronchitis of the lungs in chronic stage causes mucosal hypoxia and leads to the development of other negative morphological changes.

Excessive indulgence in strong drinks disrupts the formation of gastric mucus, after which the surface layer of the epithelium sloughs off and is not restored. And this disrupts the blood supply to the gastric mucosa. At long-term use alcohol (several years), the patient develops atrophic changes. In medicine, there is even a separate term “alcoholic gastritis”, the name of a disease that has claimed more than one life.

You should not be so careless about drinking alcohol, because at one time you can provoke acute erosive gastritis, but only when taking a single large dose of alcohol.

Some medications (Prednisolone, antituberculosis drugs, salicylates, certain antibiotics, sulfonamides, potassium chloride and others) cause gastritis of toxic etiology. But not only medications, but also working conditions can develop such a disease. For example, an excessively dusty warehouse or room with increased level concentrations of chemicals contribute to stomach irritation.

Doctors are still ambivalent about all the causes of the problem, because the origin of the disease is different for all patients. Among the etiological causes of the disease, a huge place is given to microorganisms of the mucous surface. Spiral bacterium Helicobacter pylori located under the parietal mucus on epithelial cells. These microorganisms are very active.

Pathogenesis and forms

The main signs have not yet been fully discovered. Previously, doctors believed that the chronic form of gastritis develops in a patient who has repeatedly suffered acute gastritis. Now scientists claim that chronic gastritis is an independent disease. When type A gastritis forms, infiltration of the mucous membrane with plasma cells and lymphocytes occurs. And this leads to premature death of parietal cells and disruption of the formation of new cells. The result is disastrous: severe atrophy of the glands of the mucous membrane of the fundus of the stomach. In the chronic form of gastritis type B, such changes do not occur.

During illness, the process of formation of gastric mucus, which is a protector of epithelial cells, is disrupted in patients. Sometimes observed duodenogastric reflux bile, in which pancreatic juice, when thrown into the stomach, begins to destroy lipid structures, releasing histamine and leading to degeneration of gastric mucus. All this causes the appearance of an inflammatory process, which provokes the development of a chronic form of antral gastritis with metaplasia and dysplasia of the epithelium. But this fact still remains controversial, so the exact picture of type B gastritis is not clear.

In addition to internal unnoticed changes, the patient can diagnose the first symptoms of one or another form of chronic gastritis. General and most common symptoms:

• heartburn;
• lack of appetite;
• unpleasant odor and taste in the mouth;
• pain in the upper abdomen (pressing and aching);
• belching.

The human body has one interesting feature: the pH environment of the duodenum is alkaline, while that of the esophagus is neutral. Gastric juice, which is found in different parts this body has different properties, because it is produced by certain glands in different parts of the stomach. But heartburn appears due to violations acid-base balance in one of the sections of the gastrointestinal tract.

If a patient is diagnosed with gastritis with reduced level acidity, the symptoms of the disease will change somewhat.

Patients will suffer from diarrhea, belching of air, and nausea. Aching pain will be diagnosed immediately after eating in the epigastric region.

With chronic gastritis with a high level of acidity, belching of acidic stomach contents is observed, as well as pain, which usually bothers you on an empty stomach and gradually disappears after satiety. In addition to the main symptoms, patients experience pain in the heart area, weakness and drowsiness, low blood pressure, irritability and arrhythmia.

If there is a narrowing of the antrum of the stomach or its deformation, the patient suffers from the antral variety of chronic gastritis. An increased level of secretion of gastric juice, a lack of hydrochloric acid in the gastric juice, pain in the epigastric region and dyspepsia are all symptoms of this type of disease.

Very often, the younger generation suffers from gastritis, which affects the glands of the stomach. After all, this is an early form of the disease. Upon examination, the patient can see the normal state of the gastric mucosa, but with slight thickening of the walls. Moderate foci of dystrophic changes are noticeable on the surface of the epithelium; these areas become cubic, and the thickness of the nuclei increases. Mucus is visible on the surface of the epithelium.

During the period of exacerbation, the picture worsens. For example, there is swelling of the stroma, accumulation of leukocytes in the pit area, necrosis of the integumentary epithelium, and formation of erosion.

Pain syndrome

Pain is one of the main and earliest symptoms of many diseases. But gastralgia (pain) occurs precisely in the area abdominal wall, this is the very first and surest sign of gastritis. This type of pain should not be confused with other problems abdominal cavity, which doctors call “ acute stomach" It can be cutting, pressing and stabbing pains, burning and fastening. Such symptoms
Characterize appendicitis, reflux, intestinal blockage, cancer and pancreatitis. Interestingly, the symptoms of these diseases almost never appear alone. Most often they are accompanied by additional signs of gastritis: nausea, weakness and diarrhea (constipation).

When a patient sees a doctor, without examination it is very difficult and not always possible to accurately determine the cause and signs of the disease. Thus, with an objective analysis of the patient’s condition, it is sometimes possible to detect slight pain in the pylorobulbar or epigastric region using the palpation method. After the gastroscopy procedure, a large amount of bile or mucus, swelling of the duodenal bulb and mucosa, as well as hyperemia will be noticeable.

Main signs of gastritis:

1. Acidic stomach contents.
2. Pain and heartburn.
3. Constipation.

Chronic gastritis does not always depend on the way of life; it often worsens in spring and autumn. Lack of timely and competent treatment can lead to irreversible consequences: internal bleeding, stomach cancer or peptic ulcer duodenum. But half of the patients do not notice the symptoms of this disease for years, and people live without changing their habits until a serious stage of the disease is detected.

So, the chronic form of the disease can develop over decades, with phases of remission and exacerbations constantly alternating. Every year the disease progresses and actively develops, penetrating deep into the body. Typically, the superficial form of the disease enters the atrophic phase within 20 years. The patient will feel an increase in the frequency of Achilles diarrhea, he will experience a syndrome of insufficient absorption of food, and the digestive system will malfunction.

Even though it's not fatal disease, but you should not postpone going to the doctor if you notice any symptoms of the disease. Patients should not self-medicate; they must undergo all examinations, receive an accurate diagnosis and an adequate course of treatment.

Antral gastritis, superficial and focal

Increasingly, in clinics there is a large queue of people outside the offices of gastroenterologists.

The disease has rapidly become younger, and therefore not only adults, but also the younger generation of children suffer from it.

Why does this trend arise? How to treat antral gastritis of the stomach and who is at risk? This will be discussed in this article.

Only by contacting an experienced, qualified specialist can you find out an accurate diagnosis and undergo an effective course of treatment. Therefore, you should not neglect going to the hospital.

What is gastritis

By superficial antral gastritis we mean the occurrence of a focus of the disease in the antrum of the stomach, where a food bolus is formed.

This disease is classified by specialists as chronic inflammation of the stomach, providing for some features of localization and clinical course.

Important the right approach to prescribing therapy to achieve a speedy recovery.

This type of inflammation is usually called by different names, all of them correspond to the approved International classification.

Each name reflects the characteristics of the clinical signs and forms of the disease.

Known:

• diffuse gastritis;
• non-atrophic;
• type B;
• hypersecretory gastric damage associated with Helicobacter pylori;
• surface;
• interstitial.

Experts agree that the antral superficial gastritis is the initial stage of varieties of this disease.

It causes a lot of problems for people. In a state of acute form of the disease, a person experiences heaviness, pain, as well as other symptoms that appear with fairly frequent frequency.

In this case, inflammation of the gastric mucosa occurs. This phenomenon applies to chronic diseases, since it is a consequence of an incorrect method of treating the body or even neglecting it altogether.

It is for this reason that it is important to determine whether a patient has diffuse gastritis or a superficial type of disease in order to correctly prescribe a course of therapy.

Classification characteristics

Antral inflammation in the stomach is not so common. The disease occurs almost without symptoms, and therefore it is very difficult to identify it at the first stage.

But in the chronic stage of the disease, changes in the body can no longer be avoided.

There are several types of gastritis based on the depth of the lesion:

• Superficial - when there are disturbances in the outer part of the mucosa, there are no scars, glandular cells continue to work as before. This type of disease is highly treatable.
• Erosive – inflammation affects the deeper layers, causing ulcers, erosions, and cracks. Difficult to treat. Has severe symptoms.

Causes of the disease

Antral focal superficial gastritis can occur for various reasons. But the main one is the development of Helicobacter, which is presented in 9 different species.

It is distinguished by its ability to survive in an acidic environment, moving in gel-like mucus in the stomach area.

It provides itself with a protective function by producing a variety of enzymes.

These include: superoxide dismutase, mucinase, protease, urease, etc. In fact, Helicobacter is capable of synthesizing protein, suppressing the production of hydrochloric acid by the stomach glands.

In this case, the person does not even suspect that he is a carrier of the infection, because he may not have all the symptoms of the disease. Infection is transmitted through dirty hands, water, and saliva in the case of kissing.

In the presence of risk factors, Helicobacter can be activated, giving rise to superficial antral gastritis.

It penetrates the wall of the epithelium, remaining firmly in it. As a result, it becomes inaccessible to gastric juice at all.

Factors in the development of the disease

Superficial gastritis of the antrum develops in the human body not only due to the fault of Helicobacter.

The thing is that if the functioning of the digestive tract is disrupted, then inflammation may occur.

IN in this case risk factors are:

• improper diet, which alternates between long periods of fasting and overeating;
• fast food, spicy foods, fatty foods;
• bad habits: alcohol, smoking;
• consumption of low quality foods, without vitamins and protein;
• taking medications on a long-term basis. Medicines cause irritation of the stomach walls. This should include a group that includes Aspirin, non-steroid and steroid hormones, anti-tuberculosis drugs;
• exposure of the body to stress, hard work;
• hereditary factor;
• the occurrence of allergic reactions to certain products.

Risk group

Often, superficial gastritis of the antrum of the stomach develops in people with certain pathologies, or more precisely:

• diseases of the respiratory and cardiovascular system;
• kidney disease;
• iron deficiency;
• functional failures of the endocrine system;
• caries and foci of infection in the nasopharynx and genitals;
• dysfunction of the digestive tract.

Course of the disease

Gastritis of the antrum of the stomach develops in accordance with the classical scheme:

1. infiltration of the mucous membrane occurs with the help of Helicobacter pylori subspecies, plasma cells, neutrophils, macrophages and lymphocytes;
2. follicles are formed from lymphoid tissue;
3. a process of degeneration of the epithelium is observed, as well as the appearance of focal zones of damage or diffuse changes of varying degrees.

Antral inflammation occurs against the background of increased secretion of gastric juice, provoking the growth of glandular cells and activation of their functionality due to Helicobacter.

Scientists confirm the fact that this type chronic gastritis has no connection with autoimmune processes of the human body.

If the disease lasts long enough, there is a gradual depletion of the epithelium, as well as atrophy of the mucosa, which requires replacement of the transformation of the epithelium into the intestinal version or fibrous tissue.

All this increases the risk of stomach cancer. Only a qualified doctor should diagnose the condition of the body and treat antral gastritis.

Signs and symptoms

Focal gastritis of the antral type is characterized by the occurrence of symptoms that are characteristic of any other types of chronic gastric damage.

Diagnostics will help determine the exact type of disease and prescribe the correct treatment for superficial antral gastritis.

Symptoms:

• the occurrence of pain in the epigastric region after eating or in the case of an empty stomach;
• vomiting, nausea;
• belching;
• heartburn that is not caused by the quality of food consumed;
• flatulence and bloating;
• unpleasant taste in the mouth, observed on a long-term basis;
• bowel dysfunction - alternating changes in diarrhea and constipation;
• unpleasant odor from the mouth when breathing;

If a patient develops a type of diffuse gastritis, he may be bothered by symptoms such as weakness, sudden weight loss, and lack of appetite.

In the case of the erosive form, bleeding is characteristic, both in stool and during vomiting. If the disease is not treated, you can reach a state of anemia, which will develop into an ulcer, inflammation of the pancreas.

Diagnosis of the disease

To clarify the diagnosis, the doctor will prescribe the patient to undergo:

• general blood analysis;
• test urine for gastric acidity;
• stool occult blood test;
• conducting a blood test to determine the immune composition of antibodies to confirm the presence of Helicobacter;
• X-ray of the stomach;
• fibrogastroscopic examination.

The question often arises whether ultrasound will be useful for diagnosing gastritis; it is worth noting that the stomach is a hollow organ, and therefore this study is not of great importance.

Treatment of antral type gastritis

The doctor will definitely insist on following a special diet. You need to eat 5-6 times a day in small portions so as not to overload your stomach.

It is necessary to exclude smoked foods, fried foods, sweets and spicy seasonings. It is better to eat foods that have previously been processed through a meat grinder.

It is recommended to steam or boil food. If the patient has an acute phase of development of antral gastritis, in no case should you eat fatty foods, fresh baked goods and brown bread, canned food, chocolate, sweets, whole milk, rich soups, salted fish, drink soda, alcoholic beverages and coffee, cocoa .

It is also forbidden to eat grapes. In limited portions you can eat foods with coarse fiber consisting of: vegetables, fresh fruits, drink comfort made from dried fruits.

Approximate diet for antral gastritis

The diet can be based on these types of food:

• chicken broth with white bread croutons (they need to be dried in the oven, but not fried in oil);
• boiled fish;
• porridge;
• steam cutlets;
• pasta;
• non-sour jelly;
• cheese casserole;
• vegetable puree or casserole.

Drug therapy for antral gastritis

If the human body is infected with Helicobacter, the doctor prescribes drugs to treat gastritis to destroy the pathogen.

This is a course of eradication. You need to take combinations of drugs with antibacterial properties such as tetracycline, metronidazole, ampicicline, clarithromycin.

Upon completion of the course, you must pass additional examination body. If there is an exacerbation of the condition, you need to use these drugs by injection to Once again do not irritate the gastric mucosa.

To relieve pain symptoms, you need to use no-shpa or papaverine in treatment.

To block unnecessary secretory function Gefal, Denol and Almagel are used in the gastrointestinal tract, but Cerucal is recommended to eliminate reflux.

Riboxin, anabolic steroids, and solcoseryl will help to activate the healing process of the stomach walls.

If signs of tumor transformation and bleeding are excluded, the doctor may prescribe: UHF, electrophoresis, phonophoresis or a course of diadynamic currents.

Those who have been diagnosed with chronic gastritis of the superficial antrum of the stomach are recommended to undergo a course of rehabilitation in sanatoriums.

Useful video

The inflammatory process that occurs on the gastric mucosa is called atrophic gastritis. With this disease, the number of healthy cells is greatly reduced, and a precancerous condition occurs. Before you begin treatment for atrophic gastritis, you should find out the reasons for its development. Gastritis symptoms and treatment are completely dependent on the stage of development of the disease.

• 1Clinical picture of the disease
• 2Manifestation of pathology
• 3Methods for examining the body
• 4Types of disease
• 5Therapeutic therapy
• 6Diet for illness

1Clinical picture of the disease

One of the most insidious types of gastritis is considered atrophic, developing most often in elderly and middle-aged men.

Under the influence of certain reasons, the cells of the stomach undergo so-called “atrophic degeneration” and can no longer perform their functions - to produce the components of gastric juice. Instead, they begin to secrete mucus. Atrophic gastritis usually occurs along with low or high stomach acidity. But the danger of the disease is not even that it contributes to the deterioration of the gastrointestinal tract. Today it is known that atrophic gastritis and stomach cancer are related. Atrophic gastritis is a harbinger of a more complex disease.

The insidiousness of the disease lies in the fact that in the first stages the disease passes with virtually no symptoms.

It is very easy to ignore minor discomfort or mistake it for a simple malaise.

All forms of atrophic gastritis have similar symptoms. After eating, even in small quantities, patients most often complain of a feeling of heaviness in the solar plexus area. Manifestations of gastrointestinal pathology are observed: bad breath, rumbling in the abdomen, flatulence, constipation, and less commonly, diarrhea.

Some other symptoms appear that are not directly related to diseases of the gastrointestinal tract: a sharp decline body weight, lack of vitamin B12, signs of anemia, yellowness of the skin, tingling of the tongue, headaches. Expressions may occur in oral cavity. Hormonal levels are disrupted.

Various methods are used for diagnosis; the use of CT, ultrasound, MRI, and radiography does not provide comprehensive information.

In order to obtain all the data and prescribe the correct treatment for atrophic gastritis, types of gastroscopy and endoscopy are more often used. A gastroscope allows you to determine the thinning of the stomach walls. Examination of the gastrointestinal tract allows you to obtain data on the condition of the gastric glands.

The most convenient modern method of examination is considered to be a gastropanel, which allows non-invasive assessment of the state of stomach activity. The method is based on identifying three indicators: the pepsinogen protein, which is responsible for the production of HCL, the Helicobacter pylori antibody, and the hormone gastrin 17, which controls acid production and regeneration of the stomach walls.

2Manifestation of pathology

Atrophic gastritis can be different types. Depending on the stage, a person may develop:

• surface;
• spicy;
• moderate;
• chronic atrophic gastritis.

Superficial atrophic gastritis is considered only a sign of possible inflammation of the mucous membrane. This is the most early stage, in which the manifestations are practically invisible, so it can only be determined using endoscopy. At instrumental way Research reveals the following manifestations:

• hypersecretion of cells - can only be determined by indirect signs;
• the thickness of the stomach walls is normal;
• epithelial degeneration is at a moderate level.

Contrary to popular belief, chronic atrophic gastritis is an independent disease, and not a transformation of an acute form of gastric disease. Chronic gastritis is characterized by long-term, progressive destruction of stomach cells, with dystrophic rather than inflammatory processes predominating. The motor, secretory and other functions of the stomach change significantly.

In the chronic form, the disease affects not only the stomach, but also other organs: the pancreas and endocrine glands. Due to intoxication, the nervous and circulatory systems are involved in the development of the disease.

The appearance of symptoms of the disease is associated with low or high acidity of gastric juice.

3Methods for examining the body

Most meaningful methods examinations are endoscopy, pH measurement and blood tests. Using instrumental methods, atrophic gastritis can be identified by the following signs:

• the wall of the organ may be of normal thickness or too thin;
• the presence of large gastric pits;
• gland activity is greatly reduced;
• vacuolization of glands is observed;
• condensed epithelium;
• the mucous membrane is smoothed;

Moderate atrophic gastritis - very symbol stage at which only a partial, mild degree of cell transformation is observed. The disease can be detected at this stage in only one way - by determining the number of affected cells in the area of ​​the gastric mucosa. At the same time, tissue changes are analyzed.

With this disease, the symptoms will be exactly the same as in the acute form: sharp pain, which, however, does not always appear (more often after eating spicy, fried foods), a frequent feeling of discomfort after eating.

Acute, or active, gastritis is characterized by exacerbation of inflammatory processes. Tissue swelling, destruction of the epithelium up to mucosal erosion (in rare cases) and infiltration of leukocytes outside the organ are observed.

Symptoms of the acute form: severe stomach pain, diarrhea, fever, loss of consciousness - even coma.

4Types of disease

The following types of atrophic gastritis are distinguished:

• antral;
• focal;
• diffuse.

Focal atrophic gastritis is characterized by the appearance of areas with pathological processes in the tissues of the stomach. In some cases, the disease resolves with increased acidity. An increase in the amount of hydrochloric acid in this disease is usually explained by the fact that healthy areas of stomach tissue compensate for the work of the affected ones. Basically, in terms of its symptoms, focal atrophic gastritis does not differ from ordinary gastritis.

Most common symptom considered intolerant to certain foods: too fatty foods, dairy products, etc. After eating such food, vomiting, stomach pain, and heartburn may occur. Helps make an accurate diagnosis laboratory research and instrumental.

Antral atrophic gastritis develops in the lower part of the stomach, bordering the duodenum. The manifestations of this disease are very bright and have the appearance of scarring. Visually it looks like a compacted tube. Signs of dyspepsia are moderate: belching after eating, pain in solar plexus, loss of appetite, nausea in the morning, noticeable loss of body weight. Acidity remains at the same level or, which happens much more often, decreases slightly.

At antral gastritis An instrumental examination is prescribed, which usually reveals changes and deformation of the walls of the stomach, as well as a decrease in peristalsis due to the rigidity of the walls. Tumors on the mucous membrane and ulcerative processes are often diagnosed.

Another type is diffuse gastritis. This disease is an intermediate stage, which occurs after the onset of superficial deformations of the walls of the stomach and before dystrophic changes. The most obvious sign is the presence of foci of degeneration of the gastric glands and disruption of their activity, the appearance of immature cells. Other symptoms of the disease are the presence of microstructural damage and deepening of the gastric pits.

5Therapeutic therapy

Due to the fact that there are many forms of the disease, common approach atrophic gastritis has no treatment. It has been established that the atrophy process that has begun cannot be corrected because damaged cells do not return to their original state.

Despite this, methods have already been proposed that make it possible to effectively treat the atrophic form of gastritis, regardless of its type and stage, and to stop its further development.

All forms of treatment are based on the results of the examination, since each case requires a special therapeutic approach. The treatment regimen consists of several stages.

The first stage, eradication of Helicobacter pylori, is necessary when the bacteria have a strong impact on the course of the disease. Main tasks at this stage:

• suppressing the development of bacteria, overcoming their resistance to antibiotics;
• decline dyspeptic symptoms, alleviation of the condition through the use of inhibitors;
• reduction of treatment duration;
• reducing the number of medications used to reduce the occurrence of side effects.

At the second stage, attempts are made to influence the development of autoimmune processes. A method that would fully influence the development of atrophic hyperplastic gastritis, not found yet. Usually at this stage hormonal drugs and immunocorrectors are prescribed, but they do not always give the desired effect.

The third stage is pathogenic therapy. During this period, medications from various groups are prescribed:

1. Digestive aids.
2. Parental injections to eliminate vitamin B12 deficiency.
3. Effective in some cases mineral water- they have a beneficial effect on the production of hydrochloric acid.
4. To reduce inflammation, medications containing plantain juice are used, for example, Plantaglucide. Alternatively, you can use plantain juice directly.
5. The treatment of inflammation is facilitated by Riboxin, which is increasingly prescribed to patients.
6. Drugs are prescribed to regulate intestinal motor function (Cisapride or some others).
7. In order to protect the mucous membrane, basic bismuth nitrate, Kaolin, Vikair are used.

After the end of active treatment, a period of remission begins. At this time, the main tasks are to restore digestive functions and replenish the substances necessary for this.

6Diet for illness

In order for the treatment of atrophic gastritis to produce results, the patient is prescribed special diet, which he will have to adhere to throughout the entire period of treatment and remission. In any case, with this disease, some difficulties may arise during the organization of nutrition. Before treating atrophic gastritis of the stomach, the doctor prescribes one of four types of diets developed by M. I. Pevzner.

Diet 1. Prescribed only when the symptoms of inflammation gradually subside. This method of eating helps normalize the functioning of the stomach. Cold and hot dishes are excluded from the patient's daily menu. Limit consumption of fiber-rich foods. In total, the diet includes approximately 11 dishes.

Diet 1a is recommended for patients to adhere to in the first days of treatment. The purpose of this type of diet is to have a gentle diet and reduce stress. The food should be liquid or pureed, the method of preparation is steaming or boiling in water.

Diet 2 is considered basic, aimed at stimulating the functioning of the glands. Patients' diets should be varied. The menu includes fish, lean meat, fermented milk and flour dishes, fruits and vegetables. Products can be fried in a small amount of oil, boiled, stewed and baked. In total there are about 30 dishes on the menu.

Diet 4 - for enteric syndrome, aims to improve the functioning of the stomach and reduce inflammation of the mucous membrane. Dairy products are excluded, as they are intolerant. You need to eat fractionally, that is, often, but in small portions. After the symptoms of inflammation have passed, patients are transferred to a more nutritious diet - No. 2.