Lymphocytic infiltration is a rare dermatosis of a chronic form, which is characterized by benign infiltration skin 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 pathology consists of using hormone therapy, NSAIDs, topical drugs.

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 the medical literature in 1953, when N. Kanof and M. Jessner considered it as an independent pathological process with end-to-end infiltration of lymphocytes into all skin structures. 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 immunity plays a significant role in the development of lymphocytic infiltration, 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

Most possible reasons the development of focal lymphoplasmacytic infiltration is considered to be tick bites, hyperinsolation, various infections, pathologies digestive system, the use of dermatogenic 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. On last stage cupping inflammatory reaction two simultaneous proliferation processes enhance and complement each other. Thus, foci of pathology arise.

Since lymphocytes are heterogeneous, 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 initial element of skin rashes with lymphocytic infiltration is a flat, large pink-bluish plaque or papule with clear outlines and 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 the primary element is 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.

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 is 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 number of normal cells (in 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 drugs. 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 - what is it? Doctors distinguish several types of it - inflammatory, lymphoid, post-injection and others. The causes of infiltration are different, but all its types are characterized by the presence of unusual cellular elements in the tissue (or organ), its increased density, and increased volume.

Post-injection infiltrate

1. The rules of antiseptic treatment were not followed.

2. Short or blunt syringe needle.

3. Rapid administration of the drug.

4. The injection site is chosen incorrectly.

5. Repeated administration of the drug to the same place.

The appearance of post-injection infiltrate also depends on the individual characteristics of the human body. In some people it occurs extremely rarely, while in other patients it occurs after almost every injection.

Treatment of post-injection infiltrate

There is no infection in the infiltrated tissue, but the danger of this pathology after an injection is that there is a possible risk of an abscess. In this case, treatment can only take place under the supervision of a surgeon.

If no complications arise, then the infiltration after injections is treated with physiotherapeutic methods. It is also recommended to apply to the tissue seal area. iodine grid several times a day, use Vishnevsky ointment.

Traditional medicine also offers several effective methods for getting rid of “bumps” that appear after injections. Honey, burdock or cabbage leaves, aloe, cranberries, cottage cheese, and rice can have a healing effect if a similar problem occurs. For example, burdock or cabbage leaves should be taken for treatment in fresh, applying them for a long time to the sore spot. The “bump” can be lubricated with honey beforehand. A compress made from cottage cheese also helps get rid of old “bumps”.

No matter how good this or that method of treating this problem is, the final word should belong to the doctor, since it is he who will determine what to treat and whether it needs to be done.

Inflammatory infiltrate

This group of pathologies is divided into several types. Inflammatory infiltrate - what is it? The medical encyclopedia explains everything, which talks about the ways in which inflammation occurs and indicates the reasons for the appearance of pathological tissue reactions.

Medicine identifies a large number of varieties of infiltrates of the subgroup under consideration. Their presence may indicate problems with the immune system, congenital diseases, the presence acute inflammation, chronic infectious disease, allergic reactions in the body.

The most common type of this pathological process is inflammatory infiltrate. What it is, a description of the characteristic features helps to understand this phenomenon. So, what should you pay attention to? Tissue compaction in the area of ​​inflammation. Painful sensations occur when pressed. With stronger pressure, a hole remains on the body, which levels out slowly, since the displaced cells of the infiltrate return to their original place only after a certain period of time.

Lymphoid infiltrate

One of the types of tissue pathology is lymphoid infiltrate. The Big Medical Dictionary allows you to understand what it is. It says that such a pathology occurs in some chronic infectious diseases. The infiltrate contains lymphocytes. They can accumulate in different tissues of the body.

The presence of lymphoid infiltration indicates a malfunction of the immune system.

Postoperative infiltration

For what reason can a postoperative infiltrate form? What it is? Does it need to be treated? How to do it? These questions concern people who have had to face this problem.

The development of postoperative infiltration occurs gradually. Usually its detection occurs 4-6 or even 10-15 days after surgery. The patient's body temperature rises, aching pain appears in the abdominal area, and stool retention occurs. The presence of a painful lump is determined.

In some cases, it can be difficult to determine where the infiltrate is located - in the abdominal cavity or in its thickness. For this, the doctor uses special methods diagnostics

The causes of infiltration after operations cannot always be accurately determined, but its therapy in most cases ends successfully. Antibiotics and various types of physical treatment give positive results.

Infiltration occurs very often postoperative scar. Sometimes it can appear several years after the surgical procedure. One of the reasons for its occurrence is the suture material used. Perhaps the infiltrate will resolve on its own. Although this happens rarely. Most often, the phenomenon is complicated by an abscess, which must be opened by a surgeon.

Infiltrate in the lungs

This is a dangerous pathology that requires immediate treatment. Using X-ray data and biopsy, doctors can detect lung infiltration in a patient. What it is? Pulmonary infiltration must be distinguished from pulmonary edema. With this pathology, the patient experiences penetration and accumulation of fluids, chemicals, and cellular elements in the tissues of the internal organ.

Lung infiltration most often has an inflammatory origin. It can be complicated by suppuration processes, which leads to loss of organ function.

Moderate enlargement of the lung and compaction of its tissue are characteristic signs of infiltration. Helps to recognize them x-ray examination, in which darkening of the tissues of the internal organ is visible. What does this give? Based on the nature of the darkening, the doctor can determine the type of pathology in question and the degree of the disease.

Tumor infiltrate

The most common pathologies include tumor infiltrate. What it is? It most often consists of atypical tumor cells of different nature (cancer, sarcoma). The affected tissues change color, become dense, and sometimes painful. Manifests itself in tumor growth.

Reasons for appearance

The likelihood of infiltration occurring is equally present in people of any age.

The results of the study showed that the cause of the disease can be various types of injuries, illnesses infectious nature. They can be transmitted by contact and have a lymphogenous type of spread.

An infiltrate very often develops in the tissues of the perimaxillary region. What it is? How to distinguish it from other diseases? Only an experienced doctor can assess the patient’s condition and give an accurate answer to the questions posed. The causative agents of inflammation are staphylococci, streptococci and other representatives of the microflora of the oral cavity.

A complicated condition of acute appendicitis can also cause the development of infiltrate. It occurs due to untimely surgical intervention.

Symptoms of infiltration

As the disease develops, the patient may experience slight elevated temperature. It stays at a certain level for several days. Sometimes this indicator remains normal. The infiltrate spreads to one or more parts of the body. This is expressed in swelling and compaction of tissues with a clearly defined contour. All tissues are affected simultaneously - mucous membrane, skin, subcutaneous fat and muscle membranes.

The infiltrate, which develops against the background of a complication of appendicitis, is characterized by persistent pain in the lower abdomen, fever up to 39 degrees, and chills. In this case, the patient’s recovery is possible only with timely surgical intervention. The presence of this type of infiltrate is determined during examination by a doctor (does not require special diagnostic methods).

In other cases, only a differential approach makes it possible to accurately establish a diagnosis and prescribe the necessary treatment. Sometimes, to establish a diagnosis, data from the results of a puncture from the site of inflammation are taken into account.

Specialists examine materials taken from the inflamed area. The different nature of the cells making up the infiltrate has been established. It is this circumstance that allows doctors to classify the disease. As a rule, a large accumulation of yeast and filamentous fungi is found in the infiltrate. This indicates the presence of a condition such as dysbiosis.

The main goal of treating infiltration is to eliminate inflammatory foci. This is achieved by conservative treatment methods, which include physiotherapy. The patient should not self-medicate and delay a visit to a specialist.

Thanks to physiotherapeutic treatment, resorption of the infiltrate is achieved by increasing blood flow. At this time, the elimination of stagnation occurs. There is also a reduction in swelling and pain relief. Electrophoresis of antibiotics and calcium is most often prescribed.

Physiotherapy is contraindicated if purulent forms of the disease are present. Intense exposure to the affected area will only provoke the rapid development of infiltration and further spread of the lesion.

Lymphoma of the stomach

Lymphoma of the stomach

Gastric lymphoma is a malignant non-leukemic neoplasm that originates from lymphoid cells in the wall of the organ. It usually has a relatively benign course, slow growth and rare metastasis, but the degree of malignancy of the tumor may vary. Most often located in the distal part of the stomach. Not associated with damage to peripheral lymph nodes and bone marrow. Gastric lymphomas account for 1 to 5% of the total number of neoplasias of this organ. Typically develops over the age of 50. Men are affected more often than women. In the initial stages, the prognosis is favorable. The average five-year survival rate for gastric lymphomas of all stages ranges from 34 to 50%. Treatment is carried out by specialists in the field of oncology, gastroenterology and abdominal surgery.

Causes of stomach lymphoma

The precursor of this neoplasm is lymphoid tissue located in the mucous membrane in the form of individual lymphocytes and clusters of cells. Under certain conditions (for example, with chronic gastritis caused by Helicobacter pylori infection), such accumulations form lymphoid follicles, in which areas of atypia may appear. Taking into account the fact that in 95% of patients with gastric lymphoma, various strains of Helicobacter pylori are detected during examination, this infection is considered as one of the main causes of this pathology.

Along with Helicobacter pylori, the development of various types of gastric lymphomas can be provoked by other factors, including contact with carcinogenic substances, long stay in areas with increased levels of radiation, previous radiation therapy, taking certain medications, excess ultraviolet radiation, nonspecific decrease in immunity, immune disorders in AIDS, autoimmune diseases and artificial suppression of immunity after organ transplantation operations.

Classification of gastric lymphomas

Taking into account the origin and characteristics of the clinical course, they distinguish the following types lymphomas of the stomach:

MALT lymphoma(the abbreviation comes from the Latin mucosa-associated lymphoid tissue). Included in the group of non-Hodgkin's lymphomas. This gastric lymphoma develops from lymphoid tissue associated with the gastric mucosa. Usually occurs against the background of chronic gastritis. It is not accompanied by primary damage to peripheral lymph nodes and bone marrow. The degree of malignancy varies. May metastasize to lymph nodes.

B cell lymphoma. Formed from poorly differentiated B cells. Presumably occurs as a result of the progression of MALT lymphomas; indirect confirmation of this hypothesis is the frequent combination of the two listed types of gastric lymphomas. It has a high degree of malignancy.

Pseudolymphoma. It is characterized by lymphoid infiltration of the mucous membrane and submucosal layer of the stomach. It proceeds benignly, in some cases malignancy is observed.

Taking into account the growth characteristics, the following types of gastric lymphomas are distinguished:

With exophytic growth. Neoplasms grow into the lumen of the stomach and are polyps, plaques or protruding nodes.

With infiltrative growth. Neoplasia forms nodes in the thickness of the gastric mucosa. Depending on the characteristics of the nodes in this group, tuberous-infiltrative, flat-infiltrative, giant-fold and infiltrative-ulcerative forms of gastric lymphoma are distinguished.

Ulcerative. Stomach lymphomas are ulcers of varying depths. They have the most aggressive course.

Mixed. When examining a tumor, signs of several (usually two) of the types of tumor listed above are detected.

Taking into account the depth of the lesion, determined by endoscopic ultrasound, the following stages of gastric lymphomas are distinguished:

1a – with damage to the superficial layer of the mucous membrane.

1b – with damage to the deep layers of the mucous membrane.

2 – with damage to the submucosal layer.

3 – with damage to the muscular and serous layer.

Along with the above classification, the standard four-stage classification of oncological diseases is used to determine the prevalence of gastric lymphoma.

Symptoms of stomach lymphoma

There are no specific signs; in its clinical manifestations, gastric lymphoma may resemble gastric cancer. less often - gastric ulcer or chronic gastritis. The most common symptom is pain in the epigastric region, often worsening after eating. Many patients with gastric lymphoma report a feeling of premature satiety. Some patients develop aversions to certain types of food. Characteristic weight loss is caused by a feeling of fullness in the stomach and decreased appetite. A critical decrease in body weight up to cachexia is possible.

With gastric lymphoma, nausea and vomiting are often observed, especially when eating excessive amounts of food, which further contributes to reducing portions, refusing to eat and subsequent weight loss. As the cancer process spreads, gastric stenosis may develop. In some cases, patients with gastric lymphoma experience bleeding of varying severity (including small ones, with an admixture of blood in the vomit). There is a danger of developing severe complications - perforation of the stomach wall when it grows with a tumor and profuse bleeding when gastric lymphoma is located near a large vessel. Along with the listed symptoms, there is an increase in body temperature and profuse sweating, especially at night.

The diagnosis is established taking into account complaints, medical history, external examination, palpation of the abdomen, laboratory and instrumental studies. Due to the nonspecificity of symptoms, late detection of gastric lymphoma is possible; the literature describes cases where the time period between the appearance of epigastric pain and diagnosis was about 3 years. The main method of instrumental diagnosis is gastroscopy. allowing to determine the location and type of tumor growth. When performing endoscopic examination, gastric lymphoma can be difficult to differentiate from cancer, gastritis and non-malignant ulcers.

To clarify the diagnosis, the endoscopist takes material for subsequent histological and cytological examination. A distinctive feature of taking an endoscopic biopsy for gastric lymphomas is the need to take tissue from several areas (multiple or loop biopsy). To determine the extent of the oncological process, endoscopic ultrasound and CT of the abdominal cavity are performed. To detect metastases, MRI of the chest and MRI of the abdominal cavity are prescribed. Despite diagnostic difficulties, due to their slow growth, most gastric lymphomas are detected at the first or second stage, which increases the likelihood of a successful outcome with this pathology.

Treatment of gastric lymphoma

For localized, favorable MALT lymphomas, eradication anti-Helicobacter therapy is carried out. It is acceptable to use any treatment regimen with proven effectiveness. If there is no result after using one of the standard regimens, patients with gastric lymphoma are prescribed a complicated three-component or four-component therapy, including the administration of proton pump inhibitors and several antibacterial agents(metronidazole, tetracycline, amoxicillin, clarithromycin, etc.). If complicated regimens are ineffective, chemotherapy or systemic therapy is administered, depending on the stage of gastric lymphoma.

For other forms of gastric lymphoma and MALT lymphomas that extend beyond the submucosal layer, surgical intervention is indicated. Depending on the extent of the process, gastric resection or gastrectomy is performed. In the postoperative period, all patients with gastric lymphoma are prescribed chemotherapy. IN advanced cases chemotherapy or radiation therapy is used. Chemotherapy can provoke ulceration and perforation of the stomach wall (including asymptomatic ones), therefore, when using this technique, CT scans are regularly performed to detect free fluid and gas in the abdominal cavity. In the later stages of gastric lymphoma, there is a risk of developing gastric stenosis, gastric perforation or stomach bleeding. therefore, operations are recommended even for stage III and IV tumors.

Thanks to slow growth, late invasion into the deep layers of the stomach wall and fairly rare metastasis, the prognosis for gastric lymphomas is relatively favorable. The use of eradication therapy in the early stages of MALT lymphomas provides complete remission in 81% of patients and partial remission in 9% of patients. Radical surgical interventions possible in 75% of cases. The average five-year survival rate for stage I gastric lymphoma is 95%. At stage II this figure decreases to 78%, at stage IV – to 25%.

What is lymphoid gastritis?

Treatment of lymphoid gastritis

Several more forms of rare gastritis

Medicine includes several types of gastritis, among which lymphoid gastritis, according to the international classification, belongs to special types of diseases. It occurs infrequently; according to statistical data, no more than 1% of the number of cases have it. It is characterized by the fact that the mucous membrane is damaged in an unusual way. In its wall, in place of diseased areas, lymphocytes—special cells—appear in large numbers. From them follicles (vesicles) are formed.

Lymphoid gastritis is a special type of gastritis

This disease mainly begins to develop against the background of chronic gastritis. According to doctors, the bacteria Helicobacter pylori are to blame for the appearance of such an unusual disease. These microorganisms colonize the gastric mucosa and gradually cause inflammation. The appeared lymphocytes act in two ways. On the one hand, they have a healing effect, neutralizing the pathogenic effect of bacteria. On the other hand, the follicles prevent cells not affected by the disease from producing gastric juice.

Due to the formation of follicles, the disease has another name - follicular gastritis.

Lymphoid gastritis does not cause patients very severe suffering, such as ulcerative gastritis. Patients complain of the following symptoms:

not very strong, but very frequent pain in the upper abdomen;

heartburn (this is a symptom of almost all forms of stomach ailments);

a feeling of heaviness inside the abdomen and its distension;

nausea;

unpleasant aftertaste, but not constantly, but quite rarely.

The signs are not particularly obvious, so diagnosing lymphoid gastritis is very problematic. To make a diagnosis, doctors try to use instrumental methods.

Lymphoid gastritis is quite difficult to diagnose. Even experienced gastroenterologists make mistakes. The patient is required to undergo a special endoscopic examination: the mucous membrane is examined using an optical flexible device. And the doctor sees on the display what is happening inside the stomach. As a result, the whole picture of the disease emerges. In addition, the device helps to obtain mucosal tissue for microscopic examination. A biopsy is performed. As a result, the patient is given an accurate diagnosis.

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Treatment of lymphoid gastritis

If the bacterium Helicobacter pylori is detected in the patient’s stomach, then antibacterial therapy is mandatory. Antibiotics are taken for two weeks. If the disease is accompanied by heartburn, then medications are prescribed to help reduce acidity. Symptomatic treatment is recommended.

Due to the fact that the bacterium is transmitted by contact, there is a high risk of contracting this form of gastritis through cutlery, dishes and other common objects.

The doctor prescribes medications:

painkillers;

medications that protect the mucous membrane from the effects of aggressive substances (enveloping the walls of the stomach);

drugs that restore epithelial cells.

Treatment of lymphoid gastritis will not work positive result without following a special diet. The patient should exclude from his diet all foods that cause stomach irritation. Strong broths, spicy foods, pickles, smoked foods, canned goods and spices cannot be present in food. Boiled fish and meat, crumbly porridges, vegetable purees, jelly, cottage cheese casseroles - this is exactly the food that is indicated for patients.

Meals should be frequent, but in small portions. Eating at least four times a day, and preferably six. It is advisable to eliminate alcohol completely. Mineral water is welcome. The doctor will advise which one.

Gives good results in the treatment of gastritis sharing traditional methods and treatment with folk remedies.

According to the advice of traditional healers, it is necessary to take plantain juice. It relieves inflammation, relieves pain, and has a healing effect. Propolis and fresh garlic are used as antimicrobial agents.

Traditional treatments have long courses. This leads to a good healing result and eliminates the possibility of recurrence of the disease.

Prevention of the disease is also of great importance. Since this disease is caused by bacteria and is transmitted by contact, it is advisable to provide complete isolation to the patient with obvious signs of infection. But this is practically impossible. Therefore, in order to prevent the spread of the disease, it is better to treat all family members at once. This will reduce the risk of gastritis growing.

Enlarged lymph nodes of the stomach

Gastric lymphoma is a rare disease. Its distinguishing feature is damage to nearby lymph nodes. Of the entire list of cancer diseases, 1-2% are lymphoma.

The essence of pathology

At risk are men over 50 years of age. Since lymphoma affects the lymph nodes, oncology in the stomach develops due to metastasis. Therefore, primary tumors are less common than secondary ones. Another name for the pathology is gastric malt lymphoma. Features of the pathology:

slow flow;

similarity of symptoms with stomach cancer;

relatively favorable prognosis.

There are several forms of pathology with different symptoms. In each case, the lymphoid tissue is affected along with the gastric mucosa. The increase in the incidence of lymphoma is explained by environmental deterioration, consumption of harmful, chemically contaminated food, and increased stress on the immune system. Antibodies begin to form in lymphocytes, neutralizing and destroying pathogenic stimuli and pathogenic agents. This leads to disruptions in the functioning of the immune system, characterized by a decrease in the secretion of antibodies. This encourages them to destroy their own body cells.

Mechanism

Lymphocytes are active cells of the immune system. When its functioning fails, excessive or insufficient production of these cells occurs, which leads to an increase in their aggression towards their own body. Histological analysis of stomach tissue affected by lymphoma reveals a pathological accumulation of lymphoid cells in the mucous and submucosal layers of the organ. At the same time, the lymphoid follicle infiltrates the gastric glands, which leads to digestive dysfunction. If lymphoma is initially formed in the stomach, in most cases there are no metastases in the bone marrow and peripheral lymph nodes.

In most cases, the pathological process initially affects the lymph node in the neck or groin. The stomach undergoes metastasis when local immunity decreases against the background of the development and progression of chronic gastritis, which appears as a result of Helicobacter pylori infection.

Varieties and reasons

There are:

Primary, similar to gastric cancer symptomatically and visually, but without involvement of peripheral lymph nodes with bone marrow. Appear against the background of chronic gastritis.

Secondary, affecting most of the stomach multicentrically.

Lymphogranulomatosis (Hodgkin's pathology), which develops when cancer metastasizes to the gastric walls and adjacent lymph nodes. Isolated gastric involvement is rare.

Non-Hodgkin's lymphomas, characterized by different degrees of malignancy and differentiation. They belong to large cell tumors that develop from lymphoid tissue. The cause of its appearance is damage by Helicobacter.

Lymphomatosis (pseudolymphoma), which is a benign tumor. Occurs in 10% of all cancer cases. Infiltration of the mucous and submucosal layers occurs. The tumor does not metastasize to the lymph nodes, so it is not life-threatening. But the risk of malignancy remains, so lymphomatosis must be treated. Less commonly, the pathology can develop against the background of malignant lymphoma.

95% of all gastric malt lymphomas are accompanied by intoxication with HP infection. With this form, the lymph node is always enlarged. Other predisposing factors:

features of the immune system of an individual;

genetic predisposition;

autoimmune diseases;

AIDS;

previous transplants;

long-term residence in unfavorable places with increased background radiation;

eating food saturated with pesticides and carcinogens;

long-term treatment with medications that suppress the immune system.

Symptoms

The clinical picture of lymphoid neoplasms is similar to external and symptomatic manifestations cancerous lesions and other gastrointestinal pathologies. The first sign of gastric lymphoma is an enlarged lymph node in the neck or groin. Symptoms:

Painful sensations in the epigastrium, which may intensify after a meal. The nature of the pain is dull, aching.

Quick satiety when eating small portions of food.

Rapid weight loss up to the development of anorexia.

Lack of appetite, which leads to an unconscious decrease in the amount of food consumed.

The appearance of attacks of nausea. It is possible to develop vomiting with minor overeating.

Bleeding if the tumor grows near the network of blood vessels.

Profuse sweating and fever at night.

Aversion to certain types of foods, especially meat.

Lymphoma infiltration of the stomach is often accompanied by serious complications, such as:

perforation or perforation of the gastric wall, when a through wound is formed in the tumor area;

development of severe bleeding;

the appearance of pathological narrowings, most often in the outlet section of the organ.

These complications require emergency surgery. Diagnosis is particularly difficult for follicular lymphoma, which occurs with virtually no symptoms. However, pathological follicles can be treated even in advanced form.

Kinds

Malignant lymphoma tumors of follicles in the stomach have different cellular structure, features of growth with distribution. There are 5 types of tumors that are localized in different layers of gastric tissue. The following parameters were taken for classification:

Flow form:

• polypoid or exophytic tumor growing into the lumen of the organ;
• primary nodular, formed in the mucous layer of the stomach;
• infiltrative ulcerative is the most aggressive.
• Histological feature:
• malignant;
• benign.

Character of the current:

primary;

secondary.

Form of pathology:

lymphogranulomatosis;

non-Hodgkin malt lymphoma;

pseudolymphoma.

Structure:

B cell;

T cell;

diffuse large B-cell non-Hodgkin type;

follicular.

Diagnosis of gastric lymphoma

Preliminary examination with palpation, assessment of complaints, patient history.

Blood serum analysis. With lymphoma, the erythrocyte sedimentation rate will be high, specific proteins (tumor markers) and signs of microcytic anemia will appear.

Endoscopy of the stomach. A visual inspection of the internal part of the organ is carried out. The method is not indicative due to the inability to externally distinguish a tumor from gastritis or ulcers.

Biopsy. It is carried out during an endoscopic examination. A selected piece of tumor-affected tissue is sent for histological and cytological analysis, as a result of which malignant malt lymphoma, its type and stage, are confirmed or refuted. The presence of Helicobacter is determined.

Diagnostic laparotomy. The technique is a minimally invasive operation. Refers to the most accurate.

X-ray examination. Determines the location of the enlarged tumor.

CT scan. The method allows you to determine the size of the primary tumor and the stage of spread.

Magnetic resonance imaging. Secondary foci - metastases - are visualized.

Based on the data obtained, a treatment technique is selected.

Treatment

Lymphoma is treated under the supervision of an oncologist, who selects a technique in accordance with the type, prevalence and rate of progression of the pathology.

Stage I

Early lymphoma can be cured with chemical x-ray therapy or surgery. An integrated approach is preferable, as it has a low risk of relapse. To do this, the tumor is completely excised along with part of the stomach. The organ may be completely removed. During the operation, nearby gastric lymph nodes and organs are carefully examined. After the operation, a course of chemotherapy and radiation is carried out to remove possible distant metastases.

Stage II

X-ray and chemotherapy with such powerful antitumor drugs as Prednisolone, Vincristine, and Doxorubicin are always used. The treatment regimen is prescribed in accordance with the specific nature of the pathology. If non-Hodgkin's tumors are enlarged to large sizes, they are first reduced and then removed.

Stages III and IV

Treatment is prescribed in a complex step-by-step manner:

A course of shock chemistry and radiation is carried out to reduce the size of the tumor. Apply antitumor drugs: “Prednisolone”, “Doxorubicin”, “Vincristine”, “Cyclophosphamide”, which significantly improve the effect of further surgery. The maximum radiation dose to the abdominal cavity is no more than 3700 kGy.

A gastric resection is performed with a thorough examination of nearby lymph nodes, tissues and organs. If follicles are found, they are removed along with the surrounding tissue.

Purpose of the course antibacterial therapy when a Helibacter infection is detected.

Carrying out adjuvant (preventive) therapy to reduce the risk of relapse.

If a non-Hodgkin's tumor affects blood vessels or enlarged lymphoid follicles are found, such pathologies are considered inoperable. In this case, palliative therapy is prescribed. The goals of treatment are to take medications that reduce pain and improve the condition, which will prolong the patient’s life.

Course against Helicobacter

B-cell or Helicobacter lymphoma digestive organ undergoes a special treatment method. For this purpose, special medications are used that reduce inflammation, suppress vital activity and destroy Helicobacter.

To date, there is no consensus on the preferred treatment method for this type of lymphoma, so an individualized approach is taken.

If there is no effect of drug treatment, a course of radiation and chemotherapy is carried out. The operation is scheduled for extreme cases. After this, a repeated antitumor course is indicated.

Rehabilitation

In the postoperative period, it is important to establish proper nutrition. The nutritionist draws up the menu and the required amount of food. The complexity of the situation lies in the patient’s loss of appetite due to abdominal pain. The patient must follow all the doctor’s recommendations, undergo regular examinations, and take traditional recipes as a preventive measure.

Folk remedies

The use of any prescription requires consultation with a doctor. Recipes:

Dzungarian aconite. The tincture should be lubricated and rubbed over the spine. After this, the back is tied with cotton fabric.

Sea buckthorn juice. The product is taken orally when diluted with water 1.1.

Birch buds. Taken as a decoction. Recipe: 75 g, pour 200 ml of water, boil, strain and take 60 ml three times a day before meals.

Forecast

Gastric lymphoma has a favorable prognosis when detected in the early stages. Stages III and IV are curable, but 5-year survival depends on the severity of infiltration, tumor size and its extent. Survival rate for grade I is 95%, for grade II - 75%, for grade III and IV - 25%. Complete cure possible in most cases when choosing the right treatment tactics. The outcome depends on the speed of spread of the lymphoma and the possibility of metastasis.

Nutrition and diet

The effectiveness of lymphoma treatment depends on proper nutrition and diet. The patient must receive a sufficient amount of calories and building protein to restore the body, regenerate tissue and maintain weight. Good nutrition will soon return you to normal health. But certain foods can cause problems.

Often patients refuse to eat due to pain and lack of taste during treatment. Therefore, a specific diet is being developed with a limited amount of animal protein and fatty foods. The content of vegetable protein, fiber, dairy and fermented milk products in the menu is increasing.

Products must be well boiled in water or steamed. Dishes should be prepared in liquid or semi-liquid form. It is not recommended to eat cold or hot food. Diet:

Fractional meals.

Small portions.

A large number of snacks - 6 times a day.

Ensuring rest after eating.

Avoiding overeating.

Sample menu

Despite the strict restrictions on products, a nutritionist can create a menu for gastric lymphoma that is acceptable in terms of variety and nutritional value.

Table No. 1

1. first: meatballs made from lean meat and rice, weak green tea;
2. second: apple crushed to puree.
3. Lunch: pureed vegetable soup, boiled chicken, freshly squeezed fruit juice.
4. Afternoon snack: fresh homemade yogurt.
5. Dinner: Freshly cooked macaroni and cheese.
6. A glass of goat milk before bed.

Table No. 2

7. Two meals for breakfast:
8. first: steamed omelette (can be replaced with a soft-boiled egg), tea;
9. second: crushed cottage cheese.
10. Lunch: puree soup with vegetables, boiled low-fat fish.
11. Afternoon snack: freshly squeezed juice from vegetables or fruits.
12. Dinner: heavily boiled cereal porridge with boiled chicken.

Prevention

Methods to prevent lymphoma do not completely protect against the possibility of its development due to the uncertainty of the true causes of its occurrence. But the following rules help reduce risk factors:

Do not stay for a long time in dangerous areas contaminated with radiation and other chemicals.

When living in environmentally unfavorable areas, it is recommended to constantly travel to the countryside, to nature, where the air is enriched with oxygen.

Avoid contact with pesticides.

Avoid reducing the functioning of the immune system.

Eat high-quality, fresh food.

Maintain equal intervals between meals, which will eliminate the risk of overeating or starvation.

Treat pathologies in a timely manner, but do not abuse medications.

Do not neglect consulting a doctor.

A significant step forward in the study of chronic gastritis was the study of the gastric mucosa obtained by targeted gastrobiopsy during endoscopic examination. M. Gear based on the study of biopsy samples of the gastric mucosa obtained during endoscopic examination of patients with various diseases, identifies chronic superficial and atrophic gastritis of the antrum and body of the stomach. The authors divide atrophic gastritis into moderate, moderate and severe. In their opinion, it is difficult to distinguish between superficial gastritis and incipient atrophic gastritis. R. Ottenjann and K. Elster, in addition to superficial and atrophic, distinguish chronic atrophic gastritis with intestinal metaplasia.

It is now generally accepted that various shapes chronic gastritis are stages of a single process and the main trend, according to most authors, based on long-term observations, is the progression of chronic gastritis from superficial to atrophic. The morphological shifts are based on a combination degenerative changes glandular elements, hyperplastic and atrophic processes in the mucous membrane, restructuring of the surface epithelium and glandular epithelium, inflammatory infiltration of the mucous membrane. However pathogenetic mechanism The development of chronic gastritis is interpreted differently in the literature.

According to Yu. M. Lazovsky, with chronic gastritis, deep coordination disorders occur between the two main phases of the regenerative process in the mucous membrane: proliferation and differentiation. In the early stages, a picture of dysregenerative hyperplasia is observed; in later stages, aregenerative atrophy occurs.

According to a number of authors, based on the study of the mucous membrane using light and electron microscopy, the main point in the morphogenesis of chronic gastritis is a violation of the physiological regeneration of the glands, expressed in the predominance of the proliferation stage over the differentiation stage, as well as in the premature involution of part glandular cells. This reaction of the gastric mucosa to pathological effects, in their opinion, is universal. With gastritis with damage to the glands and atrophic gastritis, changes indicate incomplete regeneration or involution of cells completing their life cycle.

A constant sign of superficial gastritis is the infiltration of the surface epithelium and its own layer of the mucous membrane by lymphoid and plasma cells.

N. Hamper considered the infiltration and release of leukocytes into the gastric cavity through the superficial or pitted epithelium as a reaction in response to food irritation, therefore, in his opinion, a diagnosis of gastritis cannot be made on the basis of lymphocytic infiltration.

S. M. Ryss, B. X. Rachvelishvili, V. P. Salupere, E. A. Kotyk, I. Valencial-Parparcen, N. Romer believe that inflammatory infiltration of the gastric mucosa is the main symptom of this disease. A nonspecific inflammatory process, starting with increased cellular infiltration of the stroma at the level of the pits, which becomes diffuse with progression, ultimately leads to atrophy of the gastric glands. Infiltration is enhanced mainly due to lymphoid and plasma cells, but with the spread of inflammatory infiltration to the basal parts of the mucous membrane, the content of neutrophilic leukocytes and macrophages increases.

V. A. Samsonov, in a histological examination of the mucous membrane of patients with peptic ulcer and gastritis, revealed leukocyte infiltration of the stomach wall and the initial part of the duodenum, as well as infiltration with plasma, lymphoid and mast cells. Only in isolated cases was it possible to note significant leukocyte infiltration of the interpitular stroma in certain areas of the mucous membrane, and only deeper than the bottom sections of the gastric pits in the mucous membrane was leukocyte infiltration always observed. The author was unable to identify any relationship between the degree of structural restructuring of the gastric mucosa and the intensity of leukocyte infiltration.

V. A. Samsonov associates the peculiar pattern of distribution of leukocytes and other cellular elements in the mucous membrane more with the functional characteristics of the gastric region than with inflammation. L.A. Fedorova, studying cellular infiltration and the state of the glandular apparatus of the gastric mucosa in a number of diseases, including chronic gastritis, came to the conclusion that the nature of infiltration has a direct connection with the depth of prevalence of changes in the glandular apparatus, and not with the nosological form of the disease.

A significant increase in the number of plasma cells as chronic gastritis progresses is considered by a number of authors as an indicator of immune and autoimmune processes developing in this disease.

Ts. G. Masevich, during an exacerbation of chronic gastritis, observed the appearance in the infiltrate, in addition to lymphocytes and plasma cells, in a large number of neutrophils, thereby confirming the data of S. S. Weil and L. B. Sheinina, Yu. M. Lazovsky, obtained by them during experimental acute gastritis.

Far from the last role in the development of morphological changes in chronic gastritis belongs to the stroma of the mucous membrane. During the atrophic process, hypertrophy of the connective tissue occurs in the muscle layer and in the own layer of the mucous membrane.

One of the most important elements of structural restructuring of the gastric mucosa in chronic gastritis is intestinal metaplasia, which is regarded as a result of impaired epithelial differentiation. Intestinal metaplasia is more often expressed in atrophic gastritis and indicates the severity of the atrophic process in the mucous membrane. Restructuring of the gastric mucosa with accompanying atrophy, intestinal metaplasia and especially uneven hyperplasia of the superficial and glandular epithelium currently considered as a precancer.

The more frequent development of stomach cancer against the background of atrophic gastritis gave M. Kekki grounds to believe that there is a genetic connection between them. Follow-up studies show that patients with atrophic gastritis die earlier, and this does not depend on age, and, in addition, they are more likely to have extragastric tumors.

When assessing the nature of morphological changes in chronic gastritis, it should be taken into account that with age the degree of damage to the gastric mucosa increases. This depends not only on factors that negatively affect the gastric mucosa, but also on the natural involution of the highly differentiated glandular apparatus and the development of connective tissue.

So, G. M. Anoshina, studying age characteristics elastic fibers of the gastric mucosa, discovered changes in elastic fibers as the structural and functional maturity of the organ develops. Even in young people, dystrophic changes in individual fibers appear, which increase in depth and prevalence in old age. These changes can probably serve as a morphological basis functional disorders gastric mucosa. An increase in the frequency of atrophic forms of gastritis with age is noted by many authors

Nevertheless, the “age factor” does not apparently play a dominant role in the development of morphological changes in the mucous membrane. Thus, most of the above-mentioned authors found that in all age groups, in 1/3 of cases, the epithelial elements of the stomach remained unaffected.

When studying the gastric mucosa obtained by gastrobiopsy in children with pathologies of the digestive organs, minor changes such as superficial gastritis are usually detected. At the same time, in adolescents and young people, morphological examination reveals atrophic changes in the gastric mucosa, which P.I. Shilov does not classify as an atrophic variant of chronic gastritis.

There is no consensus among researchers regarding the hypertrophic form of chronic gastritis. A number of scientists deny the presence of this form of stomach pathology, considering hypertrophic gastritis to be a manifestation of functional disorders; according to others, the term “hypertrophic gastritis” has citizenship rights only if it is understood as thickening of the gastric mucosa without destruction of the glandular apparatus.

The opposite point of view is shared by T. Tashev and N. I. Putilin. These authors noted thickening of the folds of the mucous membrane during fluoroscopy and gastroscopy, as well as hyperplasia of the mucous membrane with the inclusion of all glandular elements: accessory, main and parietal cells. S. Stempien in these cases uses the term “hypertrophic, hypersecretory gastropathy,” which, in their opinion, can exist as an independent nosological unit or be concomitant with ulcerative endocrinopathy, Zollinger-Ellison syndrome, etc.

Studying pathological material, R. Schindler described in detail various forms of chronic hypertrophic gastritis, including: 1) interstitial gastritis, in which thickening of the mucous membrane depends on its intermediate cellular infiltration; 2) proliferative gastritis with pronounced proliferation of the surface epithelium, but intact glandular apparatus; 3) glandular gastritis, characterized by extensive hyperplasia of the glandular apparatus. The last form of gastritis, according to the author, is common.

Other forms of hyperplasia with hypertrophy of the mucous membrane are given by K. Ottenjann and K. Elster: 1) hyperplasia of the surface epithelium (foveolar hyperplasia); 2) hyperplasia of specific glandular cells (parietal, chief, G-cells, etc.); 3) hyperplasia of lymphoid tissue.

As the authors emphasize, the causes of mucosal hyperplasia are not yet known. They cite Menetrier's disease as an example of foveal hyperplasia, and glandular hyperplasia - the morphological picture of the mucous membrane with a recurrent ulcer. In these cases, the authors also use the term “hypersecretory gastropathy.” With diffuse lymphatic hyperplasia, differentiation from malignant lymphoma is necessary.

Thus, views regarding various aspects of the morphological restructuring of the gastric mucosa in chronic gastritis are very contradictory.

In a histological and histochemical study of the mucous membrane of the body of the stomach, obtained specifically during an endoscopic examination in adolescents with chronic gastritis, we found its normal structure in 26.7% of cases. Only 8.1% of patients showed slight stromal edema in the superficial layers of the mucous membrane, increased infiltration of predominantly plasma and lymphoid cells with a small number of neutrophil granulocytes. In the antrum of most of these patients there was a pronounced chronic process, manifested by an increase in infiltration mainly by plasma cells and lymphocytes, stromal edema, replacement of glands with lymphoid tissue, erosions were sometimes observed.

The surface epithelium was either dystrophically changed, flattened, infiltrated with lymphocytes and leukocytes, weakly separated mucus, or, conversely, formed growths such as micropolyps.

Hyperplasia of parietal cells was noted in 10.5% of cases, occupying part of the pit epithelial layer, 2/3 of the glands and being localized even in the basal part of the glands. In this case, pronounced hypersecretion was observed.

In 8.1% of patients, hyperplasia of parietal cells was not observed, but there were signs of their functional tension: vacuolization, the presence of two nuclear cells. The secretion of neutral and acidic mucopolysaccharides in this subgroup of patients was also increased. In a number of cases, we noted cystic enlargement of the glands. A morphological examination of the mucous membrane of the antrum revealed diffuse and atrophic gastritis.

In 11.6% of patients, the glands in the body of the stomach were well developed, but symptoms of acute gastritis were observed (severe swelling of the stroma, alteration of the cellular elements of the glands, sometimes complete destruction of individual glands, massive neutrophilic infiltration of the stroma, up to microabscesses of the pits and glands). The vessels were sharply dilated, endothelial proliferation and perivascular neutrophilic-leukocyte infiltration were noted. In the antrum of these patients, a chronic inflammatory process in the acute stage was detected. The secretion of mucopolysaccharides was reduced. In several cases, adenomatous growths of the surface epithelium were noted.

In 25.6% of patients, the glands in the body of the stomach were also preserved, but phenomena of superficial gastritis were observed. Dystrophy of the cells of the integumentary epithelium was combined with inhibition of mucus formation and increased infiltration of the superficial layers of the mucous membrane due to plasma cells and lymphocytes. In the antrum, all patients had a chronic inflammatory process with a tendency toward atrophy of the pyloric glands and their replacement with smooth muscle and lymphoid tissue. And in this section, adenomatous growths of the surface epithelium were often detected.

In 17.4% of patients, we identified atrophic changes in the glands of the stomach. In 1st degree atrophy, in 11.6% of patients, the mucous membrane was normal, the glands were somewhat shortened and tortuous. Among the parietal cells, atrophic ones were found, in a state of necrobiosis. Visually, there was a decrease in the number of chief cells, the cytoplasm of which was PAS-positive, but not stained with Alcian blue. The surface epithelium is often flattened, and the PAS reaction was weakly positive. The pit epithelium was usually unchanged.

With atrophy of the 2nd degree (5.8%), the mucous membrane is thinned, the main glands are preserved in small quantities. The cellular elements of the glands are often atrophic, the parietal cells are vacuolated, the main cells are partially replaced by mucus-forming cells, acidic mucopolysaccharides were not detected. The surface epithelium was flattened, the gastric pits were deep and convoluted. In this case, stromal edema was observed with excessive infiltration of plasma cells, lymphocytes, and in some cases with a small number of neutrophilic leukocytes. Pseudopyloric glands were often located in groups in the gastric mucosa. A similar process was observed in the antrum of these patients. Some patients had microerosions in this section.

Erosions (10.5%) had different stages of development: acute, in the healing period, or already epithelialized. The nature and intensity of infiltration depended on the stage of the erosive process. Typically, the infiltration consisted of neutrophilic leukocytes. The surface epithelium was flattened only at the edges of the defect, and neutral mucopolysaccharides were detected in small quantities in the apical part of the cells. The fundic glands were mucused, and at a short distance from the erosion they were of normal structure. With deep tissue destruction, one could observe the destruction of part of the glands with necrosis of cellular elements and pronounced predominantly leukocyte infiltration, covering a fairly large area of ​​tissue. Among the cellular elements of the glands, the number of indifferent mucus-forming cells increased, in contrast to the surface epithelium, which contains a small number of neutral mucopolysaccharides.

In a number of adolescents, the clinical symptoms corresponded to the clinical picture of duodenal ulcer, despite the fact that endoscopic examination did not reveal erosive and ulcerative lesions in the stomach and duodenum. This group of adolescents also had no history of gastric ulcer, which was the basis for the attending physicians to regard their disease as chronic gastritis. In this regard, we compared data from a histological study of biopsy samples of the mucous membrane of the antrum, body of the stomach and duodenal bulb.

At the same time, the histological picture of the mucous membrane of the bulb was normal in 15.8% of adolescents, except that in 10.5% of patients there was slight swelling in the subepithelial layer, as well as increased infiltration of lymphocytes and plasma cells. In the antrum of the same patients, 5.3% had normal mucous membrane, and in the rest it corresponded to the picture of superficial and diffuse chronic gastritis. The morphological picture of superficial duodenitis, noted in 63.2% of adolescents, coincided with superficial gastritis of the antrum in 21% of patients, while the rest had a diffuse (36.8%) and atrophic (5.3%) process. Diffuse bulbitis was detected only in 21% of adolescents and was combined with chronic diffuse gastritis of the gastric outlet. In a morphological study of the mucous membrane of the body of the stomach, superficial gastritis was found in 42.1%, and hyperplasia of the parietal cells of the stomach - in 21% of adolescents. In 36.8% of patients, the structure of the mucous membrane was normal.

Thus, a comparison of the results of a histological study of the gastric mucosa and duodenal bulb made it possible to identify the morphological picture of gastroduodenitis in the majority of adolescents. Since this issue requires special consideration, we will return to it a little later.

Our studies have shown that the morphological changes in the mucous membrane of the body and the antrum of the stomach are quite diverse. First of all, attention is drawn to the preservation and normal structure of the glandular apparatus of the stomach in the overwhelming majority of adolescents (82.6%). True gastritis (a pronounced inflammatory process in the mucous membrane) was much less common than atrophic changes in the glands of the body of the stomach. In the antrum, diffuse and atrophic gastritis is observed in 89.5% of cases. Significant differences were noted in the morphological picture of the antrum and body of the stomach when compared with the data of a morphological study of the mucous membrane of the duodenal bulb. It was noteworthy that superficial bulbitis was more often combined with gastritis of the antrum of the stomach, but chronic gastritis was rarely detected in the mucous membrane of the stomach body. Although microerosions occurred in only 10.5% of adolescents, however, given the small piece of mucous membrane taken during biopsy, one can think of a greater frequency of this pathology in adolescents.

In a number of cases, despite the fact that endoscopic examination of the stomach showed a picture of superficial gastritis, light-optical examination of biopsy samples of the gastric mucosa did not reveal characteristic morphological signs of chronic gastritis.

To identify possible ultrastructural disorders, these patients were examined using electron microscopy. At the same time, cells were found with preserved microvilli on the apical surface, along with a reduction of microvilli and smoothing of the cytolemma of the free pole of the cells. The number of secretory granules in some cells was significantly reduced. The structural features of the surface epithelium included the expansion of intercellular spaces. In individual cells, processes of vacuolization and expansion of the tubules of the cytoplasmic reticulum were observed, both in the apical part of the cells and in the perinuclear zone and in the basal part of the cells. Hyperplasia of the lamellar complex and destruction of mitochondria were also revealed. In addition, migration of lymphocytes along expanded intercellular spaces through a layer of epithelial cells and infiltration by neutrophilic leukocytes were noted.

The cellular elements of the glands of the mucous membrane of the antrum and body of the stomach were not changed.

Interpretation of ultrastructural changes in the surface epithelium in the absence of disturbances in the main and parietal cells presents certain difficulties. Taking into account the rapid turnover of the epithelial layer of the stomach, the listed ultrastructural changes can also be interpreted as a result of involutive changes that occur in a cell completing its life cycle. However, the presence of similar changes in the mucous membrane in a number of patients who have a morphological picture of superficial gastritis during a light-optical study of biopsy specimens, as well as clinical symptoms, does not allow us to categorically reject the pathology in these cases. Probably, the study of the ultrastructure of the mucous membrane can provide significant assistance in studying the dynamics of chronic gastritis in adolescents, especially in the absence of sufficient morphological data for this disease.

Thus, in the morphogenesis of chronic gastritis in adolescents, in addition to dystrophy and disruption of the physiological regeneration of glands, true inflammatory processes in the mucous membrane are also of certain importance. Signs of inflammation of the mucous membrane in chronic gastritis have been noted by other authors. This is reflected in the endoscopic picture of the gastric mucosa (severe swelling, hyperemia, thickening of the folds). The clinical picture of the disease is more vivid, but in no way resembles duodenal ulcer. The decrease in acid production in the overwhelming majority of these patients may be associated with both an alteration of the main glands of the stomach and a violation of microcirculation. The latter is characterized by expansion and congestion of arterial and venous vessels with the phenomena of perivascular edema (indicating a violation of vascular permeability), with the formation of serous exudate, compressing the glands and leading to their dysfunction.

Atrophic gastritis was detected in 17.4% of adolescents. The data obtained coincide with the results of our previous studies of the gastric mucosa in patients with chronic gastritis, obtained by aspiration gastrobiopsy. This coincidence is hardly accidental and serves as proof of the true prevalence of atrophic changes at this age. It should also be noted that there is a pronounced parallelism between the data of endoscopic, functional and morphological studies of the stomach in patients with grade 2 mucosal atrophy.

Infiltration of the stroma of the gastric mucosa tended to intensify with the deepening of the atrophic process. In this case, infiltration of lymphoid and plasma cells with a small number of eosinophils predominated. Does such infiltration serve as an indisputable sign of an inflammatory process? As I.V. Davydovsky points out, such “large cell” infiltrates can be observed outside of any inflammation. They often witness metabolic processes associated, for example, with a violation of the secretion of mucous membranes, and in the presence of a significant number of plasma cells are characteristic of autoimmune processes. Other authors also point to the possibility of an immune mechanism in the development of chronic atrophic gastritis.

Literature data show that with type A gastritis (immune gastritis), which occurs in B-deficiency anemia, as a rule, there are circulating antibodies to the parietal (lining) cells of the gastric mucosa and a high level of gastrin in the blood. While with type B gastritis (as a result of impaired regeneration and differentiation of the epithelium), this is not observed. If the first type of gastritis occurs in 5% of the population, then the second - in 20%.

Atrophic gastritis is observed mainly in female adolescents who have suffered from viral hepatitis, dysentery, lamblia cholecystitis, and suffering from biliary dyskinesia. This once again confirms the well-known functional-morphological connection of the digestive organs.

It is also possible to note a tendency towards an increase in the duration of the disease in adolescents with chronic atrophic gastritis, although direct parallelism has not been identified. It is convincingly shown not only the absence of a characteristic clinical picture in atrophic gastritis, but also the discrepancy in a number of cases between clinical symptoms and the severity of the atrophically changed gastric mucosa. In this regard, the question posed by V.P. Salupere is logical: is atrophic gastritis a disease if in most cases it does not cause any distress to the patient, and the patient and the doctor are not aware of it without special research? The author answers this question in the affirmative, believing that from the point of view of the development of stomach cancer, the presence or absence of complaints in a patient with gastritis does not matter. It is difficult for us to agree with this approach to this problem and here’s why. First of all, it is impossible to approach this issue unambiguously: whether or not a given individual has atrophic changes in the stomach, assessing them immediately as a pathology and, thus, absolutizing morphological findings. In our opinion, this issue must be resolved dialectically in each specific case. In this regard, we are very impressed by the point of view of I.V. Davydovsky, who wrote: “Under physiological conditions, atrophy is observed already during the development of the individual, starting from the first months of intrauterine life, especially during the aging period of the organism. Atrophy acquires the features of a pathological phenomenon if it is not completed somewhere or if such completion occurs in a time frame that does not correspond to the normal development of the individual.” At the same time, the author emphasized great importance biological factors, namely: species and hereditary. From these positions, the assessment of atrophic changes in the gastric mucosa in a teenager and in an elderly individual cannot be assessed equally. In the first case, atrophic changes should undoubtedly be assessed as a pathology, and in the second it can be involutional, coinciding with the period of aging. The data of L. I. Aruin and V. G. Sharov, based on electron microscopic examination of the gastric mucosa obtained by biopsy, also indicate signs of involution in the main glands of the stomach with atrophic gastritis. These data allowed them to come to the conclusion that the morphogenesis of chronic gastritis is based on a violation of the physiological regeneration of the glandular epithelium. By the way, V.P. Salupere himself points out that gastritis in people under 40 years of age is precisely the form (case) of the disease, the study of which expands the possibilities of discovering the patterns of development of this disease.

The frequency of atrophic gastritis does not correspond to the frequency of gastric cancer, and at present we cannot say which forms of gastritis can be considered an obligate precancerous condition. However, long dynamic observations for patients with atrophic gastritis can detect early gastric cancer.

The results of our studies showed that the pyloric antrum is involved in the gastric process much more often (81%) than the body of the stomach. In this respect, our findings are consistent with those obtained in adults.

Many authors make the development of the gastric process in the antrum of the stomach dependent on the presence of duodenogastric reflux. The question of the significance of duodenogastric reflux in the genesis of not only chronic gastritis, but also gastric ulcers, as well as the corresponding nature of clinical symptoms, is very complex and has not been fully clarified.

Duodenogastric reflux can occur in the absence of any symptoms of macroscopic and morphological changes in the gastric mucosa. In this respect, our results are consistent with data obtained in adults. It is believed that duodenogastric reflux most often occurs with stomach and duodenal ulcers, cholelithiasis, as well as after operations on the stomach and bile ducts. Duodenogastric reflux plays an important role in the pathogenesis of stress erosive and ulcerative lesions of the stomach. Animal experiments have shown that duodenal contents increase cellular infiltration in the gastric mucosa, reduce the number of parietal cells and lead to changes in the glands. Wherein acidic environment in the stomach increases the damaging effect of bile acids. According to our data, duodenogastric reflux in adolescents is observed more often with increased acid-forming function of the stomach. And if we take the point of view of G. Eastwood, then we should expect more pronounced morphological changes in the mucous membrane in this category of adolescents than in cases where there is no duodenogastric reflux. However, the results of our research do not support the above point of view.

Observations by S. Niemela showed that nausea and abdominal pain after eating are more common in patients with duodenogastric reflux than without it. Nausea, heaviness in the epigastrium and flatulence became more frequent as the concentration of bile acids and lysolecithin in the gastric contents increased (the difference is not statistically significant).

According to S. Niemela, in patients with duodenogastric reflux, a normal morphological picture of the mucous membrane of the antrum of the stomach was observed in 23.9% of cases, and in the absence of reflux in 37.3%. Accordingly, in the body of the stomach these ratios were 27.7 and 40%. At the same time, morphological changes in the mucous membrane of the body of the stomach were more pronounced than in the antrum. It is also noteworthy that the severity of duodenogastric reflux does not depend on age.

Thus, the inconsistency of the data obtained indicates the difficulty of assessing duodenogastric reflux both in normal and pathological conditions, so this issue needs further study.

In addition to atrophic changes in the mucous membrane of the antrum, hyperplastic growths of the superficial and pit epithelium are also found in adolescents. It should be noted that focal hyperplasia in the form of outgrowths of at least 0.1 cm in diameter, they are quite clearly detected during endoscopic examination. Hyperplastic growths are more often observed in patients with increased acid-forming function of the stomach. This may serve as a sign of increased regeneration of the surface epithelium at this age, and also play a certain protective role during high acid production. At a certain stage, this process can acquire pathological features, as evidenced by the presence of adenomatous growths and polyps in a number of adolescents. It is noteworthy that adenomatous growths occur against the background of the normal structure of the glands. Such a macroscopic picture can be observed with nodular lymphatic hyperplasia. Histological examination of biopsy specimens reveals more or less closely spaced lymphatic follicles in the mucous membrane, which cause flattening of the epithelium. As the authors point out, more diffuse lymphatic hyperplasia is characterized as pseudolymphoma. In these cases, differential diagnosis with malignant lymphoma is difficult.

Based on the importance of histological and histochemical studies in the diagnosis of chronic gastritis, we analyzed the results from the standpoint of the morphological features of the mucous membrane of the body of the stomach, since in the outlet section of the stomach, as a rule, there was a histological picture of chronic, predominantly diffuse gastritis.

The clinical picture was dominated by the symptom complex characteristic of duodenal ulcer (periodic hunger, night pain mainly in the epigastric region, decreasing after eating or antacids). The most common dyspeptic symptom was heartburn (52.2%).

Hyperplasia of parietal cells and morphological signs of their functional activity, found in 16 adolescents, were reflected in increased acid production in the vast majority of patients (81.3%). Clinically, 68.8% of patients had symptoms characteristic of duodenal ulcer.

In both subgroups, the majority of patients were adolescent males. Here is a clinical example.

Patient L., 16 years old, was admitted with complaints of pain in the epigastric region, often on an empty stomach. The pain is aching, without irradiation, short-lived, and goes away after eating. Notes heartburn after eating, constipation. Ill for 2 years. At the beginning of the disease, the pain occurred immediately after eating; in the last six months, the pain pain syndrome changed: hungry, night pain appeared, quite intense, which subsided after eating. He studies at school, eats irregularly (except for the last 2 months) (2-3 times a day), does not follow a diet. The mother suffers from chronic gastritis. Objectively: upon palpation, the abdomen is painful in the epigastrium and pyloroduodenal area.

X-ray of the stomach and duodenum: symptoms of gastritis. Esophagogastroduodenoscopy: the esophagus and cardia are not changed. There is a significant amount of fluid in the stomach mixed with bile. The mucous membrane of the body of the stomach is pink and shiny. Folds of the mucous membrane with a diameter of up to 0.8 cm, are tortuous, can be traced to the exit section, and are well straightened with air. The mucous membrane of the outlet section is pale pink; there are areas of hyperplasia, such as “millet grains,” which remain unchanged when air is insufflated into the stomach. Peristalsis along the outlet section is rhythmic and shallow. The pylorus is open, the mucous membrane of the bulb and duodenum is without features. There is reflux of intestinal contents mixed with bile.

Conclusion: follicular hyperplasia of the mucous membrane of the antrum of the stomach, duodenal dyskinesia.

Analysis of gastric contents: amount on an empty stomach - 110 ml, after stimulation - 135 ml. Basal acid production - 5.8 mmol/l, serial - 10.4 mmol/l.

Morphological study. Body of the stomach: the surface epithelium is normal, mucus formation is normal, the main glands are well developed, there are a large number of parietal and mucus-forming cells among the cells, stromal infiltration is normal. In the antrum: the main glands are normally developed and have a normal cellular composition. The basal part of the mucous membrane and the submucosal layer are fibrously changed, infiltrated with lympholeukocytes and macrophages. In the submucosal layer there are vasculitis.

Conclusion: Antral gastritis and hyperplasia of parietal cells in the main glands of the gastric body.

Duodenal bulb: duodenal (Brunner's) glands are well developed. The villi are short and full-blooded. The surface epithelium is somewhat flattened. In the stroma there is swelling and cellular infiltration with lymphocytes, plasma cells and a small number of leukocytes, especially a lot of eosinophils. Mucus production of goblet cells is suppressed.

Conclusion: chronic duodenitis in the acute stage.

An ulcer-like clinic was also observed in 54.5% of patients with a morphological picture of superficial gastritis against the background of unchanged main gastric glands. Increased acidity levels in these cases were observed less frequently than in other morphologically distinguished subgroups. The morphological picture of superficial gastritis in 63.6% of cases corresponded to the endoscopic picture, and in 27.3% the endoscopic picture of the gastric mucosa was normal. The number of male and female adolescents in this subgroup was approximately equal.

Atrophic changes in the gastric mucosa in 15 adolescents were endoscopically confirmed in 73.3% of patients, and acid production in the majority was reduced both in the basal and sequential phases of secretion. The clinical picture in patients of this subgroup was more typical of chronic cholecystitis and biliary dyskinesia. Among the patients, 73.3% were female adolescents. The duration of their disease was longer than in other subgroups. The following observation can serve as an illustration of this subgroup.

Patient T., 16 years old, was admitted to the department with complaints of aching pain in the epigastric region without irradiation, mainly after eating. Deterioration of health is noted in the spring-autumn period (nausea in the morning, unstable stool, heaviness in the epigastric region). I've been sick for about 3 years. Doesn't follow diet or diet. The mother suffers from chronic gastritis. Objectively: upon palpation, the abdomen is painful in the epigastrium, more so on the right.

X-ray of the stomach and duodenum: symptoms of gastritis. Esophagogastroduodenoscopy: there is little fluid in the stomach, the mucous membrane is swollen, hyperemic, the folds are well straightened with air, the mucous membrane of the outlet section is pale pink with areas of follicular hyperplasia. The pylorus is open, the mucous membrane of the bulb is slightly hyperemic.

Conclusion: superficial gastritis with hyperplasia of the antral mucosa. Superficial bulbitis.

Analysis of gastric contents: amount on an empty stomach - 8 ml, after stimulation - 55 ml; basal acid production - 0.87 mmol/l, serial - 2.4 mmol/l.

Morphological study. Body of stomach: chronic erosive gastritis with atrophy of the glands of the 1st-2nd degree. Antrum: chronic atrophic-hyperplastic gastritis. Duodenum: slight catarrhal irritation in the mucous membrane.

Very interesting, in our opinion, was the subgroup with the morphological picture of acute gastritis described above.

In these cases, endoscopic diagnosis coincided with histological data, since there was pronounced hyperemia of the mucous membrane, swelling, thickening of folds with mucus deposits. Acid production in the majority of patients (60%) was reduced. In this connection, we believe that parietal cells, being in a state of severe depression, cannot respond to their stimulation. The clinical picture in these patients was quite clear. The pain occurred immediately after eating and was quite intense. Taking antacids did not give the corresponding effect. Dyspeptic symptoms included discomfort after eating, belching of air, nausea, and vomiting.

In a number of adolescents, pain was most often localized in the right hypochondrium and was constant, aching and of low intensity. Often patients noted heaviness in the epigastrium, more on the right. Paroxysmal pain was observed much less frequently.

As a rule, adolescents associated the occurrence of pain in the right hypochondrium with errors in eating (fatty, fried foods), and less often with psycho-emotional stress. In addition, quite often teenagers complained of a feeling of bitterness in the mouth. Upon palpation and percussion of the abdomen, they revealed positive symptoms of Kehr, Mendel, and Ortner. These symptoms were not always combined with pain in the right hypochondrium and at the same time were noted in the clinical picture of duodenal ulcer.

Numerous literature data show that chronic gastritis in a significant percentage of cases is complicated by concomitant disorders of the motor function of the biliary tract and inflammatory processes in them. In this regard, we performed an ultrasound examination on 53 adolescents. Since an isolated examination of the gallbladder would lead to an incomplete examination, all organs of the upper abdomen (liver, biliary system, pancreas, spleen, stomach, blood vessels, retroperitoneal space) were examined using ultrasound in all adolescents.

The study revealed the following changes: deformation of the gallbladder in 2 (3.8%), compaction in 20 (37.7%) and thickening of its wall in 1 (1.9%), kinks in 2 (3.8%) and constrictions in the gallbladder cavity in 9 (17%), inhomogeneity of the cavity in 4 (7.5%) adolescents.

The listed changes on the echogram indicated previous or existing inflammatory processes. Naturally, in some cases, congenital anatomical changes in the gallbladder (kinks, constrictions) are possible among them, which can be a prerequisite for functional and inflammatory disorders.

In 16.3% of adolescents, local pain was detected under the sensor in the area of ​​​​the gallbladder projection. After taking a cholecystokinetic breakfast, hypomotor dyskinesia of the gallbladder was noted in 11 (20.7%) adolescents, hypermotor dyskinesia in 17 (32.1%), and normotension in 25 (47.2%). It must be said that, despite a significant percentage of changes in the gallbladder and disorders of its motility detected during ultrasound examination, only in 35.9% of these patients the characteristic clinical symptoms gave reason to think about pathology of the biliary tract.

Biliary dyskinesia can also be detected by X-ray examination (cholecystography). However, the absence of any radiological signs characteristic of chronic noncalculous cholecystitis, as well as a certain risk of radiation, reduces diagnostic value this research method in adolescents.

The method of chromatic duodenal intubation can provide significant assistance in diagnosing diseases of the biliary tract in adolescents (especially non-calculous cholecystitis).

Although consideration of various aspects of biliary tract pathology is not included in our tasks, with all of the above we would like to once again draw the attention of the adolescent doctor to the need for a thorough differential diagnosis diseases of the digestive system in adolescents. Moreover, as our observations show, combined diseases of the digestive system in adolescents are not uncommon.

Thus, a comparison of the data obtained makes it possible to identify certain clinical variants of the course of the disease in adolescents with chronic gastritis, with their characteristic morphological, endoscopic and functional features of the gastric mucosa. Along with this, in almost every subgroup there were patients whose clinical picture of the disease was difficult to attribute to one or another variant. In addition, differences in the frequency and severity of pain and dyspeptic syndrome were probably determined by the individual characteristics of the body.

As our studies have shown, the correspondence of morphological, endoscopic and functional examination of the stomach is not always observed. The agreement between the results of morphological and endoscopic examination reaches 56-67%, and with the morphological picture of acute gastritis endoscopically in 100%, pronounced superficial gastritis is revealed. Therefore, the endoscopic research method, assessing superficial changes in the mucous membrane various departments stomach, largely reflects the essence of the processes occurring in the deeper layers of the mucous membrane. How to evaluate in some cases the absence of morphological changes in the mucous membrane with an endoscopic picture of superficial gastritis? This is largely due to the non-physiological nature of endoscopic examination and the reaction of the vascular apparatus of the gastric mucosa. There is no doubt that the presence of focal processes in the mucous membrane (intestinal metaplasia, atrophy, the nature of infiltration, as well as hyperplasia of glandular cells, etc.) goes beyond the diagnostic capabilities of the endoscopic method. A comparison of secretory and acid-forming functions with data from a morphological study of the gastric mucosa shows that in adolescents in the early stages of development, chronic gastritis is focal. This is convincingly evidenced by data on acid production, which is often normal or even increased during atrophic changes in the gastric mucosa. In turn, the lack of parallelism between the data of functional and morphological studies of the stomach indicates the complexity of neurohumoral hormonal regulation secretory function of the stomach, which is difficult to take into account.

Based on the above, we came to the following conclusions:

1. Diagnosis chronic gastritis» brings together adolescents with various clinical symptoms, data from functional, endoscopic and morphological studies. Chronic gastritis is diagnosed in them only on the basis of X-ray and endoscopic findings and pronounced focal lesions of the upper digestive tract.

2. The presence in a number of patients of clinical symptoms characteristic of duodenal ulcer, normal and often high acid-forming gastric production, the absence of morphological changes in the mucous membrane of the body of the stomach during histological and endoscopic examination excludes the eligibility of the diagnosis of chronic gastritis.

3. Chronic gastritis does not have a characteristic clinical picture. It is often caused by a concomitant disease (chronic cholecystitis, dysentery, etc.).

4. In some cases, the discrepancy between the data of morphological, endoscopic and functional studies of the stomach in the examined adolescents is associated with the different capabilities of the above methods for diagnosing chronic gastritis.

5. Endoscopic and morphological methods of studying the stomach significantly complement each other. Using the first method, they obtain a general picture of the mucous membrane, exclude or confirm the presence of focal lesions (polyps, ulcers, erosions, etc.), their nature, specify the location of the biopsy, and to a certain extent assess the functional state of the stomach (detection of mucus, fluid, thickness of folds, severity of peristalsis, etc.). In turn, the morphological study of biopsy material allows us to specify the features of the process in a particular endoscopic picture of the mucous membrane, to find out its direction, which is of great importance for understanding the essence and predicting the possible outcomes of this process. In addition, it allows further work to more accurately interpret endoscopic changes in the gastric mucosa. In this connection, the need for a biopsy of the mucous membrane may be limited to cases that require clarification of the nature of its lesion, especially if the data from clinical, functional and endoscopic studies do not correspond.

6. Diagnosis of chronic gastritis should be based on a comprehensive assessment of clinical symptoms, functional studies stomach, as well as endoscopic and, if necessary, morphological study of its mucous membrane.

Articles about gastritis:

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 in 37% of patients the origin of the disease was traumatic, 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. All soft tissues of this area are affected - skin, mucous membrane, subcutaneous fat and muscle tissue, often several fascia with inclusion of lymph nodes in the infiltrate. That is why we prefer the term “inflammatory infiltrate” over the term “cellulite,” which also refers to such lesions. The infiltrate can resolve into purulent forms of inflammation - abscesses and phlegmons, and in these cases it should be considered as a prestage of purulent inflammation, which could not be stopped.

Inflammatory infiltrates may have a traumatic origin. They are localized in almost all anatomical parts of the maxillofacial region, somewhat more often in the buccal and area of ​​the 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 subfebrile body temperature, relatively clear contours of the infiltrate, the absence of signs of purulent tissue melting and severe pain on palpation. Other, less pronounced, distinctive signs are: the absence of significant intoxication, moderate hyperemia of the skin without revealing tense and shiny skin. Thus, the inflammatory infiltrate can be characterized by a predominance of the proliferative phase of 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, the increase in symptoms of acute inflammation determines the prognosis of the process. 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 surgical treatment is performed.

Which doctors should you contact if you have Inflammatory infiltrate?

Infectious disease specialist

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In recent years, due to the active implementation in clinical practice endoscopy, in the diagnosis of diseases occurring with diarrhea syndrome, methods of morphological examination of biopsy samples of the intestinal mucosa have become widespread, allowing not only to confirm a preliminary clinical diagnosis, but also to evaluate the dynamics of the process, the nature of the course of the disease, and the effectiveness of the treatment. Using electron microscopy, histochemical, immunoluminescent, enzymological and other modern methods research, a morphologist can help in diagnosing the most subtle, initial changes, when specific clinical manifestations may still be missing.

The accuracy of morphological diagnosis largely depends on the technique of taking a biopsy. The biopsy specimen should be as little traumatized as possible, without coagulation damage. It is necessary that the material sent for research be absolutely informative, sufficient in the number of pieces and their sizes. Small-sized biopsies do not always provide an idea of ​​changes in the entire surface of the mucous membrane of the small or large intestine and can cause false negative results. For diffuse lesions (for example, common forms of ulcerative colitis), biopsies should be multiple, taken from different parts of the intestine.

Research methods.

Biopsies obtained during endoscopic examination are examined primarily using light microscopy. In this case, histological methods of staining the material are usually used to obtain an overview picture. To assess the secretory function of the intestinal epithelium, histochemical methods are used to identify neutral (CHIK reaction) and acidic (Alcian blue staining) glycosaminoglycans. Material from tumors and polyps is stained with picrofuchsin according to van Gieson to detect connective tissue stroma. In some cases, Sudan III or IV staining is used to identify lipids. To study regenerative processes in intestinal epithelium use the Feulgen reaction (for DNA) or staining with gallocyanin and alum chromate (for DNA and RNA).

Can help diagnose some diseases histoenzyme-chemical methods, allowing to identify certain enzymes and determine their activity. For example, in celiac disease, a deficiency of specific peptidases is found that ensures the deamination of gliadin in the intestine.

Indicative in this case is the study of biopsy samples taken before and after a gluten-free diet.

Electron microscopic examination allows us to monitor at the ultrastructural level the most subtle changes that develop in various diseases.

By using morphometric methods you can obtain objective information about the condition of the intestinal mucosa, calculate the height and number of villi, the depth and number of crypts, the content of bordered epithelial cells and goblet cells, interepithelial lymphocytes, assess the thickness of the mucous membrane, infiltrate cells in the stroma, etc.

Histoautoradiography makes it possible to visually assess the varying degrees of intensity of biochemical processes in the cells of the intestinal mucosa and allows, based on the determination of DNA synthesis, to draw a conclusion about the dynamics of the mitotic cycle.

Immunomorphological methods(in particular, the immunoluminescent method) help to identify the components of immune reactions in tissues (antigen, antibody, complement) and establish the connection of these reactions with the nature of developing morphological changes.

The biopsy obtained by endoscopy, in addition to conventional light microscopy, can be examined using stereoscopic microscopy. This method does not require pre-processing of the material and takes little time. At the same time, the intestinal mucosa retains its light, which makes it possible to evaluate intestinal villi under conditions close to natural. Finally, from a biopsy obtained during endoscopy, an impression smear can be prepared and cytological examination. The advantage of this method is the rapid (same day) receipt of an answer about the nature of the pathological process.

Morphological changes in the intestinal mucosa in various diseases.

At chronic enteritis , arising, for example, as a result of radiation injury, with long-term use of non-steroidal anti-inflammatory drugs, immunodeficiency states, etc., morphological changes develop, characterized by chronic inflammation, disorders of epithelial regeneration, which culminate in atrophy and structural restructuring of the mucous membrane. Therefore, the morphological classification of chronic enteritis is based on the presence or absence of atrophy. There are chronic enteritis without atrophy of the mucous membrane and chronic atrophic enteritis. In turn, chronic enteritis without atrophy of the mucous membrane is divided depending on the depth of pathomorphological changes into superficial and diffuse.

At chronic superficial enteritis the thickness of the mucous membrane of the small intestine, as well as the ratio of the lengths of villi and crypts, do not change. With this form of enteritis, uneven thickness of the villi and club-shaped thickening of their apical sections are noted. Bordered epithelial cells are dystrophic, acquire a cubic shape or become flattened; the nuclei of some cells are pyknotic, their cytoplasm is vacuolated. Some of the cells are desquamated, destruction of the basal membrane of the epithelial lining and exposure of the villous stroma occur. The number of goblet cells is unchanged or may even be increased. The lamina propria of the mucous membrane at the level of the villi is diffusely infiltrated with lymphocytes, plasma cells, and eosinophils.

Histochemical study of border epithelial cells indicates a decrease in oxidoreductases and alkaline phosphatase, a significant decrease or disappearance of neutral and acidic glycosaminoglycans in the area of ​​the “brush” border. Electron microscopy reveals deformation, shortening and irregular arrangement of microvilli, and the absence of a glycocalyx on their surface. These changes serve as a morphological substrate for subsequent disturbances in the processes of digestion and absorption.

At chronic diffuse enteritis further progression of structural changes is noted, which is manifested by an increase in dystrophic and necrobiotic changes in the epithelium and the spread of the process to the entire depth of the mucous membrane of the small intestine. The inflammatory infiltrate from the villous area penetrates between the crypts up to the muscular plate of the mucous membrane and further into the submucosal layer. Along with infiltration in the stroma, vascular congestion, edema, the appearance of thin collagen fibers, and hyperplasia of lymphoid follicles are noted. Often, villi exposed in the apical part are found, as well as adhesions, “arcades” between the enterocytes of nearby villi, which arise as a result of healing of superficial erosions. The number of goblet cells is slightly reduced, their secretion is liquid and contains little mucin.

At chronic atrophic enteritis There are 2 types of damage. In option 1 (hyperregenerative atrophy), atrophic changes affect the villi, which thicken, shorten, and fuse together. The crypts retain their normal length, but over a long period of time they become longer due to hyperplasia. Option 2 (hyporegenerative atrophy) is characterized by significant shortening of both villi and crypts.

In both cases, along with pronounced atrophic changes in the epithelium, diffuse inflammatory infiltration of the stroma and proliferation of connective tissue displacing the crypts are noted. Deep changes in the crypts should be considered typical: their number decreases significantly, resulting in the ratio of villi to crypts being 1:3-1:2 (with the norm being 1:4-5).

The inflammatory infiltrate is usually represented by lymphocytes and plasma cells; during an exacerbation, a predominance of polymorphonuclear leukocytes and eosinophils is observed. Leukopedesis of the epithelium is noted.

A histoautoradiographic study of DNA synthesis showed that in chronic enteritis, epithelial proliferation accelerates and its differentiation is delayed (the second phase of the regenerative process). This is evidenced by the appearance of incompletely differentiated cells on the surface of the villi, the expansion of the generative zone, as well as an increase in the number of DNA-synthesizing cells in this zone.

Morphological changes in all types of enteropathies are the same and are reduced to dystrophic and atrophic processes in the mucous membrane of the small intestine without pronounced exudative reactions. The mucous membrane becomes thinner. In this case, as a rule, a hyperregenerative form of atrophy is possible: the villi are shortened, often deformed, and the crypts are elongated. The number of enterocytes is reduced, the cytoplasm of the surviving cells is vacuolated. In the lamina propria of the mucous membrane there is a moderate infiltration of lymphoplasmacytic elements and eosinophils. There are macrophages with high activity of lysosomal enzymes. Electron microscopic examination of bordered epithelial cells reveals swelling of mitochondria, fragmentation of the endoplasmic reticulum, shortening and reduction in the number of microvilli. In the later stages, total villous atrophy and severe sclerosis of the mucous membrane and submucosal layer develop.

At disaccharidase enteropathy the morphological changes described above are extremely poorly expressed. The diagnosis is made exclusively histo- and biochemically. In this case, a deficiency of enzymes that break down lactose and/or sucrose is detected.

At celiac enteropathy(non-tropical sprue, sprue-celiac disease) morphological changes are represented by various types of damage to the mucous membrane of the small intestine with gliadin (a fraction of gluten - a protein contained in cereals). Microscopically, in addition to hyperregenerative atrophy of the mucous membrane, a significant decrease in the number of goblet cells and a sharp decrease in the RNA content in the bordered epithelial cells are detected. A characteristic feature is also a significant number of interepithelial lymphocytes in the villi of the mucous membrane of the small intestine, as well as an increase in the number of cells synthesizing IgA, IgM, IgG. In some cases of nontropical sprue, a picture of collagenous colitis is detected.

A histoautoradiographic study reveals an increase in the number of cells in the phase of DNA synthesis, indicating increased proliferation of the epithelium, as well as the appearance of incompletely differentiated epithelial cells from the generative zone in the villi. Changes develop predominantly in the proximal part of the small intestine, where, as a result of the digestion and absorption of gluten, gliadin has an adverse effect on the mucous membrane. In biopsy samples, in addition to the changes described above, using histoenzyme-chemical reactions, it is possible to detect an insufficient content of enzymes that break down gliadin.

At intestinal lipodystrophy (Whipple's disease) Rigidity of the walls and segmental expansion of the lumen of the small intestine, thickening of the folds of the mucous membrane, fibrinous deposits on the serous membrane are noted. The mesentery is dense, the mesenteric and sometimes para-aortic lymph nodes are enlarged, they contain an excess amount of chylous fluid, the nodes resemble caseous-like masses.

In histological examination of biopsy samples of the small intestinal mucosa in patients with intestinal lipodystrophy, enterocytes have a normal structure, with a preserved “brush” border. The villi are somewhat thickened and shortened. Lymphatic vessels are sharply dilated and contain protein-lipid masses in the form of lumps, which are stained red with Sudan III. In the lamina propria of the mucous membrane, diffuse infiltration of round or polygonal macrophages with a pale-colored nucleus and foamy cytoplasm containing PAS-positive inclusions is detected. PAS-positive macrophages are also found in the submucosal layer of the small intestine, para-aortic and mesenteric lymph nodes.

Electron microscopic examination reveals bacilli-like bodies about 1-3 µm long, 0.2-0.4 µm thick, with a three-circuit membrane in which the oval vacuole. Some macrophages are destroyed and bacilli-like bodies are found in the intercellular space.

Morphologically, 2 stages of intestinal lipodystrophy can be distinguished: early stage accumulation of protein-lipid substances occurs in the lymph nodes and lymphatic vessels; at a later stage, lipogranulomas develop.

Morphological changes during nonspecific ulcerative colitis depend on the nature of the disease (acute or chronic form).

In the acute form of nonspecific ulcerative colitis, the folds of the mucous membrane are significantly thickened or, conversely, smoothed, sharply swollen, congested, covered with translucent mucus, pus-like deposits or a thin layer of fibrin. Numerous erosions and ulcers are visible in the mucous membrane. The ulcers are located randomly (unlike Crohn's disease), their definite orientation to the lumen of the colon is not observed. Ulcers vary in size, but are often large, irregular shape, with undermined overhanging edges. Even large ulcers usually remain shallow and are localized in the mucous membrane; their bottom, as a rule, is the submucosa. Often, along with typical ulcers, numerous erosions in the form of “wormholes” are visible, while the mucous membrane resembles moth-eaten felt. In the initial stages of the disease, erosions and ulcers may be absent and changes in the mucous membrane of the colon are minimal.

A characteristic sign of the acute form of ulcerative colitis are pseudopolyps. In this case, in the mucous membrane of the colon, along with ulcers, single or multiple protrusions of a stalactite nature ranging in size from several millimeters to several centimeters are found, which often resemble true glandular polyps. These formations are islands of mucous membrane preserved between ulcers (fringed pseudopolyps), or areas of granulation tissue growing at the site of healing ulcers (granulomatous pseudopolyps).

Sometimes the ulcers penetrate deep into the intestinal wall, forming pockets between the submucosal layer and the mucous membrane. In this case, the mucous membrane can be torn away and then the inner surface of the colon looks like a solid ulcer. With deep ulcers and destruction of the muscular lining, the wall of the colon becomes thinner (up to 1 mm or even less), resembling tissue paper, and the lumen of the damaged area of ​​the intestine expands sharply.

Single or multiple microperforations may occur in a thinned intestinal wall.

Histologically in initial stage diseases in the mucous membrane of the colon, inflammatory changes predominate. The infiltrate consists mainly of lymphocytes with an admixture of polynuclear leukocytes, plasma cells, eosinophils and is located in the lamina propria of the mucous membrane, without penetrating into the submucosal layer. Hyperemia of microvessels (mainly venules and capillaries), stromal edema, and moderate hyperplasia of lymphoid follicles are pronounced.

Then polymorphonuclear leukocytes begin to accumulate in the infiltrate, which penetrate through the perivascular space into the thickness of the intestinal wall, through the integumentary epithelium through leukopedesis into the intestinal lumen, and through the epithelium of the crypts into the lumen of the latter. Cryptitis develops, in which obliteration of the distal parts of the intestinal crypts (Lieberkühn's glands) occurs, the number of desquamated epithelium and leukocytes sharply increases, and a crypt abscess is formed. Crypt abscesses open in the fundus, their contents break into the submucosa and an ulcer forms.

At acute form nonspecific ulcerative colitis is characterized by the dominance of destructive processes: when opening single crypt abscesses, numerous small ulcers are formed; the formation of large ulcers occurs when the merged crypt abscesses are opened and inflammation passes from the mucous membrane to the submucosa. At the bottom of the ulcer there are extensive foci of necrosis, intramural hemorrhages, and vessels with signs of fibrinoid necrosis. Fresh and organized blood clots are found in the lumen of many vessels. In some ulcers, the bottom is lined with granulation tissue, diffusely infiltrated with lymphocytes, plasma cells, a small number of neutrophilic leukocytes, and eosinophils. The destructive process may involve the intermuscular nerve plexuses, where in such cases a picture of toxic aganglionosis is revealed.

At chronic form Nonspecific ulcerative colitis in the mucous membrane is dominated by reparative sclerotic processes. Ulcers undergo granulation and scarring, while the colon is grossly deformed, often significantly shortened, its wall thickens due to hypertrophy of the muscular layer, and the lumen narrows unevenly. The mucous membrane of the colon sharply smoothes out, acquiring a whitish appearance. As a result of reparative regeneration of the epithelium around ulcers and scars, numerous granulomatous and adenomatous pseudopolyps are formed, sometimes imitating the picture of diffuse polyposis. Some ulcers scar with the formation of rough, extensive scar areas of irregular shape. Complete epithelization of ulcers, as a rule, does not occur.

Histological examination reveals a picture of chronic productive inflammation in the intestinal wall. The infiltrate contains many plasma cells, no polymorphonuclear leukocytes, and the number of eosinophils varies widely. It is characteristic that lymphoplasmacytic infiltration persists even during a period of long-term remission. In the vessels there is a picture of productive endovasculitis with sclerosis of the walls, narrowing, and sometimes obliteration of the lumen.

Regeneration of epithelium with nonspecific ulcerative colitis turns out to be imperfect, as evidenced not only by pseudopolyps, but also by the nature of the newly formed mucous membrane in the areas of epithelization of ulcers: full-fledged crypts are not formed, goblet cells remain single. In the epithelium of the atrophied mucous membrane, dysplasia of varying degrees of severity is often observed, which can be considered as a risk factor for the subsequent development of colorectal cancer.

Macroscopic changes in the intestine with Crohn's disease usually turn out to be the same type regardless of location. Inflammatory process begins in the submucosal layer and spreads to all layers of the wall. At the site of the lesion, the intestinal wall thickens and becomes dense to the touch; in appearance - depending on the length of the process (from 8-15 cm to 1.5-2 m) - it is figuratively compared to a “hose” or “suitcase handle”. Such areas are especially often found in the jejunum and ileum.

Damage in Crohn's disease is extremely rarely isolated. The process is usually multifocal in nature and spreads like “kangaroo jumping”, when foci of ulceration, which always have clear macro- and microscopic boundaries, alternate with areas of unchanged mucous membrane. This sign can be considered quite typical for Crohn's disease, allowing one to exclude nonspecific ulcerative colitis based on the macroscopic picture.

Appearance ulcers of the intestinal mucosa turn out to be very characteristic: they are long, narrow, with smooth edges, deep, often penetrating to the serous membrane and even into the surrounding tissue. The ulcers are arranged in parallel rows along the axis of the intestine, resembling “rake marks.” At the same time, slit-like ulcers are formed, deep, like knife wounds, oriented in the transverse direction. Islands of edematous mucous membrane, enclosed between intersecting fissure ulcers, resemble a “cobblestone street.”

Slit-like ulcers that penetrate through all layers of the intestinal wall sometimes form intramural abscesses, but more often they contribute to the formation of adhesions and fistulas between the loops of intestines and neighboring organs(urinary and gallbladder, vagina), in some cases external fistulas occur.

Microscopic changes in Crohn's disease are diverse. The most characteristic sign of the disease should be considered the formation of nonspecific granulomas, formed against the background of productive inflammation that develops in all layers of the intestinal wall, and consisting mainly of epithelioid cells, sometimes with giant cells of the Pirogov-Langhans type. Granulomas do not contain foci of caseous necrosis, and tuberculous mycobacteria are never detected in them. These granulomas resemble those in sarcoidosis, but unlike the latter, they are smaller in size, do not have clear boundaries, and the giant cells detected in these granulomas contain fewer nuclei. It should be emphasized that granulomas are detected in Crohn's disease only in half of the cases, and taking into account the often isolated nature of granulomas, research is necessary to detect them large quantity biopsies and preparation of serial sections.