Formation of lymph follicles in the stomach. Lymphoid follicles in the stomach

Lymphoid nodule)

a limited accumulation of lymphoid tissue in which lymphocytes develop; are present in the lymph nodes, tonsils, spleen, mucous membrane of the stomach, intestines, larynx and some other organs.

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. encyclopedic Dictionary medical terms. - M.: Soviet encyclopedia. - 1982-1984.

See what “Lymphatic follicle” is in other dictionaries:

- (folliculus lymphaticus; synonym lymphoid nodule) a limited accumulation of lymphoid tissue in which lymphocytes develop; are present in the lymph nodes, tonsils, spleen, mucous membrane of the stomach, intestines, larynx and some... ... Large medical dictionary

- (Latin folliculus, “sac”) a round, oval or pear-shaped formation in various organs vertebrates and humans, performing various functions. Ovarian follicle (folliculus ovaricus) Hair follicle (follikulus... ... Wikipedia

A; m. [from lat. foliculus sac] Physiol. A vesicle-like formation in animal and human organs that performs various functions (lymphatic nodule, vesicle in which an egg is formed, etc.). * * * follicle (from lat. folliculus ... ... encyclopedic Dictionary

follicle- A; m. (from Latin foliculus pouch); physiol. A vesicle-like formation in the organs of animals and humans, performing various functions (lymphatic nodule, vesicle in which an egg is formed, etc.) ... Dictionary of many expressions

Large medical dictionary

- (nodulus lymphaticus, BNA) see Lymphatic follicle ... Medical encyclopedia

Mesenteric part - small intestine is located in the lower part of the abdominal cavity, its length is 4-6 m, and its diameter is 2-4 cm. The proximal part of the small intestine is called jejunum(jejunum) (Fig. 151, 158, 169, 171), is approximately 2/5 and without visible boundaries... ... Atlas of Human Anatomy

- (nodi lymphatici) peripheral organs immune system, performing the function of biological filters, as well as lymphocytopoiesis and antibody formation. Lymph nodes are soft, elastic to the touch, pinkish colored formations. They have an ovoid... ... Medical encyclopedia

I Esophagus (esophagus) is the section of the digestive tract that connects the pharynx to the stomach. Takes part in the swallowing of food; peristaltic contractions of the muscles of the stomach ensure the movement of food into the stomach. The length of the leg of an adult is 23 30 cm,... ... Medical encyclopedia

TYPHOID FEVER- TYPHOID FEVER. Contents: Etiology......................... 160 Epidemiology.................. 164 Statistics....... ............ 167 Pathological anatomy........ 187 Pathogenesis................... 193 Clinical picture ............... 195 Complications ... Great Medical Encyclopedia

- (pseudofolliculus; pseudo + follicle) a sharply hyperplastic lymphatic follicle in gigantofollicular lymphoma, characterized by the proliferation of light reticular cells in the form of fields surrounded by a lymphoid shaft... Large medical dictionary

lymphoid tissue are viable lymphocytes that persist along the periphery of the explant. In groups of these elements, on the 4-5th day of cultivation, mitoses are detected, and subsequently secondary lymphoid follicles are formed in their place.

In the formation of secondary lymphoid follicles in organ cultures, a special type of connection between reticular cells and lymphocytes can be seen. In many cases, the lymphoid follicle forms around characteristic spherical structures formed by reticular cells.

In birds, B cell differentiation occurs in the bursa of Fabricius, the folds of which contain lymphoid follicles that have a cortical and medullary zone.

Reduction of lymphoid follicles in the marginal zones of the spleen.

The splenic capsule is somewhat wavy, the trabeculae are thickened and hyalinized. The lumens of the central arteries are narrowed, their wall is homogeneous and hyalinized. In some cases, lymphoid follicles are reduced in number and volume; lymphocytes in them are preserved only in the form of a narrow belt around the central arteries. In areas of preserved lymphoid tissue, pycnoform lymphocytes are visible.

The submucosa of the small and large intestines is sharply swollen, loosened, and in most cases infiltrated with cellular elements with a significant number of plasma cells. The same swelling is even more pronounced on the part of the stroma of the villi of the small intestine. Among the edematous tissue of the submucosal membrane of the large intestine, there are perivascular hemorrhages (Fig. 15). Lymphoid follicles of the large intestine were not expressed. The epithelial cover in the superficial areas of individual villi and folds is necrotic, impregnated with fibrin, and the cells are desquamated (Fig. 16). In the deep layers of the lateral

Subacute poisoning. Administration of /5 from LD50 for 1 month causes a lag in body weight gain, depression of the central nervous system, anemia and an increase in the content of methemoglobin in the blood. Histologically - parenchymal degeneration in the liver, hyperplasia of lymphoid follicles in the spleen.

In some rats killed at various times after the onset of dusting, a few loose or more compact nodular accumulations of macrophages were found in the lungs, located in the lumens of the alveoli, in the interalveolar septa and in the perivascular and peribronchial lymphoid follicles. The protoplasm of macrophages sometimes looked cellular, was palely stained with eosin, and had a grayish tint. The nuclei in these cells were often absent. Sometimes small gray specks of dust could be seen in the protoplasm of lscrophages. In animals covered with dust as if during

In most experimental rats killed after 2 and 5 months. after the administration of polyvinyl butyral, in the lungs, against the background of emphysema and congestion, individual macrophages were visible, scattered in the lumens of the alveoli between the cells of the peribronchial and perivascular lymphoid follicles. The protoplasm of some macrophages contained phagocytosed small black dust particles.

The described compact accumulations of macrophages in the lung tissue and in the peribronchial and perivascular lymphoid follicles were found mainly in experimental rats

In surviving rats killed after 1 3 b and 9 months. after the administration of substances, pinpoint or larger blue spots, up to 2-3 mm in diameter, were noted in the lungs under the pleura and on the incision. The bifurcation lymph nodes were slightly enlarged and colored blue. Under the pleura, in the lumens of the alveoli, in the interalveolar septa and in the lymphoid follicles, a blue substance was found, located in the protoplasm of macrophages or lying freely (Fig. 5). In addition, in rats killed after 6 and 9 months. after intratracheal administration of fat-soluble pure blue anthraquinone b/m, individual accumulations of the substance located in the interalveolar septa were surrounded by a small number of elongated connective tissue cells. No changes were found in the remaining internal organs following the administration of the substances.

Peribronchial lymphoid follicles are noticeably enlarged, and a proliferation of reticular cells is observed in their peripheral parts. Here you can see dilated lymphatic vessels with a picture of lymphostasis. On the part of the bronchial epithelium, there are phenomena of a proliferative-destructive nature.

Starting from the 5-6th day of cultivation, regeneration of lymphoid tissue occurs in the cortical region of the explants. As with the explantation of lymph nodes, Tai and with the cultivation of the thymus, regeneration occurs in the form of the formation of lymphoid follicles, often having characteristic cleared centers. Such a structure is characteristic of lymph nodes, but is not found in the intact thymus in vivo, which reflects the different immunological roles of these organs. It is known that antigens do not penetrate into the thymus and differentiation of antibody-forming cells does not occur in it. At the same time, when an antigen is directly introduced into the thymus, secondary follicles are formed in it and plasma cells appear

Morphologically, immunized cultures did not differ from non-immunized ones. As usual, in the first 4 days, most of the lymphoid tissue was destroyed and the stroma was preserved. This was followed by regeneration with the formation of lymphoid follicles in the cortex. The medulla recovered poorly, and plasma cells were observed as rarely in immunized cultures as in nonimmunized ones.

The huge population of lymphocytes in the body can be divided into sedentary and wandering lymphoid cells. Most lymphocytes circulate in the body through the blood and lymph. At the same time, a significant number of lymphoid cells are localized in organs, being a component of the lymph nodes, spleen, Peyer's patches, and non-encapsulated lymphoid follicles (in the loose connective tissue of the mucous membranes and skin). The division of many lymphocytes into sedentary and wandering is not absolute. There is constant redistribution between these two populations.

The white pulp is composed of periarteriolar lymphoid muffs (PALM), many of which contain lymphoid follicles. It is surrounded by a marginal zone filled with numerous macrophages, antigen-presenting cells, slowly recirculating B lymphocytes, and normal killer cells. The red pulp contains venous canals (sinusoids), separated by splenic cords. Blood enters the splenic tissue through trabecular arteries, which give rise to branched central arterioles. Some of these arterioles end in the white pulp and feed the reproductive centers and the marginal zone of the follicle, but the majority reach the marginal zone or areas adjacent to it. Some branches of the arterioles enter directly into the red pulp, ending in the splenic cords. From the venous sinusoids, blood collects into the pulpal veins, then into the trabecular veins and from them into the splenic vein.

Histological structure of the lymph node. The cortical (C), paracortical (P) and medullary (M) regions are visible. The section is stained to reveal the localization of T cells. Most of them are in the paracortical region and a certain amount is present in the reproduction center (CR) of the secondary lymphoid follicle, in the cortical region and medullary cords (MT). (Photo courtesy of Dr. A. Stevens and Prof. J. Lowe.)

Single lymphoid follicle in the colon. This nodule of lymphoid tissue is located in the mucosa and submucosa of the intestinal wall (arrow). (Photo courtesy of Dr. A. Stevens and Prof. J. Lowe.)

A dome-shaped projection formed by the intestinal mucosa, in an area devoid of villi. The surface epithelium in this area, called follicle-associated epithelium (EAE), contains M cells. In depth

Hyperplasia is a process of pathological cell proliferation. Lymphofollicular hyperplasia is an increase in follicular tissue of the mucous/submucosal layer. The disease occurs in patients of all age categories, regardless of gender, food preferences and regardless of place of residence.

Lymphofollicular hyperplasia is diagnosed in the endocrine sphere, but most often affects the digestive system. What causes the predominance of pathology in the gastrointestinal tract? Of course, the number of predisposing factors - disease digestive system in the chronic stage, consumption of a large number of carcinogens, level of stress. Hyperplastic changes in endocrine organs are detected against the background of endocrine or systemic disorders. For example, lymphofollicular damage to the thymus gland is observed with existing pathology of the pituitary gland.

, , , , , , , , ,

ICD-10 code

D13 Benign neoplasm other and ill-defined digestive organs

D13.1 Stomach

Causes of lymphofollicular hyperplasia

The appearance of hyperplasia is associated with a variety of negative impacts on tissue, leading to an increase in cell number. They can trigger the pathogenic mechanism related problems– obesity, liver dysfunction, hyperglycemia, etc. Hereditary factor experts also consider it a risk factor.

Highlight following reasons lymphofollicular hyperplasia:

• dysfunction of the internal secretion of the gastric mucosa;
• hormonal abnormalities;
• malfunctions nervous regulation digestive tract;
• the harmful effects of carcinogens that activate pathological cell division;
• exposure to specific tissue breakdown products;
• blastomogenic effect;
• the presence of chronic, autoimmune, atrophic diseases of the digestive system (often gastritis of these forms);
• presence Helicobacter bacteria pylori;
• permanent nervous disorders and stress;
• herpes virus infection;
• disorders of gastric and 12-gut motility;
• pathologies of an immune nature.

, , , , , , , , , , , , ,

Symptoms of lymphofollicular hyperplasia

The manifestations of pathogenic symptoms largely depend on the location of the pathological focus. Generalized signs are considered to be an increase in temperature, a feeling of weakness, a quantitative increase in lymphocytes and a decrease in albumin levels. It should be noted that often with a benign nature of the lesion, there are no symptoms of lymphofollicular hyperplasia. Negative symptoms are common in neglected and especially difficult cases hyperplastic lesions of the gastrointestinal tract, which are characterized by pain in the abdominal area (often in the epigastrium) in the presence of dyspeptic disorders.

The stages of hyperplasia are classified according to the size and distribution of the follicles:

• zero – lymphoid follicles are absent or poorly expressed, small in size and chaotic in position;
• the first is a diffuse, single proliferation of small follicles;
• the second is a dense, diffuse distribution without merging into conglomerates;
• third - crowding of follicles sometimes into large colonies, their mucous membrane can be hyperemic;
• fourth - erosive areas, pronounced hyperemia of the mucosa with the presence of fibrin plaque, the mucous membrane is matte in color, an increase in the vascular pattern is observed.

Based on the above features of the formation and course of pathology, we can conclude:

• lymphofollicular hyperplasia of the gastrointestinal tract gives clinical manifestations only at stages 3-4 in the form of intestinal bleeding, pain syndrome varying intensity of the abdominal area;
• detection of the disease in other cases is a random event, since there are no specific symptoms.

Lymphofollicular hyperplasia of the gastric mucosa

The complex structure of the gastric mucosa is due to the performance of many functions, including secretory activity, protection and participation in the process of peristalsis. A healthy mucous membrane is the key to the proper functioning of the entire digestive system.

Excessive proliferation of epithelial cells with simultaneous thickening of the walls of the mucosa is called lymphofollicular hyperplasia of the gastric mucosa. Pathology is often accompanied by the formation of growths or polyps. The cause of the disease is considered to be neurological and hormonal changes. Lymphofollicular hyperplasia rarely transforms into oncology. Appearance cancer cells in most cases, epithelial dysplasia contributes, in which healthy cells of the mucous layer develop into cells with a pronounced atypical structure. The most dangerous is mucosal metaplasia, characterized by digestive dysfunction and a high likelihood of developing malignant tumors.

Making a diagnosis and carrying out appropriate treatment are the main tasks of a gastroenterologist. Moreover, therapeutic methods are selected individually for each pathology.

Lymphofollicular hyperplasia of the antrum of the stomach

According to statistical data, the cause of damage to the antral region of the stomach in the presence of chronic gastritis is due not only to a reaction to inflammation (the causative microorganism in in this case acts as Helicobacter pylori), but is a consequence of weakened immunity. Immune changes in combination with gastritis, as practice shows, are detected under conditions of low acidity, which in turn is a prerequisite for the appearance of autoimmune diseases.

The study of pathology in childhood led to the conclusion that lymphofollicular hyperplasia antrum stomach is a consequence of autoimmune rheumatic disease, and not the action of bacteria. Of course, availability pathogenic flora and autoimmune disorders significantly increases the risk of hyperplasia.

Changes in the mucosa often lead to the appearance of polyps, the localization of which in the antrum accounts for about 60% of all cases of gastric damage. Polyps of an inflammatory nature, in other words hyperplastic, occur with a frequency of 70 to 90%, developing from the submucosal or mucous layer. They are round, cylindrical, dense formations with wide base and a flat top.

Lymphofollicular hyperplasia of the ileum

Bottom part small intestine called the ileum, lined from the inside with mucous membranes with an abundance of villi. The surface is equipped with lymphatic vessels and capillaries involved in the absorption of nutrients and nutrients. So fats are absorbed by the lymphatic sinus, and sugars with amino acids are absorbed by the bloodstream. The mucous and submucosal layers of the ileum are represented by circular folds. In addition to absorbing necessary substances, the organ produces special enzymes and digests food.

Lymphofollicular hyperplasia of the ileum is formed as a consequence of immunodeficiency and proliferative processes of the intestinal wall. Disorders are detected by a specific reaction to external irritation of the lymphoid tissue of the intestinal sections. Clinical manifestations pathological condition:

• loose stools (with frequent urges up to 7 times per day);
• inclusion of mucus/blood in the stool;
• abdominal pain;
• a sharp decrease in body weight;
• increased gas formation, bloating and rumbling in the stomach;
• a noticeable decrease in the body's defenses.

The disease can be differentiated by blood, urine, stool tests, as well as examination using fiber endoscopy. As a rule, lymphofollicular hyperplasia is diagnosed exclusively in the terminal zone of the ileum, which indicates the secondary nature of the pathological process and does not require therapeutic intervention. As a therapeutic and preventive measure, a strict diet with restriction of a number of foods may be recommended. If we are talking about serious inflammation If cancer or Crohn's disease is suspected, then treatment with medications or surgery is used.

Diagnosis of lymphofollicular hyperplasia

The difficulty of early detection of the pathological condition of the mucous membrane lies in the asymptomatic course of the disease in the first stages of formation. Often, the detection of lymphoid follicles occurs accidentally during colonileoscopy for other indications. Unfortunately, patient requests begin with the appearance intestinal bleeding or unbearable abdominal pain, which corresponds to last stages diseases.

An increase in the mucous layer in the stomach and intestines can be examined using endoscopic technologies, which include colonoscopy, FGDS and sigmoidoscopy. Diagnosis of lymphofollicular hyperplasia is also carried out by radiography using contrast agents. X-ray examination helps to assess the extent of spread of newly formed cells, and endoscopic examination allows obtaining biological material for histology.

Confirmation of the diagnosis of lymphofollicular hyperplasia indicates the need for constant monitoring of the condition in view of the possible development of abnormal areas into malignant tumors.

, , , , , , , [

The presence of malignant tissue makes it necessary surgery. Hyperplasia of parts of the digestive system may require resection of the stomach or excision of a section of the intestine. The rehabilitation period depends on the severity of the disease, the success of the operation and the general condition of the patient. An important point after surgical manipulation Constant monitoring remains to exclude relapses and complications.

Identification of a pathological focus in the endocrine or hematopoietic system with signs of a malignant process requires long-term combined treatment that combines surgical techniques and chemotherapeutic effects.

Treatment of benign lymphofollicular hyperplasia, as a rule, is not carried out.

Prevention of lymphofollicular hyperplasia

Considering the fact that lymphofollicular hyperplasia in most cases is asymptomatic, it is possible to identify pathology at the inception stage only by regular examinations. Therefore, regular visits medical institution for the purpose of passing preventive examination is mandatory.

Prevention of lymphofollicular hyperplasia includes recommendations general: healthy and good nutrition, maintaining a daily routine, moderate physical activity, having time for rest and relaxation, minimizing stressful situations, giving up addiction to tobacco/alcohol/drugs.

It should be noted that those who like to self-medicate with medications or folk remedies are at risk, since severe symptoms of hyperplasia occur only on late stages formation of pathology. Neglected processes are difficult to treat and develop into chronic forms diseases require complex surgical interventions, can transform into malignant neoplasms.

Prognosis of lymphofollicular hyperplasia

The number of patients with chronic diseases of the digestive system is steadily growing. Such pathologies are increasingly being identified in childhood, leading to severe consequences and even disability. The presence of Helicobacter pylori in the gastrointestinal tract is associated with the development of autoimmune gastritis, which in turn is provoked by the herpes virus. As, for example, with mononucleosis caused by Epstein-Barr infection, damage to the epithelium of the digestive organs is observed with clear signs lymphofollicular hyperplasia.

For quality treatment of autoimmune gastritis chronic course Early diagnosis remains the determining factor. Gastritis of the autoimmune type has a pre-atrophic form, corresponding to an immune response that provokes lymphofollicular hyperplasia.

The earlier the disease is detected, the better the prognosis for lymphofollicular hyperplasia. By complex therapy, which includes a treatment regimen for chronic gastritis (a combination of interferon with immunocorrection and valacyclovir), eliminates the pathological focus of the gastric mucosa, normalizes the body's defenses and achieves stable remission.

The diagnosis of lymphofollicular hyperplasia must be confirmed by clinical, morphological, endoscopic, virological and immunological data. Only after the above studies can high-quality and effective treatment be prescribed.

Lymphoid gastritis – chronic form Gastritis is a rare form that occurs in only one patient out of a hundred diagnosed cases. The disease is an inflammatory and degenerative change in the gastric mucosa. Under the influence of negative factors, lymphocytes (immune blood cells) leak and accumulate in the tissues, leading to the formation of follicles (growths) on the surface. Therefore, this type of disease is called follicular gastritis.

Follicles that appear in damaged areas may grow large sizes. They prevent the secretion of gastric juice, disrupt the digestion process and intestinal function.

Clinical studies have established the causes leading to the onset of the disease.

• Helicobacter pylori (lymphoid, similar to antral gastritis, in the vast majority of cases caused by bacterial infection);
• genetic predisposition;
• poor nutrition;
• alcohol abuse;
• smoking;
• stress.

The listed factors individually and in combination create comfortable conditions for the proliferation of Helicobacter. The immune system tries to fight the pathogen by increasing the number of lymphocytes in the affected areas. However, chronic processes and the lack of comprehensive treatment lead to the formation pathological changes.

The manifestation of signs of the disease is weak. Not noted severe pain, as opposed to acute forms.

Patients often come to the doctor with complaints of:

• mild pain in the upper abdomen, disturbing on an empty stomach or after eating;
• nausea;
• sour belching;
• heartburn;
• unpleasant taste in the mouth;
• white coating on the tongue;
• feeling of discomfort and heaviness in the abdomen;
• stool disorder.

Symptoms occur infrequently, many seek help in advanced cases. The type of gastritis is dangerous: thickening of the lymphocytic layer and progressive degeneration of mucosal tissue without proper treatment often leads to erosion (with high acidity) or stomach cancer (with low acidity).

Diagnostics

It is difficult to identify lymphoid gastritis. The difficulty is due to the similarity of symptoms with other types of gastritis.

Several methods are used for diagnosis:

• Laboratory research. The patient passes clinical tests urine and feces, fecal occult blood test, general blood tests, biochemical blood test, detection of Helicobacter.
• Endoscopy. The method is known: a flexible probe with a camera at the end is inserted into the stomach through the esophagus. On the monitor, the doctor has the opportunity to see the condition of the mucous membrane, the presence and nature of changes.
• Biopsy. It is done together with endoscopy. A piece of stomach tissue is taken through a probe for analysis.
• Ultrasonography. It is carried out in individual cases and helps to identify the extent of the proliferation of lymphoid tissue.

Usage endoscopic method allows us to determine that the patient has lymphoid, and not Helicobacter pylori caused by a similar infection. The variant is localized in and has acute erosive changes in the mucosa.

Treatment

For the treatment of follicular gastritis, like others chronic diseases Gastrointestinal tract, it is necessary to use a set of measures.

Treatment is individual for each case, depending on clinical picture. The symptoms are not clearly expressed, the situation will gradually worsen, and the disease will become more difficult to treat.

Drug treatment

If diagnostic studies have confirmed the presence of Helicobacter in the microflora of the gastric mucosa, the doctor first of all prescribes a triple regimen of irradiation (destruction) of the pathogen. Includes an inhibitor (a drug that reduces the production of stomach cells of hydrochloric acid) and two antibiotics.

If the treatment does not work, in addition to the inhibitor, a colloidal drug is prescribed, which creates a film on the damaged areas and stimulates the production of protective mucus. Antibiotics are replaced by others.

Then medications are prescribed that restore epithelial cells. The doctor may prescribe painkillers.

Unconventional methods of treatment

Treatment with folk remedies in combination with using medicinal methods gives good results. Before starting therapy, to avoid exacerbations, you should definitely consult a doctor.

In herbal medicine, herbal infusions are recommended to relieve symptoms and chronic manifestations of lymphoid gastritis.

Other methods

Lymphoid gastritis is accompanied by treatment with other products.

• Plantain juice is useful for the treatment of exacerbations in the gastrointestinal tract. It has antispasmodic and anti-inflammatory effects, promotes the restoration of mucosal tissue. You should drink 50 g of fresh juice a quarter of an hour before meals for two weeks.
• Fresh potato and cabbage juices have a detrimental effect on Helicobacter. The dosage regimen is similar to that of plantain juice.
• Honey has the ability to reduce acidity. Allowed to be used for lymphoid gastritis. You need to dissolve honey (10 g) in a glass of water and drink it before meals 20 minutes a day three times. Alternative medicine recommends a decoction: dilute honey in fresh plantain juice (in equal parts). Cook for 20 minutes over low heat, drink 20 minutes before meals.
• Propolis has antibacterial and anti-inflammatory effects. For oral administration, a pharmacy tincture is used. For 100 ml of water, take 10 drops and drink half an hour before meals. The course of admission is two weeks. However, propolis must be used with extreme caution; the product is considered a strong allergen.
• Recommended sea ​​buckthorn oil. The beneficial substances in it fight bacteria, heal and restore soft fabrics. Take 5 ml of oil half an hour before meals.
• People with reduced secretion are advised to drink half a glass of blackcurrant juice three times a day.
• There is advice to use fresh leaves and juice of Aloe Arborescens. In addition to healing and antimicrobial properties, the plant can stimulate the growth of malignant cells. You will definitely need to consult a doctor when using the plant for treatment.

Diet

In order for lymphoid gastritis to be cured, the number of relapses is minimized, and gentle nutrition is indicated. In diet therapy for acid-related gastrointestinal diseases, dishes are divided into three groups:

1. Recommended. Allowed are lean meat, fish and poultry, soft-boiled eggs or scrambled eggs, soups in lean broths, non-acidic and low-fat dairy products, well-cooked porridge, boiled, baked or steamed vegetables, and non-sour fruits. It is allowed to take weak coffee and tea diluted with milk. It is allowed to eat marshmallows, marshmallows, milk caramel and ice cream (not on an empty stomach). It is better to eat wheat bread and slightly dried.
2. It is recommended to limit. This group includes sausages, salted and canned fish, caviar, hot and sour soups, sour and fatty dairy products, and cheeses. The restrictions include homemade baked goods, rich bread and pasta, spicy and hard-to-digest vegetables, spices, sour fruits and berries, dried fruits, juices and compotes. It is allowed to add butter in small quantities to ready-made porridges and soups; after eating, eat a small piece of chocolate or candy.
3. Not recommended. It is necessary to completely exclude from the diet fatty meats, smoked meats, fried foods, raw eggs, soups and borscht with rich broths, legumes, confectionery (especially with butter creams), spreads, carbonated drinks, alcohol.

A special diet provides for split meals 4 to 6 times a day. If you feel full after eating, you need to reduce the size of portions and give preference to pureed, steamed dishes, boiled vegetables and pureed soups. In any case, the diet is prescribed individually and agreed with the attending physician.

Prevention

Chronic diseases are different from acute forms sluggishly ongoing processes formed over the years and habits. To achieve good results in overcoming ailments, including lymphoid gastritis, preventive measures are necessary.

• If the cause of the disease is Helicobacter pylori, all family members should be examined to avoid relapses. If no symptoms are noticeable, a pathogen carrier is likely present.
• It is necessary to undergo an annual examination by a gastroenterologist.
• Get rid of bad habits: smoking (especially on an empty stomach), alcohol.
• Establishing a diet as a habit for life is the key to the health of the digestive system and the whole organism.
• Follow the diet for a year after establishing stable remission. It is gradually possible to introduce previously excluded foods into the diet.
• Moderate physical exercise will help restore psycho-emotional balance and launch the body’s self-healing processes.

In the normal mucous membrane there are only single lymph nodes. They are usually located in the pyloric region and do not contain light centers. As a rule, they cannot be identified in biopsy material. The detection of follicles, especially follicles with light centers, is considered a sign of Helicobacter pylori gastritis.

1.2.7.2. Blood vessels.

The blood supply to the stomach is provided by arteries arising from the celiac trunk. They anastomose well on the surface of the stomach, in the muscularis propria, and form a plexus in the submucosa, from where the arteries penetrate the mucous membrane. Arterial microvessels are located horizontally along the muscular plate of the mucous membrane. Capillaries extend from them perpendicular to the surface, rising to the epithelial lining and forming a network surrounding the glands. Terminal arterioles (metaarterioles) are formed by a single layer of smooth muscle cells.

The capillary network of the antrum of the mucous membrane is coarser and less regular than in the fundus. Alkaline phosphatase activity is expressed in the walls of the capillaries (Fig. 1.47). In the basal part of the mucous membrane they are considered arterial, in the superficial venular.

With light microscopy, it is impossible to distinguish blood capillaries from lymphatic ones; electron microscopy characteristic fenestration is visible (89).

1.2.7.3. Lymphatic vessels.

Almost all lymphatic capillaries are located in the basal part of the mucosa, above the muscular plate. In the submucosa and around the muscular plate there is a lymphatic plexus. Lymphatic vessels run along large veins and arteries

Distribution peculiarity lymphatic vessels explains the rarity of metastases in superficial cancers. Tumor growth into the submucosa

leads to sharp increase frequency of metastasis and intramural (submucosal) spread of cancer.

In the same time early cancer on the background atrophic gastritis metastasizes more often. This is due to the fact that with atrophy of the mucous membrane, lymphatic capillaries penetrate into the superficial sections (90).

1.2.7.4. Nervous system.

The innervation of the stomach wall is carried out by the branches of the sympathetic nerves (solar plexus) and parasympathetic systems. The peculiarities of gastric neurons include the content of a number of hormones in them, including those that are synthesized in endocrine cells. Immunohistochemically, vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), catecholamines, gastrin releasing peptide (GRP), bombesin, substance P, enkephalin, somatostatin, gastrin, cholecystokinin, neuropeptide Y, and galanin (9) were found in the nerves.

GRP regulates HCL secretion and peptide hormones, there are especially many GRP in the nerves in the mucous membrane, they are located in the pyloric region, around the glands. Using double immunostaining of gastrin and GRP, contacts between GRP fibers and gastrin-producing cells were identified (91). This indicates the presence of an integral neuroendocrine system. In the submucosa, peptide-containing nerve fibers are located in and around the ganglia.

Bombesin was found in the nerve fibers of the mucous membrane and muscle layer (91,92), the main function of which is to stimulate the synthesis and secretion of gastrin and, to a lesser extent, somatostatin, as well as influence the motor function of the stomach.

1.3. Elements of gastric physiology

1.3.1. Secretory function of the stomach

1.3.1.1. Secretion of HCL and pepsinogen

Despite the fact that the phenomenon gastric secretion was discovered more than 150 years ago, only in recent decades has direct evidence been obtained that the secretion of hydrochloric acid is carried out by the parietal cells of the gastric mucosa. The concentration of hydrogen ions in gastric juice is a million times higher than that in the blood and tissues. The energy required for this is produced by the parietal cell through aerobic metabolism, which includes the production of high-energy phosphate bonds. The functions of parietal cells are regulated by a complex system of mutual

actions various factors, present both in the gastric mucosa and in the bloodstream, suppressing or stimulating the synthesis and secretion of HCL.

The main achievement of gastric physiology in recent decades has been the discovery of various mechanisms of functioning of parietal cells during the digestion of food. When food enters the stomach, acid secretion is stimulated as a result of increased vagal activity, stretching of the stomach, as well as the chemical effect of food components on the gastroduodenal mucosa. For a long time no objective methods have been found for studying secretion in humans, since both probe methods and pH measurements of gastric juice evaluate the final criterion - acidity or acid production, which is the result of complex interactions of factors stimulating and suppressing acid formation. And only in recent years have methods emerged that make it possible to study the secretory process at the cellular level, using isolated gastric glands or a culture of parietal cells. These methods are also applicable to biopsy material taken from humans. They represent an excellent model for studying the secretory process at the cellular level from both biochemical and morphological points of view.

The parietal cell membrane contains receptors for various mediators - histamine, acetylcholine, gastrin, somatostatin. The functions of these receptors are now known. In addition, there are receptors for prostaglandins, vasoactive intestinal peptide, glucagon, and secretin, but their physiological effect on the parietal cell has not been fully studied. The main stimulator of secretion in in vitro experiments was histamine and its effect is associated with the influence on the receptor-adenylate cyclase complex.

This receptor is designated as H 2 receptor. Stimulation of secretion by histamine does not require the presence of calcium ions extracellularly; on the contrary, stimulation of an isolated parietal cell with gastrin requires the presence of a phosphodiesterase inhibitor and necessarily calcium ions outside the cell. Moreover, it is believed that when stimulated by gastrin, histamine is necessarily involved in this process. In vitro experiments showed that gasgreen is a weak stimulator of secretion from an isolated parietal cell, or does not affect the secretory process at all (93). Similar experiments with acetylcholine showed that it is a very weak stimulant; it turned out that its effect was also potentiated by histamine (94), although this effect was not confirmed in studies of isolated glands taken from humans.

Thus, it is clear that the binding of the H2 receptor to histamine and the activation of adenylate cyclase with subsequent metabolism of cyclic adenosine

monophosphate (cAMP) is the main pathway for stimulating acid secretion. In experiments on isolated gastric glands, it was shown that the secretory tubules of parietal cells are the site of acid formation (95). Using intact parietal cells, it was possible to establish that acid secretion depends on the activation of adenylate enzyme, which, carrying out a number of reactions unknown to us, activates H-K'-ATPase, an enzyme specific to parietal cells, localized in the microvilli of secretory tubules (96). The mechanisms of action of this enzyme are reduced to the electrically neutral exchange of potassium ions for hydrogen ions. Stimulation of the parietal cell with histamine increases the affinity of potassium ions for cell membrane and thus, in the presence of potassium chloride around the secreting surface, potassium is exchanged for a proton, which leaves the parietal cell.

Regulation of histamine-stimulated secretion of the parietal cell is carried out in various ways, in particular, through the regulation of secretion of histamine itself in the tissues, which will be discussed below. Directly in the parietal cell, the influx of histamine is regulated by the somatosgatin receptor, which is associated with the H 2 receptor. It has been found that binding of somatostatin to it causes suppression of secretion, but it is not clear whether this is due to inhibition of adenylate cyclase or a decrease in the sensitivity of the H 2 receptor to histamine (97). This is how the secretory process occurs at the level of the parietal cell.

There are two types of gastric secretion: basal and stimulated. Basal is the spontaneously existing secretion of HCL in the absence of any stimulating influences. The level of basal secretion varies depending on the time of day, has individual fluctuations, and can be said to tend to follow a circadian rhythm (98). The lowest level of secretion is observed between 5 and 11 a.m., while the maximum level is found between 2 and 11 p.m. The level of basal secretion varies from day to day, but no significant correlation was found between serum gastrin concentrations and circadian rhythms of basal acid secretion (99). Therefore, at present there is no reason to believe that fluctuations in basal secretion in different persons or the same individual are in any way associated with changes in serum gastrin levels.

Basal secretion is most likely due to stimulation by impulses constantly coming from the fibers of the vagus nerve to the receptor apparatus in the acid-producing area of ​​the gastric mucosa. And although today there is no method that could adequately and directly determine the tone of the vagus, nevertheless, it can be judged by the basal concentration of pancreatic polypeptide, which, as is known, is released mainly as a result of the activity of the vagus. The study of this parameter showed that the concentration of pan

serum creatic polypeptide changes synchronously with changes in the level of basal secretion (100), which suggests that basal secretion is controlled mainly by vagal tone. It is possible that such vagal stimulation maintains or preserves the sensitivity of parietal cells to hormonal stimuli during the interdigestive phase. The secretion that occurs under their influence is called stimulated.

In the body, the stimulated secretory process is regulated by various influences, which in a certain sequence have a direct or indirect effect on the parietal cells. Based on time and the interaction of various factors, it is customary to distinguish three phases of gastric secretion: cerebral, gastric and intestinal.

The brain phase begins with the production of gastric juice under the influence of conditioned reflexes. The anticipation of food or the sight of it is accompanied not only by the secretion of saliva, but also by gastric juice. When food enters the mouth, stimulation of taste and olfactory receptors leads to an additional unconditioned reflex increase in secretion. The centers of secretory reflexes lie in the diencephalon, limbic cortex and hypothalamus. From here, excitation travels to the stomach through the fibers of the vagus nerve. The result of this is the release of gastrin, an increase in the concentration of which in the blood by 5-15 pg/ml can be detected in healthy individuals. However, stimulation of the acid-producing zone of the stomach by vagal fibers is more important, since even after resection of the antrum duodenum secretion stimulated by a test breakfast remains significant, while after proximal gastric vagotomy it decreases to a much greater extent. During this secretion phase, a slight increase in the production and release of gastrin into the blood begins to stimulate mast cells and histaminocytes located around the parietal cells to release histamine, which in turn binds to the H 2 receptor and triggers the entire intracellular biochemical chain, the result of which is release of HCL into the lumen of the glands and stomach. But this process develops like an avalanche already in the second phase of secretion - gastric, when gastrin is released in much larger quantities. The stimulators of gastrin secretion in this case are food components, amino acids, proteins, dipeptides, calcium compounds, which are rich in animal products; fats and carbohydrates stimulate gastrin secretion to a much lesser extent. In most laboratory animals, gastrin release is stimulated by distension of the gastric antrum, but this has not been confirmed in humans (101).

The release of gastrin continues at the beginning of the intestinal phase, when

Chronic gastritis, L.I. Aruin, 1993