Atrophic hyperplastic gastritis

The hyperplastic form of atrophic chronic gastritis differs from the other by the expressed ability of a part of the cells of the gastric mucosa to actively grow (proliferate).

The process is accompanied by the destruction of the useful for the functioning of the epithelium, which produces hydrochloric acid and components of gastric juice. As a result, chronic inflammation in the stomach is maintained, functional connections with neighboring organs participating in digestion are violated.

Diagnosis and treatment of atrophic hyperplastic gastritis requires evaluation of the structural changes formed as a result of proliferation, differentiation with malignant growth. According to the International Statistical Classification, the disease is taken into account in the group of "Other gastritis" under code K29.6.

What is known about prevalence?

It has been established that for such a disease as atrophic hyperplastic gastritis, about 5% of the total chronic pathology of the stomach occurs. His varieties are detected with varying frequency.

For example, giant hypertrophic gastritis affects both adults and children. And men are 3.5 times more likely than women, and more typical for the age category of 30 years and older. Polypous appearance is typical for women 40-45 years old.

What are the forms of hyperplastic proliferation?

The method of studying the stomach with the help of a fibrogastroscope and studying biopsy specimens from different parts of the affected tissue made it possible to reveal microscopic changes accompanying hyperplastic cell proliferation.

In the zones of inflammation, the process of mitosis (division) of cells changes. As a result, the order of the superfluous abundance is disrupted, the folded structure of the gastric mucosa changes, thickened folds appear (rigid), which can not stretch and increase the volume of the stomach upon ingestion of food.

In the submucosal layer (submucous) instead of elastin fibers dense knot formations are formed, different in size and crowding. Structural disorders are located in different parts of the stomach (in the body, cardia, antrum). Against the background of growth of the epithelium, glandular cells that produce gastric juice, surrounding the mucous atrophy are suppressed and destroyed.

Histological examination reveals plots of clogging and destruction of the epithelium

Causes

The appearance of mucosal atrophy is explained by external and internal causes. External impact is provided by:

• violations of the regime and the usefulness of the food (long periods of hunger, abnormal diets, enthusiasm for fatty meat, lack of sufficient volume of vegetables and fruits);
• the effects of alcohol and nicotine;
• professional and household poisoning with toxic acids, alkalis, heavy metal salts;
• sensitivity to medicines.

Internal causes are combinations of disadvantaged factors, which include:

• infection with Helicobacter pylori;
• the presence in a person of severe nervous and endocrine disorders that disrupt the regulation of recovery of the epithelium of the stomach;
• deterioration of the supply of tissues due to the defeat of the vascular network by atherosclerosis, the formation of venous stasis with thrombosis;
• dysfunctional heredity.

These causes are significant for any form of atrophy. In order to create a hyperplastic process on this background, it is necessary additionally:

• autoimmune disorders (pernicious anemia);
• infection with cytomegalovirus against the background of high activity of Helicobacter pylori;
• gross changes in the regulation of mucus production by glands, especially in the region of the bottom of the stomach;
• ; eosinophilia in the peripheral blood, caused by parasitic diseases (ascariasis, anisakidosis, filariasis);
• a certain mutation at the genetic level, it is revealed that the unhealthy heredity is formed due to disorders in the normal structure in the genes of β-catenin, the suppressor of the MEN1 tumor in the Zollinger-Ellison syndrome (pancreatic islet tumor accompanied by increased gastrin production and activation of gastric acid secretion in the stomach)
• congenital abnormalities of the stomach and its tissues (for example, Cronkhete-Canada syndrome - polyposis of the entire gastrointestinal tract with the formation of cysts in the growth, necrotic polyps).

Anisakidosis is common among marine life, a person becomes infected while consuming salted fish or cooking fresh fish, which is accompanied by eosinophilia

Are there risk factors?

To the factors contributing to the hyperplastic flow of atrophic gastritis, experts reckon the presence of a person's food allergies (40% of cases in children are associated with intolerance to gluten-celiac disease), beriberi, hyperglycemia in diabetes and kidney disease, accompanied by kidney failure.

It has been established that long-term use in the treatment of gastritis of drugs blocking the production of hydrochloric acid (a group of proton pump inhibitors, omeprazole and analogues) leads to a significant increase in the risk of excessive activation of polyps in the zones of gastric pits and major glands.

The mechanism of development

The development of hyperplastic growth of epithelial cells on the gastric mucosa causes an excess of mucus production. At the cellular level, the division is stimulated by special growth factors. Synthesis of acid in parietal cells is simultaneously suppressed. This mechanism explains the parallel processes of hypertrophy in individual areas with a gradual atrophy of the surrounding tissue.

Symptoms of atrophic hyperplastic gastritis

The clinical signs of atrophic hyperplastic gastritis differ somewhat depending on the type of pathology. But the initial symptoms are usually the same and manifest as a feeling of heaviness in the epigastric region after eating fatty meat dishes, spicy condiments, pickles.

The disease lasts for a long time without complaints. But with a retrospective questioning of the patient, the doctor can identify:

• frequent heartburn;
• nausea;
• bloating;
• rarely vomiting of food eaten;
• occurrence of a raid on the tongue;
• a burp with an unpleasant odor.

Since at the initial stage the acidity remains normal or elevated, the pains in the epigastric region can be cramped (spastic), less often described as aching or pressing

In cases of an erosive form of gastritis, pain increases with the body tilting, walking. Exacerbations are associated with spring and autumn periods. In fecal masses and vomiting, impurities of blood are detected. With giant hypertrophic gastritis, symptoms are often absent. Some patients still note nausea, diarrhea, weight loss, lack of appetite, rare gastric bleeding.

In the blood of such patients, the level of protein (albumin) is significantly reduced. This contributes to additional swelling of the stomach tissue. Hyperplastic gastritis is a chronic disease. It flows with periods of exacerbations and remissions. These symptoms characterize the stage of exacerbation.

Types of disease

The last classification of gastritis is called at the place of its adoption Sydney. Not all domestic gastroenterologists agree with its conclusions. In the practice of Russian doctors, there are several varieties of hyperplastic gastritis.

Focal

Another name is "nodal endocrine-cell hyperplasia", benign hyperplasia in the form of a tumor in diameter less than 15 mm. It is based on the proliferation of endocrine cells, which stimulates the excess of the hormone gastrin.

It occurs more often in patients with pernicious anemia caused by vitamin B12 deficiency. "The culprit" of tumor growth is the mutated tumor suppressor gene MEN1, it has to do with multiple endocrine lesions.

Surface

The process involves only the uppermost layer of prismatic epithelium on the gastric mucosa.

Diffuse

The diagnosis is made with the multiple nature of hypertrophic changes, regardless of the etiologic factor.

Polypous

According to the classification, "multifocal atrophic gastritis with focal hyperplasias", multiple or single polyposis sprouts (focal and diffuse forms), consisting of glandular cells, are found on the mucosa. More often associated with massive Helicobacter pylori infection, autoimmune processes, decreased acidity.

Characteristic for patients after 50 years

Erosive-hyperplastic

In another way, called lymphocytic-erosive gastritis, against the background of leukocyte infiltrates and hypertrophy of the folds, nodules and areas of mucosal tissue erosion are visible, more often in the zone of the pits of the cardial, pyloric and gastric body. The acidity index of gastric juice can be different.

Hyperplastic granular

Or "granular" - is close to a focal lesion, on the mucous there appear formations in the form of growing drops up to 3 mm in size, a multiple character is possible, the mucous membrane looks bulky and edematic. Most often affects the antrum department. Muscles become dense and sedentary. It is observed in men 40-50 years.

Hyperplastic reflux-gastritis

Mandatory includes casting and damage to the mucosa of the antrum by the alkaline content of the contents of the duodenum. The most significant aggressive agents are bile acids.

Antral

Or rigid antral gastritis differs in sharply broken folds in the antrum, they are thickened, change direction, on the surface are covered with polyps. The pyloric part of the stomach gradually cicatrizes and narrows, the peristalsis sharply decreases. The production of hydrochloric acid ceases.

The giant hypertrophic

Or polyadenomatous gastritis - Menetrier's disease. It is characterized by proliferation of folds along the large curvature of the stomach, the release of epithelium from the pits with excessive production of mucus. Cells that synthesize mucus grow into the muscle layer and form cysts. Reduced acidity is accompanied by loss of protein, dystrophy.

As you can see, the main differences can be determined only by the type of mucosa in fibrogastroscopy and histology of biopsy specimens

Complications

The lack of timely treatment leads to unpleasant consequences of hyperplastic growth:

• the structure of the mucous membrane of the stomach is broken, atrophy of a more or less severe degree appears;
• the participation of the stomach in the process of digestion decreases, as the production of gastric juice decreases in parallel with the destruction of parietal cells;
• body weight is lost;
• gastric motility is disturbed, which leads to paresis, reflux damage to the esophagus;
• the intensity of protein metabolism decreases, the decrease of albumins affects the restorative processes in all organs and tissues;
• hypovitaminosis is accompanied by anemia;
• Hyperplastic granular and hypertrophic gastritis have the greatest ability to degenerate into an ulcer and a cancerous tumor, every fifth case is transformed in the polyposis.

Diagnostics

In addition to fibrogastroscopy in diagnosis, x-ray examination of the stomach, less often ultrasound, is important. Indirect signs can be suspected on the basis of laboratory tests. For this, a clinical and biochemical blood test is performed (it is important to identify eosinophilia, signs of anemia), an immunoenzymatic blood test for Helicobacter pylori.

Treatment

Conservative treatment of hyperplastic gastritis is carried out only with confirmation of diagnosis, determination of acidity.

The nutritional requirements do not differ from other forms of gastritis:

• frequent consumption of food in small quantities;
• excluded freshly baked bread, culinary products;
• not allowed fatty, fried, smoked foods and meals;
• with a painful syndrome go to kissels, liquid porridges, rubbed soups;
• meat and fish can be in the absence of pain eat in boiled form, in steam cutlets, meatballs, casseroles;
• curd is shown;
• use kefir and other sour-milk products is better to specify with the attending physician, it depends on the level of acidity;
• vegetables with fruits are recommended in the form of diluted juice, rubbed with heavy forms, without special restrictions for superficial gastritis.

Identification Helicobacteria, according to modern views, needs a course of eradication with antibiotics (Azithromycin, Clarithromycin) and Trichopol.

Duration of the course and dosage is selected by the physician individually, there may be substitutions caused by hypersensitivity of the organism

With an increase in acidity, inhibitors of the proton pump (Ranitidine, Omez, Misoprostol) are used. Drugs are not indicated for severe achlorhydria, low acidity. To support and protect the mucosa, bismuth preparations are shown: De-Nol, Ventrisol, Bismofal. Aluminum compounds are not less active: Gelusil, Gastal, Compensane.

In severe pain syndrome appoint:

• Bruskopan.
• Pirentsepin,
• Gastril.

Replenishment of protein losses is necessary due to diet, course intake Methionine, with severe complications - intravenous transfusion albumin, frozen plasma. Operative treatment may be necessary with frequent repeated bleeding, suspicion of a tumor transformation. If possible, endoscopic interventions for electrocoagulation of polyps, laser exposure are used.

Folk treatment for hyperplastic growth is contraindicated. It can not fully take into account the state of the mucosa, the level of acidity. Herbal remedies are able to activate the disturbed growth of the epithelium.

Patients are recommended vitamins, especially B12 and P, they prevent the development of anemia

Forecast

The prognosis of hyperplastic atrophic gastritis is determined by the form of the disease. For treatment, it is unfavorable. The patient can survive long enough provided that the doctor's recommendations are followed. All my life I will have to follow a diet, drink supportive medications, undergo examinations.

How dangerous is transformation into a tumor in advance to be impossible. The above examples indicate the probability, but do not mean an obligatory outcome. The multiple nature of hyperplastic atrophic gastritis and moderate clinical manifestations pose the task of conducting mass preventive studies in the prophylactic medical examination of the population.