Atrophic gastritis

It is clear from the title that atrophic gastritis should represent one of the forms of inflammation of the stomach. However, this opinion was backward by 200 years, when at autopsy doctors found patients in the thin wall of the stomach and could not understand exactly what caused this.

There are still disputes over the classification, causes, role in the general pathology of the digestive tract, the significance of acidity changes, the use of the most informative examination and optimal treatment.

Which facts have to be considered?

The true prevalence of gastric atrophy is unknown, because not all the population is examined gastroscopically. If we assume that atrophic gastritis follows gastric autoimmune processes and represents the outcome of Helicobacter pylori infection, the researchers consider it to be the possible culprit of pathology in 60% of the adult population. The facts show the following.

The insidiousness of the disease consists in a mild symptomatology, even in the long course, so 10-15% of the sick people turn to the doctors. This leads to low detectability and belated anticancer measures.

It is proved that it is with atrophic gastritis that there is a disturbed growth of the epithelium, which turns into a precancerous state. Chronic atrophic process in the stomach is the initial stage of many disorders in the etiology of liver, intestine, pancreas.

Serves as a complication or consequence of prolonged inflammatory process, including with non-atrophic antral gastritis. Varieties differ in the depth of the lesion of the stomach, localization, massive capture of the area of ​​inflammation, the presence of erosion.

Acute form accompanies the toxic effect of the poison, extreme factors( acids, poisons, alkalis), therefore passes by gastroenterologists, and is treated as one of the manifestations of toxicologists. The patient gets to therapists in case of chronic symptoms.

Reasons for

All causes of atrophic gastritis are divided into exogenous( external) and endogenous( internal).To exogenous include eating disorders, the intake of toxic products into the stomach. Food can cause a disease in the case of:

• irregular eating, long periods of fasting, subsequent overeating;
• incomplete masticating for problems with teeth, oral diseases,
• lack of timely prosthesis, if the elderly person has nothing to eat;
• habits for snacks "dry";
• hobbies fast food, smoked products, fatty meat dishes, products with contrasting temperature.

Of the incoming toxic substances in the body, the gastric mucosa is most sensitive to:

• nicotine;
• coal, cotton and metal dust;
• salts of lead, arsenic;
• alcohols;
• medicines containing salicylates, prednisolone, sulfonamide compounds.

Endogenous causes of gastric damage in atrophic gastritis can be the processes of disturbing the physiological recovery of the gastric mucosa( regeneration of the epithelial tissue), helicobacteria, disorders of the nervous and endocrine regulation of the activity of gastric secreting cells in stress, diseases of the nervous system, myxedema, dysfunction of the pituitary gland and adrenal glands.

The list continues the disturbed blood circulation of the stomach wall, insufficient blood flow in regional vessels( atherosclerosis, thrombosis), venous congestion( at high pressure in the portal system) and weighed heredity.

The development mechanism of

The essence of the processes occurring at an atrophic gastritis is reduced to the cessation of the activity of a part of the cells of the mucous membrane for the production of constituent elements of gastric juice, including hydrochloric acid. Changes begin with replacing production with mucus. Usually, the activation of acid formation is observed at the beginning, then the transition to a significantly reduced acidity.

Most researchers hold the view that Helicobacter pylori plays its role only at the first stage of the disease. It contributes to an increased consumption of acidity, some of it spends on the work of its own enzyme systems. This helikobaktery completely violates the ability of the gastric mucosa to protect itself from external influences, destroy incoming other pathogens and toxic substances from food.

In the future, the main pathological direction is considered autoimmune. The organism perceives its own cells as foreign cells and reacts by producing antibodies to them. Since such agents( antigens) are epithelial cells, they are destroyed during the reaction, so the process of recovery( regeneration) is blocked.

In a healthy person, the epithelium is completely renewed every 6 days. Mucus production does not replace gastric juice. Complete cells are replaced with connective tissue. The wall of the stomach is gradually thinner, stops participating in digestion. Undigested food accumulates in the stomach cavity, which stimulates an increased synthesis of gastrin.

. Most often, the transformation occurs in the areas of the intestinal epithelium( metaplasia, dysplasia).A similar condition is called precancerous. After what time period there will be a transition to cancer, it is impossible to say exactly. The problem is whether the atrophic gastritis can be cured at this stage rests on preventing the further degeneration of the epithelium with the help of diet, diet, and medicines.

Atrophied areas of the mucous membrane lose their properties forever. The result of therapy depends on how much it is possible to maintain the remaining cells, to compensate for the reduction of the working epithelium.

Symptoms of atrophic gastritis

Severe pain syndrome with vivid clinical manifestations is typical for a hyperacid state. Since atrophic changes occur against a background of reduced acidity up to complete absence( achilias), then the clinic of the disease for a long time does not have the characteristic signs and complaints of patients.

Usually leading questions the doctor manages to find out the general symptoms for all types of a gastritis:

• feeling of gravity in the field of an epigastrium after meal;
• frequent nausea;
• eructation - is caused by reflux( reverse casting) of food from the stomach into the esophagus;
• bloating and rumbling of the abdomen;
• bad breath;
• susceptibility to constipation, rarely diarrhea.

You can detect manifestations of digestive deficiencies and its effects on the body:

• weight loss;
• signs of avitaminosis and anemia( dry skin, brittle and hair loss, sores in the mouth, burning tongue, yellowing of the skin, headaches, dizziness);
• the change in the hormonal balance, expressed in men in impotence, in women - in violation of menstrual function, the inability to become pregnant;
• increased nervousness, insomnia.

Diagnosis of

Symptoms of atrophic gastritis can already be detected by diagnostic methods at an early stage. The most informative method is fibrogastroscopy. It allows you to examine the walls of all parts of the stomach, the vascular system, take material( gastric juice, mucosal slices) for research, use preliminary coloring( chi-histoscopy), which helps to identify areas with functional abnormalities more quickly.

It is possible to histologically study the degree of dystrophic disorders in tissues, atrophy of glands, to measure the acidity of gastric juice by intragastric method, to reveal Helicobacteria in the antrum.

The most promising blood test for the detection of impaired gastric functions is gastropanel. It includes:

• detection of antibodies to Helicobacter pylori;
• study of pepsinogen I, pepsinogen II( the most significant proteins in the production of hydrochloric acid), their ratio allows you to judge the number of intact glands in the epithelium, so the method is considered a marker of the atrophic process;
• gastrin 17 - a local hormone that affects the regulation of the secretory function of the epithelium, tissue repair and motor muscle of the muscular wall of the stomach;
• antiparietal antibodies to the Castle factor - reveals antibodies to the structural components of parietal gastric cells( do not administer vitamin B12 two days before the study).

To study the functional state of the stomach apply daily pH-metry in the stomach contents, analysis of the activity of pepsins, proteolytic activity. The detection of Helicobacter pylori infection is verified by microscopic examination of biopsies, respiratory urease test.

Indirect information can be obtained from the study of stool. Atrophic gastritis reveals a lot:

• unchanged muscle fibers;
• connective tissue;
• fiber and starch;
• signs of dysbiosis.

For a comprehensive assessment, a specialist should compare the results with histological studies, fibrogastroscopy data. Results will tell the doctor how to properly treat atrophic gastritis in a particular case.

Degrees of atrophy

Fibrogastroscopic method of investigation allows not only to diagnose, but also to estimate the degree of loss of healthy cells:

• with mild degree - 1/10 part of parietal cells is lost;
• in the case of secondary - atrophy occupies 10-20% of the gastric mucosa;
• for severe changes - more than 1/5 of the epithelium is absent, replaced by scar tissue and transformed cells.

Distinctive features of acute and chronic atrophic gastritis

Acute and chronic forms of atrophic gastritis are not related, in the sense that chronic is not a transformation of untreated acute( active).

The main differences are presented in the table

Symptoms of	Acute	Chronic
Features of pathogenesis	Exposure to gastric mucosa	The adjacent organs associated with the stomach are anatomically or functionally involved: duodenum, esophagus, liver, gallbladder, pancreas, endocrine system, nervous and hematopoietic system
Symptoms	severe abdominal pain; vomiting; diarrhea; temperature increase;fainting; state of coma. Specific symptoms depend on the specific venom. The patient may die due to general intoxication, heart attack or respiratory arrest.	pain syndrome is absent or weakly expressed; is dominated by dyspepsia in the form of nausea, eructations, flatulence, constipation.
Symptoms detected on fibroadastroscopy	wall swelling; enlargement and blood vessel stasis; sites of leukocyte infiltration; destruction of epithelial cells; less often - erosion.	thinning of the wall; mucosal smoothness; epithelial flattening; deficiency of the secreting glands; mild leukocyte infiltration; cell degeneration.

Types of atrophic gastritis

The development of diagnostic methods with visual and cytological confirmation of the nature of the changes made it possible to identify several varieties of atrophic gastritis. They have their own preferential ways of development, differ in the severity of the symptoms and in the clinical prognosis.

Superficial atrophic gastritis is the easiest form of the disease. The acidity of the gastric juice is normal or slightly reduced. There is thickening of the walls, abundant production of mucus. Histologically - moderately expressed dystrophy. A good result is given by diet, herbal treatment, folk methods.

Focal - is characterized by areas of alternation of altered and normal gastric tissue. A healthy epithelium takes on an increased production of acid, as a result, the acidity is not changed. Often accompanied by intolerance of certain types of products( milk, eggs, fatty meat).

After use, there is nausea, vomiting, epigastric pain. Erosive - the main sign is the disturbed blood circulation in the inflammation zone. On fibrogastroscopy visible patchy hemorrhages, accumulation of blood vessels.

are found in the affected area. The patient shows signs of gastric bleeding:

• black liquid stool;
• vomiting with blood;
• acute weakness;
• heartbeat;
• lowering blood pressure.

It is caused by alcohol, prolonged use of medicines, respiratory viruses. Antral is a form of atrophic gastritis located at the exit to the duodenum. It is accompanied by scarring of the inflammation zone. The walls become dense( rigid).Clinical signs are moderately expressed. Typical transformation into the stomach ulcer.

Diffuse is an intermediate stage from superficial damage to complete dystrophy. On the epithelium, foci of degeneration, hyperplastic growth of immature cells appear, and ridge and pits are formed on the walls of the stomach. Histology shows the defeat of the structural basis of the glandular epithelium. About the features of the clinical course and the formation of hyperplastic gastritis can be found in this article.

Treatment of atrophic stomach gastritis

A single treatment strategy for atrophic gastritis can not be, because the symptoms are poorly expressed and too different in species and degree of injury. The general opinion of gastroenterologists - in connection with the inability to transform the altered cells back into the glandular epithelium, it is necessary to direct therapy to prevent the further process of scarring and cancer degeneration.

Treatment of atrophic gastritis in women and men does not differ. The specific choice of drugs is determined by the attending physician after examination and comparison of clinical data with an objective view of the internal surface of the stomach on fibrogastroscopy.

The complex of therapeutic measures necessarily includes:

• dietary recommendations and treatment;
• course of eradication - destruction of Helicobacterium;
• use of proton pump inhibitors;
• for the suppression of the autoimmune process - steroid hormones are used only with the predominance of signs of pernicious anemia, until there are ways to cope with this kind of inflammation;
• vitamin therapy to compensate for body losses( B12 in injections).

Proton pump inhibitors are prescribed with increased acidity to inhibit the internal mechanism of secretion:

• Omeprazole,
• Omez,
• Esomeprazole,
• Rabeprazole,
• Pantoprazole,
• Ranitidine.

In case of an anacidic state with a substitutive purpose, Acidin-pepsin, gastric juice, Abomin is prescribed. To stimulate the secretion of hydrochloric acid are suitable:

• mineral water( Narzan, Essentuki No. 4, 17, Mirgorodskaya), drink before meals for 15-20 minutes;
• broth of wild rose, potato juice, diluted juices of lemon, tomato;
• collections of herbs with plantain, wormwood, St. John's wort, thyme.

Plantaglyucid is widely used - a granular form of plantain, which is conveniently dissolved in warm water. To support regeneration, Solcoseryl is prescribed. To drugs that improve the motor function of the stomach, include Cisapride, Domperidone, prokinetics. They are necessary in detecting a reduced tone of the sphincter of the stomach.

Why is eradication needed?

Helicobacter pylori removal helps:

• suppress further development, addition of other bacteria, growth of antibiotic resistant strains;
• to shorten the duration of gastritis treatment;
• to reduce the negative effects of drugs;
• approximate the acidity of gastric juice.

The most effective treatment regimens are those that combine the antibiotics tetracycline and penicillin series and Metronidazole( Trichopolum).Actively used modern means of De-Nol - a drug based on bismuth citrate. Doses are selected individually.

Features of food

The diet for atrophic gastritis should be high in calorie and stimulating glandular mucosa. Serious restrictions are connected only with severe pain syndrome. For a few days, liquid cereals, soup-mashed potatoes, mashed meat, meatballs are recommended.

In case of painless current it is recommended:

• to establish a constant diet, not to allow long breaks;
• cook only for a couple, exclude fried and canned dishes, you can bake;
• sour-milk products( kefir, cottage cheese, low-fat varieties of sour cream);
• of eggs is better to make an omelet;
• vegetables stewed;
• shows buckwheat, rice, oatmeal;
• fruit juices boil with boiled water.

No matter how many people live with atrophic gastritis, they should always stick to the diet. No one will definitely predict the transition to cancer. It is established that the worst prognosis in people after 50 years and in the presence of hereditary complication. Teaching a child the rules and habits of healthy eating helps reduce the likelihood of illness among family members.