Helicobakter pylori enters the stomach with saliva, contaminated food, not sterile medical equipment. The stomach is always a small amount of urea, which is derived from the blood through the stomach and intestines. From urea by the enzyme urease Helicobacter own forms ammonia, which, being alkaline, neutralizes hydrochloric acid, and creates favorable conditions for the microorganism. Another enzyme produced by a bacterium - mutsinaza - destroys the protein mucin in the gastric mucus and thins mucus. With this Helicobakter pylori penetrates the layer of protective mucus and epithelial cells attached to the mucosa in the antral stomach.
Helicobacter can be attached only to cells blennogenic columnar epithelium. Epithelial cell is damaged, its function is reduced. Next, multiply rapidly and Helicobacter colonize the entire mucosa in the antral stomach. In the mucosa there is an inflammatory process due to the fact that a large number of other enzymes produced by the organism lead to the destruction of cell membranes, alkalization normal acidic environment of the stomach. Ammonia acts on the endocrine cells of the stomach, increasing the production of hormonal substances and reducing the production of gastrin hormone, resulting in increased secretion of hydrochloric acid.
Gradually increasing and there is an inflammatory reaction of the gastric mucosa. Helicobakter pylori produces substances called cytotoxins. These substances cause damage to the mucosal cells and can lead to erosion and ulceration of the stomach. If you do not release helicobacter these substances, the ulcer is formed and the process stops at the stage of chronic gastritis. First, Helicobacter colonize the antrum (in the transition region of the stomach into the duodenum). At this stage of the disease secretory function is preserved or even increased, since the main secretory cells of the stomach are not in the antral part and in the area of the body and fundus of the stomach.
There are the following forms of gastric helicobacter defeat:
Latent form of H. pylori infection or carriage. In such a patient Helicobacter long live the mucosa of the stomach antrum, but no complaints there. However, the study of the gastric mucosa of chronic gastritis are all the same.
Acute gastritis. This condition occurs infrequently. If all the same acute gastritis occurs, it occurs with pain in the stomach, nausea, vomiting. Then the acute effects subside, and acute gastritis becomes chronic.
Chronic atrophic gastritis. This gastritis develops gradually. Usually first appears atrophic process in the stomach, which was first inhabited by Helicobacter - in the antral part. The process is then applied to the entire stomach. At the same time gradually decreases inflammation and atrophy spread to the entire gastric mucosa.
Chronic gastro. In this form of the disease in the process involves the duodenum. The changes start first in the duodenal bulb. There is swelling, redness, inflammation, erosion, occur. All this ends with atrophy, which gradually extends down the length of the intestine.
Peptic ulcer disease. It is believed that both gastric ulcer and duodenal ulcer develops on the background of already existing chronic gastritis caused by Helicobakter pylori.
World Health Organization defines Helicobakter pylori as a carcinogen by the first group. This means that the proven effects of H. pylori on the incidence of tumors of the stomach and duodenum. In early disease, when Helicobacter colonize only gastric antrum, there is a chronic gastritis without atrophy and with intact and sometimes increased secretion of the stomach.
Usually these are young patients. They have pain in the stomach after 1-2 hours after eating. Sometimes there are so-called "hunger pains" that arise in the morning on an empty stomach. The patient is worried about heartburn - a burning sensation behind the breastbone, which can be excruciating. Appears belch with sour taste. The appetite for such a patient is usually kept in full, weight loss does not occur. There is a tendency to constipation.
The examination revealed a slightly furred tongue, pain during palpation in the upper abdomen, usually on the right of the midline. Further, in the course of the process of helicobacter extend to the whole stomach and begins a gradual process of atrophy of the glandular cells of the mucous membrane. Accordingly, gradually decreasing the secretory function of the stomach, there is insufficient production of hydrochloric acid, enzymes of gastric juice. The patient is deteriorating appetite, nausea, dry mouth.
You may receive a metallic taste in the mouth. Belching released. Its sour taste gives way to flavor food or rotten eggs. If the patient develops duodenal contents reflux into the stomach, belching may have a bitter character. After the meal, patients notice heaviness in the stomach, a feeling of fullness. The intensity of pain is reduced, the pain becomes dull. Often patients complain of bloating, rumbling in the abdomen. Tendency to constipation followed by increased stool, enhanced separation of gases and diarrhea. The examination revealed a thick coating on the tongue, cracks in the corners of his mouth. When abdominal palpation point tenderness in the area of the stomach. The patient is often reduced body weight.
Diagnosis of helicobacter gastritis set by X-ray studies fibrogastroskopii, histological studies. For the diagnosis of H. pylori infection is carried out cytology: use fingerprints or smears pieces of gastric mucosa taken at fibrogastroskopii. Used and various other methods of determining Helicobakter pylori in the gastric mucosa. We study the secretory function of the stomach using a thin probe (sensing the stomach) or by intraventricular pH-metry.
Treatment of helicobacter gastritis is conducted under the general rules of treatment of chronic gastritis. If the gastritis occurs erased, treatment may not be required. But in the event of relapse, a combination of gastritis with duodenitis, the presence of erosions on the mucous membranes, there is a need for eradication (removal) Helicobakter pylori. To destroy the helicobacter obligatory in triple therapy.
Treatment of chronic gastritis helicobacter includes three components:
Antibiotic. This is usually amoxicillin or clarithromycin, tetracycline, sometimes.
Antimicrobial drug - metranidazol (trihopol, tinidazole).
Proton pump inhibitor (omeprazole, rabeprazole), or bismuth preparations.
This regimen is used for 7-14 days and allows for the destruction of Helicobacter pylori in 90% of patients.
Chronic gastritis is almost always disappears after the removal of helicobacter. When you have finished taking medication, be sure to conduct a study of gastric mucosa in the presence of Helicobakter pylori. Sometimes there is the question of treatment of H. pylori in patient's family. Re-infection usually occurs rarely and its frequency is no more than 1-2%.
