In 1983, for the first time, a connection was found between spiral-shaped bacteria( Helicobacter pylory), with gastritis, which led to fundamental changes in the understanding of the nature of gastrointestinal diseases.This discovery made possible the use of antimicrobial agents, for the destruction of bacteria.Infection with bacteria passes through the fecal-oral route or only through the oral cavity.Helicobacter chronic gastritis usually develops at a young age( up to 20 years) and for developed countries, the incidence of the population is 50%, and in developing countries, the infection rate of the population reaches 90%.
Factors for the development of chronic helicobacterial gastritis
Bacterial colonization in the human body occurs due to such properties of Helicobacter pylori, as:
- Flagellum allows bacteria to move in the mucous layer and gastric juice.
- Attaching a bacterium to the cells of the stomach to destroy their eco-skeleton.
- Generation of H. pylori substances that cleave urea fou
- Ability to suppress some immune responses.
The development of the disease is caused by violations of mucosal protective functions, the integrity of membranes of epithelial cells and inflammation of the mucous membrane.The increased risk of infection with bacteria lies in the fact that the diagnosis of positive chronic gastritis with Helicobacter leads to an increase in the incidence of stomach cancer, which is diagnosed 3-6 times more often than with other types of chronic gastritis.
Treatment of bacterial types of diseases of the gastrointestinal tract is a mixed therapy, including antibiotics and, suppressing the acidity of the environment, substances.The use of such drugs as omeprazole, clarithromycin and metronidazole creates an unfavorable environment for H. pylori and contributes to their destruction.
Forms of Helicobacter Chronic Gastritis
- Superficial so-called non-atrophic gastritis, proceeds without changes in the glands.Changes in the form of flattening of epithelial cells and fuzzy boundaries between cells are localized only in the antrum part of the stomach.Initially, subepital edema occurs, and later the stomach develops pangastritis.
- Atrophic( autoimmune) chronic gastritis is characterized by death of the glands of the gastric mucosa.In the beginning, atrophy has a character of foci and is not expressed clearly.Then atrophy affects the entire mucosa of the stomach.
Non-standard forms of helicobacterial gastritis, such as chemical, lymphocytic, eosinophilic and granulomatous, are characterized by epithelial changes in varying degrees of damage, up to the formation of a cyst.The symptomatology of the disease depends on the type of chronic gastritis in Helicobacter pylori.For non-atrophic disease, the manifestations are pain in the hypogastric and peripump region, occurring before meals, and sometimes after eating, especially if the diet is violated.Dyspepsia, combined with a painful syndrome, is manifested by heartburn, a belch with a sour aftertaste.Sometimes nausea and vomiting are also possible.
For the second type of chronic gastritis, which is mainly manifested in the elderly and middle age, it is characteristic of a feeling of overeating, heaviness in the stomach, belching with an unpleasant aftertaste in the mouth.There may also be a manifestation of flatulence and unstable stools.Other types of the disease are accompanied by pain of varying intensity, vomiting, diarrhea, loss of appetite and a sharp decrease in weight.The identification and character of the treatment of positive chronic gastritis, Helicobacter, is determined after laboratory and instrumental examinations.