Hyperplastic gastritis: symptoms, treatment, diet, prognosis

A single classification of hyperplastic gastritis is not available at present, but gastroenterologists use the so-called Sydney system of gastritis classification (which was adopted by the participants of the 9th World Congress of Gastroenterology).

Experts emphasize that - regardless of localization, degree of severity and stage (exacerbation or remission) - this is a chronic hyperplastic gastritis. In the domestic gastroenterology, the following types of this pathology are distinguished:

• Focal hyperplastic gastritis or nodal endocrine-cell hyperplasia is the development of a basally located benign carcinoid gastric tumor (<1-1.5 cm in size) resulting from hyperplasia of endocrine enterochromaffin cells, the proliferation of which is stimulated by hypergastrinemia (an excess of the hormone gastrin). Most often, this pathology is observed in patients with chronic atrophic gastritis, vitamin B12 deficiency (pernicious anemia), as well as mutations of the suppressor gene of the MEN1 tumor (leading to multiple endocrine neoplasias).
• Diffuse hyperplastic gastritis is diagnosed in cases where the hypertrophic changes in the gastric mucosa of any etiology are of a multiple nature.
• Superficial hyperplastic gastritis is characterized by involvement in the pathological process of only the upper single-layer prismatic epithelium of the gastric mucosa.
• Polypous hyperplastic gastritis, which many specialists define as atrophic-hyperplastic, but officially it is called multifocal atrophic gastritis with focal hyperplasias. The appearance on the mucosa of the body walls of the stomach of multiple, consisting of cells of glandular tissue of polyps, is associated with infection with Helicobacter pylori infection, as well as hypochlorhydria and hypergastrinemia of autoimmune etiology. As a rule, pathology begins to manifest itself in adulthood; has both a focal and diffuse form.
• Erosive-hyperplastic gastritis or lymphocytic-erosive gastritis (which has already been mentioned above) differs not only in leukocyte infiltrates in the gastric mucosa and hypertrophies of its folds. Nodular formations and areas of chronic erosion of the mucosa can also be observed (especially in the foveal region of the cardial, fundal and pyloric glands). The level of acidity of gastric juice can be different.
• Hyperplastic granular gastritis (or granular) is attributed to focal mucosal hypertrophies when multiple 1-3 mm hemispherical outgrowths are formed on it, which causes the mucous membrane to swell and become bumpy. At the same time, the stiffness of her muscular plate, the submucosa, and also the folds of the mucosa and the muscular membrane of the stomach are noted. Typical localization is the antral department, the mucosa of which has a large amount of secretory cells producing additional mucosal secretions with a granular cytoplasm and the incorporation of mucous granules. According to clinical observations, this pathology is more often detected in middle-aged men.
• Hyperplastic reflux gastritis is accompanied by a throw into the stomach of the contents of the duodenum, causing the mucosal epithelium of the stomach to be damaged by the components that make up the duodenal secretion (in particular, bile acids).
• Antral hyperplastic gastritis or rigid antral gastritis manifests itself in the disturbance of the physiologically normal relief of the mucosa, up to the change in the direction of the folds, and also in the presence of polyposic lesions on their surface. Because of this, the main and lining cells of the fundal glands can be atrophied, which leads to achlorhydria (stopping the production of hydrochloric acid). In addition, the pyloric part of the stomach becomes deformed and the gastric peristalsis decreases.

Among the rare hereditary pathologies, there is a giant hypertrophic gastritis - chronic hypertrophic polyadenomatous gastritis or Menetrier's disease. It is characterized by hypertrophy of the mucous membrane in the gastric fossa and a significant increase in gastric folds, inadequate secretion of HCl and excessive production of protective gastric mucin. A low level of hydrochloric acid leads to an inability to digest proteins and absorb nutrients, causing diarrhea, weight loss, peripheral swelling of soft tissues. However, since inflammation is minimal or completely absent, in the medical literature, Menetries disease is classified as a form of hyperplastic gastropathy.

Finally, distinguish active hyperplastic gastritis, which has three degrees of leukocyte (neutrophilic) infiltration of focal mucosal hyperplasia. In fact, this is a chronic hyperplastic gastritis, in which the severity of the inflammatory process, determined by the histological examination of tissue samples, is ranked according to the scale of the penetration of polynucleated T cells into the structures of the gastric mucosa.