Gastritis is acute or chronic inflammation of the stomach. Two forms of gastritis are differentiated – acute and chronic ones. Acute gastritis is usually caused by high doses of concentrated alcohol, irritative meal, pathogenic microbes (e.g. Salmonellas, staphylococcus, pseudomonas) and different toxic chemicals.
Acute gastritis may affect all layers of the stomach wall. Due to the kind of inflammatory exudation serous, hemorrhagic, fibrinous and purulent acute gastritis are differentiated. Acute inflammation of the mucous membrane is accompanied by hypersecretion of a mucus (acute catarrhal gastritis). Acute gastritis usually needs dietary treatment and in most cases ends by self-recovery.
Chronic gastritis (ChrG) represent themselves the original diseases and generally does not have a direct relationship with acute one. Morbidity of ChrG is rather high, both adults and children suffer from the diseases.
Three principal types of ChrG are differentiated: autoimmune (chronic gastritis of A type), bacterial (chronic gastritis of B type) and chemical (chronic gastritis of C type).
ChrG-A. The incidence of the disease is low (not more 5% from all ChrG). ChrG-A is caused by autoantibodies to parietal cells of the mucosa mainly of the fundic part of the stomach. Microscopically prominent infiltration of the mucosa by lymphocytes and especially by plasma cells is found. Plasma cells produce mainly IgG instead of normal secretory IgA. The autoimmune affection of the mucosa leads to depressed secretion of pepsin and hydrochloride acid with achlorhydria (lack of HCl) and achylia (lack of HCl and pepsin).
ChrG-B is caused by different bacteria especially by Helicobacter Pylori (HP). The bacterium was discovered in 1983 by B. Marshall and J. Warren. It is established that contamination occurs in childhood and with age proportion of infected adult people increases up to 60-65%. As not all infected people develop gastritis the mechanism of bacterial gastritis is closely related with local immunodeficiency. HP multiply mainly in the mucus of the antrum and release the urease. The enzyme neutralizes the hydrochloric acid and thereby creates favorable conditions for subsequent damage of the cells of the gastric glands. The early stage of the process is characterized by hypersecretion of the gastric juice (hyper acid gastritis), later on, atrophic changes develop with loss of gastric secretion. Morphologically HP-gastritis is characterized by the predominance of neutrophil infiltration of the mucosa, formation of erosions of the mucosa (erosive gastritis) and lymphoid follicles in the submucosa. Atrophic changes of the mucous membrane are accompanied by intestinal metaplasia of gastric glands.
ChrG-C develops in patients with chronic duodenal reflux (regurgitation of the duodenal contents into the stomach) with predominant lesion of the antrum (reflux gastritis). The mucous membrane of the antrum is affected by alkaline duodenal contents with an admixture of the bile acids. Morphologically reflux-gastritis is characterized by prominent hyperplasia of the gastric pits with papillomatous epithelial vegetations. Reflux-gastritis is considered as a precancerous disease. Another type of ChrG-C can be found in patients treated with non-steroid anti-inflammatory drugs. Morphologically it is similar to reflux-gastritis.
Irrespective of etiology two morphological types of ChrG are differentiated – without atrophy of the mucosa (superficial ChrG) and atrophic one. In superficial ChrG inflammatory infiltration (neutrophils, lymphocytes) can be seen only in the superficial parts of the mucous membrane. Progression of the process is accompanied by involvement of the whole mucosa with its possible atrophy. In atrophic gastritis the folds of the mucosa are smooth, the mucosa itself becomes very thin and blood vessels of the submucosa are well seen. Microscopically the quantity of the mucosal glands is diminished as well as the quantity of glandular cells producing pepsin and hydrochloride acid. On the contrary the quantity of mucus producing cells of the necks of the glands increases. Not rare atrophic gastritis is accompanied by metaplasia and intestinal dysplasia of the mucosa. In view of this chronic atrophic gastritis is considered as the disease with high risk of malignant transformation.
In accordance with the modern classification of gastritis (Sydney, Australia, 1990) the diagnosis of gastritis should include etiology (autoimmune, bacterial, reflux and some others), morphology (with or without atrophy), and topography (gastritis of the fundus, body or antrum of the stomach) of the process. Topography and morphology of the disease can be revealed only in gastric biopsy examination. Biopsy specimens should be taken from different sites of the stomach – fundus, body and the antrum (not less than 3 pieces).