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The authors review the used classifications of chronic gastritis: Modified Sydney system, Atrophy Club classification, and Operative Link for Gastritis Assessment (OLGA). Their concept apparatus: the grade and stage of gastritis, intestinal metaplasia as a marker of gastric mucosal athrophy is considered. The possibilities of interpreting the pathologist's report and clinicomorphological comparisons are discussed. The OLGA Classification, which is to predict the gastric cancer risk determined by the degree of mucosal atrophy (a stage of chronic gastritis), is noted to have an indubitable merit. A simplified classification, according to which the grade and stage of gastritis are determined by the modified visual analog scale for mucosal changes in the body of the stomach and its antral part, is proposed. Whether the postmortem study protocol for gastric biopsy specimens can be modified is discussed.

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The surgical material of 1,340 cholecystectomies as a result of cholelithiasis was analyzed. Heterotopy of the stomach mucous membrane into gallbladder was discovered in two cases; its heterotopy into the common bile duct with an ulcer formed in the heterotopic section of the mucous membrane in the fundic part of stomach was discovered in one case.

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A new international classification of gastritis retained basic principles of the Sydney system-combination in the diagnosis of etiology, topography and morphological features. This makes the diagnosis close to the nosological one. The advantage of the classification is its visual-analogous scale of evaluation of the morphological changes degree. It will ensure higher reproducibility of the morphological results and will decrease the controversies between morphologists. Subdivision of chronic atrophic gastritis into the subtypes-autoimmune (etiology) and multifocal (morphology)-is lame. Likewise, so-called peculiar forms of gastritis are not covered. Nevertheless, this modified classification may be considered as acceptable for diagnostic and research goals.

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International Agency for Research on Cancer recognized as sufficient the evidence of Helicobacter pylori (HP) infection carcinogenicity and placed it into the 1st group of carcinogens. The results of the studies performed during last years are discussed. They showed the involvement of HP in the development of stomach cancer. HP enhances mitogenesis of epithelium with translocation of immature cells on the surface of stomach mucous membrane and thus forms the targets for mutagenic and carcinogenic influences. HP takes part in the formation of mutagens, primarily of free oxygen radicals. Achlorohydria is the outcome of HP-gastritis and results in the bacterial growth in the stomach which participate in the formation of N-nitrosocompounds-well known carcinogens. Antitumor stomach defense is weakened by the decrease in the stomach of ascorbic acid, carotin and tocopherol resulting from HP-infection.

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Antral biopsies of 33 duodenal ulcer patients (15 with hypergastrinemia, group 1 and 18 with normal fasting serum gastrin, group 2) and also 13 healthy volunteers were studied for D- and G-cell density and HP-status. Basal acid output (BAO), maximal acid output (MAO) and serum somatostatin were also evaluated. G- and D-cell density was measured by PAP-immunostaining technique. Serum gastrin and somatostatin levels were studied by radioimmunoassay. HP-status was evaluated histologically with the use of semiquantitative enhanced method. Both groups of patients had decreased D-cell density compared with control (p < 0.05). Patients from group 1 had significantly increased BAO, MAO, G-cell density, index of infective load of HP, index of adherence of HP, comparing with group 2 (p < 0.05), and decreased serum somatostatin level and D-cell density compared with group 2. There were no significant differences found in serum somatostatin level, BAO, G-cell density, serum gastrin level between group 2 and control (p > 0.05). Hyperfunction of G-cells arose from impaired paracrine secretion of somatostatin, that strongly associated with increased index of infective load and increased index of adherence of HP to epitheliocytes of gastric antrum.

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The diagnosis of chronic hepatitis (CH) should include the information on CH etiology, the presence or absence of CH activity as well as its morphological characteristics. CH may be of a viral etiology (the type of the virus should be mentioned in the diagnosis), autoimmune, drug-induced and alcoholic. The etiology can be established by means of the clinicomorphological analysis using immunological and immunohistochemical techniques. Sometimes it is possible to do so after routine staining of biopsies. Portal, lobular and periportal hepatitis are distinguished morphologically. Instead of the indefinite term chronic persisting hepatitis it is recommended to recognize active and non-active hepatitis.

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An objective method of histological evaluation of stomach mucosa contamination with H. pylori proposed by the authors comprises contamination index, contamination density, adhesion density, adhesion index. The response to antibacterial therapy and other factors can also be determined. Chronic gastritis activity is characterized by the activity in surface area, in pits and in lamina propria. The method is simple, reproducible, time-effective, convenient both for diagnosis of chronic H. pylori gastritis and follow-up of the treatment results.

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The authors analysed the immediate and late results of selective proximal or truncal vagotomy with excision of the ulcer from the gastric lumen or wedge resection of the stomach in patients with various localization of the gastric ulcers. The best results were produced (Visick I-II) in patients after selective proximal vagotomy with excision of the ulcer from the gastric lumen (in 93%), the results were poorer in selective proximal vagotomy with wedge resection of the stomach and in truncal vagotomy with excision of the ulcer or wedge resection of the stomach (only in 20%, 38%, and 30% of patients, respectively). The results were unsatisfactory (Visick IV) mainly after vagotomy with wedge resection of the stomach due to recurrences and postvagotomy functional disorders. The authors claim only limited use of organ-preserving operations to be admissible.

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74 patients with GSU are studied. These ulcers occur more frequently than ordinary ulcers in aged persons against the background of various diseases. "True" GSU are localized mainly in the proximal regions. GSU combined with duodenal ulcers have a course with grave complications requiring urgent surgery. GSU located in the central parts are characterized by chronic ulcer symptoms, and those located at the periphery by the symptoms of acute ulcers (centrifugal progression). Confluence of adjacent ulcers occurs at the centripetal progression. Epithelization is lacking at the edges of the majority of GSU this indicating the predominance of the destructive processes.

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A review of the recent literature on the association between Helicobacter pylori (HP) and stomach carcinoma (SC) is presented. It is established that SC occurs 6-8 times more frequently in persons infected with HP than in non-infected. HP is considered as a co-factor in the development of SC: HP stimulates proliferation of stomach epitheliocytes and is able to produce free radicals having mutagenic properties. Some authors compare the role of HP in the development of SC with that of tobacco in the development of lung cancer. HP possesses procarcinogenic properties which are manifested if contamination occurs during childhood and when combined with genetic and environmental factors.

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Repeat biopsy examinations (38 specimens) from 18 patients with primary biliary cirrhosis (PBC) showed association of the most active PBC with pronounced ductule proliferation, especially with ductule necrosis. The semiquantitative R. Knodell technique allows defining most characteristic histological parameters and correlations. In 3 patients the biopsies helped detect a combination of PBC with viral hepatitis resultant in cirrhosis. Repeat biopsies contribute to specification of the initial diagnosis, to evaluation of PBC activity and progression.

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The author describes the morphological substrate and pathogenesis of the most common enteropathies (gluten enteropathy, collagen sprue, Whipple's disease, common variable immunodeficiency), discusses the potentials and limits of morphological methods for differential diagnosis of enteropathies, emphasizes the high informative value of duodenal biopsies that are as good as jejuno-biopsies. He considers it incompetent to use the term "chronic enteritis" which is widely spread in our country. The term stands for nosological diagnosis, making the treatment of patients worse.

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