[Possible combination of eosinophilic infiltration of the stomach, small and large intestines with psoriasis]. / O vozmozhnom sochetanii éozinofil'noi infil'tratsii zheludka, tonkoi i tolstoi kishok s psoriazom.

The combination of the eosinophilic infiltration of the stomach, small and large intestine with psoriasis is described. Diarrhea and syndrome of the disturbed absorption in eosinophilic gastroenteritis coincided with exacerbation of the skin disease. Clinical regression of both conditions with disappearance of peripheral eosinophilia occurred simultaneously. Participation of T-cell immunity and IgE is suggested as a pathogenetic mechanism of eosinophilic gastroenteritis and psoriasis.

[Reparative characteristics of gastric and duodenal mucosa in ulcer]. / Kharakter reparatsii slizistoí obolochki zheludka i dvenadtsatiperstnoí kishki pri iazvennoí bolezni.

Mucosal repair in the stomach and duodenum was assessed clinically and morphologically in various ulcer phases in 475 patients with gastroduodenal ulcer. It was found that poorly scarring ulcers are characterized by severe impairment of regeneration with epithelial proliferation prevailing over its differentiation. Participation of immune system, primarily T-cell component, in regeneration regulation is shown. Helicobacter pylori is not involved in repair. Superoxide dismutase activity in red cells and ulcer edges mucosa is prognostically significant indicating the disease phase, completeness of ulcer process.

[Reparative processes in peptic ulcer (clinico-morphologic study)]. / Reparativnye protsessy pri iazvennoi bolezni (kliniko-morfologicheskoe issledovanie).

475 patients with stomach ulcer (1984-1993) were studied using various methods: endoscopical, immunological, biochemical, bacteriological and morphological. Morphology of exacerbation and type of reparative processes in normal scarring and torpid course of disease are presented. Under adequate regeneration there is an activation of immune system, first that of T-cell compartment. Torpid course is characterized by a grave regeneration disturbance and depression of the immune system. The interpretation of the so-called "red scar" is given: it reflects different stages of the epithelial regeneration, however in 4.8% of duodenal ulcers and in 11.2% of stomach ulcers it masks a torpid course. Helicobacter pylori has no influence on the reparative processes. Adequately chosen therapy improves and accelerates ulcer scarring.

[Diagnostic criteria of pyloric helicobacter infection in peptic ulcer]. / Kriterii diagnostiki piloricheskogo khelikobakterioza pri iazvennoi bolezni.

Helicobacter pylori (HP) in 41 patients (10 with stomach ulcer and 31 with duodenum ulcer) was found in gastro-biopsies from the stomach antrum before and after the treatment. The following methods to reveal HP were used: Giemsa staining, immunoperoxidase reaction with polyclonal monospecific antibodies against HP, urease rapid test. HP was also revealed in the blood serum by antibodies against HP by means of enzyme immunoassay. Electron microscopy was performed in 5 patients and bacteriologic study in 10 patients. Immunohistochemical method allows one to judge about real HP colonization of the gastric mucosa. Bacterioscopy with Giemsa staining gives good results but they are not true markers of HP presence this being explained by other methods. Serologic enzyme immunoassay gives an idea about the patient contamination, but not about HP eliminations as a result of treatment. Urease-test is adjuvant.

[The use of histamine H2-receptor blockaders in the clinical picture of internal diseases]. / Primenenie blokatorov gistaminovykh H2-retseptorov v klinike vnutrennikh boleznei.

The analysis of the literature, the material, and the results of the authors' own studies concerning the comprehensive investigation of blockers of histamine H2-receptors are presented. The attention is paid to the reparative action of drugs of this group, side effects, interaction with other drugs. The limitations and possibilities of their use in various diseases proceeding with gastric hypersecretion and hyperchlorhydria are determined.

[Congenital hypoplasia of the pancreas with lipomatosis and bone marrow dysfunction (Shwachman syndrome)]. / Vrozhdennaia gipoplaziia podzheludochnoi zhelezy s lipomatozom i disfunktsiei kostnogo mozga (sindrom Shvakhmana).

The description is given of Shwachman syndrome in a male of 17, with a long anamnesis of malabsorption syndrome, granulocytopenia, repeated bronchopneumonia, somatogenic subnanism and hypogonadism. The death resulted from acute cardiovascular insufficiency. Post-mortem examination revealed exocrine pancreas hypoplasia with lipomatosis, Wirsung duct atresia, fibrocholangiocytosis and fat hepatosis, visceral anemia, delay in the maturation of granulocytes in the bone marrow, somatogenic polyglandular endocrinopathy, metabolic myocardium necrosis, calcinosis of the small arteries wall, lymphoid tissue atrophy, focal pneumonia of the upper lobe of the left lung.

[Campylobacter pylori and the reparative processes in peptic ulcer]. / Campylobactwer pylori i reparativnye protsessy pri iazvennoi bolezni.

The paper deals with reparative potential of gastric and duodenal mucosa in ulcer in connection with the presence and quantity of Campylobacter pylori (CP) which is found practically in all patients not only with duodenal localization of ulcer but with mediogastric and pyloroantral localization as well. No correlation between the CP presence and CP mucosa colonization on the one hand and the type of reparative processes in the mucosa is found. The presence or the absence of CP as well as the degree of CP mucosal dissemination have no influence on the clinical course of the ulcer. Antiulcer treatment aiming at aggression factors (histamine H2-receptors blockers) and protective factors (enprostil) and lacking antibacterial activity improves the reparative processes but does not influence CP. Thus, CP is not etiological and probably is not a main pathogenetic factor in ulcer development. Its participation in the genesis of ulcer is possibly brought about under conditions of suppression of local protective mechanisms.