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Biomedical subjects

T L Lapina

Publications and source records attributed to T L Lapina.

14 recordsLinked to original sources
PubMed1997

[Reparative characteristics of gastric and duodenal mucosa in ulcer].

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.

Adult↗
PubMed1993

[Diagnostic criteria of pyloric helicobacter infection in peptic ulcer].

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.

Azure Stains↗
PubMed1990

[Campylobacter pylori and the reparative processes in peptic ulcer].

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.

Adult↗
PubMedDate not supplied

[The role of apoptosis and proliferation of epitheliocytes in morphogenesis of Helicobacter pylori-associated gastritis].

77 patients with chronic Helicobacter gastritis verified endoscopically and exacerbation of duodenal ulcer were examined. H. pylori infection was identified by the rapid ureasa test (CLO-test) and Giemza staining. The patients received 7-day three-component therapy for eradication of H. pylori. Apoptosis and proliferation were studied in 16 patients in serial sections with the use of monoclonal antibodies. Eradication of H. pylori resulted in relief of inflammation and transformation of active gastritis in inactive one. H. pylori-associated gastritis is associated with activation of apoptosis of gastric mucosa epithelial cells and epitheliocytes proliferation. H. pylori eradication alters correlation between apoptosis of epitheliocytes and their proliferation: successful eradication of the infection decreases apoptosis, high proliferative activity of epitheliocytes persists reflecting enhancement of regeneration in gastric mucosa.

Amoxicillin↗
PubMedDate not supplied

[Atrophic gastritis caused by Helicobacter pylori as a precancer disease].

1-3% persons infected with H. pylori develop atrophic gastritis annually. Probability of stomach mucous membrane atrophy in such patients is 50%. H. pylori increases risk of carcinoma development 4-6 times. Experimental infection of mice and mongol gebrils results in neoplasia. CagA- and VacA-positive H. pylori strains have the most pronounced effect in relation to enhancement of inflammation and mucous membrane atrophy. The association was noticed between certain human gene alleles IL-1, IL-10, TNF-alpha on the one hand, incidence of stomach carcinoma and atrophic gastritis with hypochlorohydria, on the other. Results of efficiency of H. pylori treatment in inverse development of gastritis are contradictory. Nevertheless, such therapy is studied as a possible method of carcinoma prophylaxis.

Animals↗
PubMedDate not supplied

[Reparative processes in peptic ulcer (clinico-morphologic study)].

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.

Adult↗
PubMedDate not supplied

[Peptic ulcer and liver pathology (an analysis of 6456 autopsy observations during 1983-1992)].

The incidence of various forms of stomach ulcer, their combination with liver diseases and pathogenetic relationships of these two pathological types have been studied on the material of 6456 autopsy cases for 1983-1992. High incidence of nonspecific reactive hepatitis in both gastric and duodenal ulcer and that of liver cirrhosis and cirrhosis-carcinoma in the pyloro-duodenal ulcer is established. A role of gastrin as a promoter in the development of liver cirrhosis and carcinoma in pyloroduodenal ulcer is suggested. The role of nonspecific reactive hepatitis in chronization of the hepatic pathological process is not excluded.

Adult↗
PubMedDate not supplied

[Possible combination of eosinophilic infiltration of the stomach, small and large intestines with psoriasis].

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.

Eosinophilia↗
PubMedDate not supplied

[Ulcer disease: new facts--new issues].

Involvement of Helicobacter pylori in pathogenesis of ulcer, the role of inflammation induced by the bacteria and possible mechanisms of hypergastrinemia are considered. The results of therapy directed to eradication of H. pylori from the clinical and pathogenetic point of view are presented. The role of H. pylori in asymptomatic gastritis and in gastric and duodenal ulcer is discussed. The information on genetic variability of H. pylori and its strains with different pathogenicity distinguished on the basis of genes encoding vacuolising cytotoxin and cytotoxin-associated protein is provided.

Cytotoxins↗