[Barrett's syndrome].
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Biomedical subjects
Publications and source records attributed to I V Popova.
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Two variants of dysplastic hepatocytes are revealed: small and large which are characterized by cell atypia and probably result from the disturbance of regenerative processes. The disturbance of the liver lobule architectonics is also a feature of dysplasia. The degree of hepatocyte dysplasia assessed by morphometric indices (nuclei surface, ratio of ellipticity) and its frequency increase with progression of the pathological process: chronic persistent hepatitis----chronic active hepatitis----liver cirrhosis----hepatocellular carcinoma. More frequent observation of the hepatocyte dysplasia in viral liver conditions (HBsAg in dysplastic hepatocytes) indicates the role of hepatitis B virus in the development of hepatocyte dysplasia. Increase of DNA content and nuclei polymorphism are observed in small and large dysplastic hepatocytes when the degree of dysplasia is increasing, this making these cells closer to cells of hepatocellular carcinoma and favouring the concept of hepatocellular carcinoma development in the foci of dysplastic hepatocytes, particularly in liver cirrhosis.
Liver cirrhosis (LC) comprises 2.1% of 17,458 autopsies in the pathology department for the period from 1962 to 1987, the incidence has increased during the last decade. LC is more frequent in males than in females (ratio 1.36:1.0), the highest incidence in males being at the age of 40-49 years, in females 50-59 years. The main etiological factors of LC, growing in importance, are hepatitis B virus (28.6%) and ethanol (26.1%). The incidence of primary liver carcinoma is 0.9% of all the autopsies, hepatocellular carcinoma (HCC) being predominant (86.3%); it develops more frequently in LC of viral and ethanol etiology. This liver carcinoma has become more frequent in the last decade. Primary liver carcinoma, particularly HCC, is more frequent in males than in females (ratio 3.1:1.0), age peak between 50 and 59 years in males and 60-62 years in females.
The clinicofunctional and morphological status of the stomach, biliferous system, pancreas, large and small intestine was studied in 83 patients with Sjogren's syndrome and disease (SS and SD). Chronic gastritis with secretory insufficiency was shown to develop in SD. Morphological changes of the gastric mucosa were represented by chronic gastritis with glandular involvement and chronic atrophic gastritis of immune genesis. Pathology of the extrahepatic system of bilification was detected in 87% of patients. The most common pathologies diagnosed in these patients were chronic cholecystitis (51%) and biliary dyskinesia (25%). Changes of the chemical composition of the bile (arise of its lythogenic properties) were observed. Various disorders of pancreatic function were detected in 85% of SS and SD patients. X-ray and endoscopic investigations revealed duodenal, intestinal and colon hypokinesia, less frequently signs of enteritis and colitis in one-third of the patients. The irritable colon syndrome was found in 40%. On the whole, involvement of different parts of the intestine was observed in 92%. Morphological changes in the duodenal and sigmoid colon mucosa were typical of chronic diffuse duodenitis and sigmoiditis in a subacute SD course, and chronic atrophic duodenitis and sigmoiditis in a chronic SD and SS course.
Primary biliary cirrhosis (PBC) of the liver is considered to be an autoimmune liver disease in which an immune aggression is directed against small biliary ducts--mitochondrial antigens of a biliary epithelium. The targets of an immune aggression in PBC may also be the histocompatibility antigens of the biliary ducts epithelium. This makes PBC resembling so-called disease "graft against host". The destruction of bile ducts in PBC is brought about through the mechanisms of an immune cytolysis and is manifested morphologically by the symptoms of the delayed hypersensitivity response. Cholangiole proliferation develops along the ductal destruction, sclerotic changes and cholestasis increase in their intensity. Small-nodular cirrhosis develops at the final stage of disease. Systemic manifestations of PBC are associated with a circulation of immune complexes containing hepatobiliary antigens. Cross-immune reactions are also of importance in the mechanisms of extrahepatic lesions.
Stomach secretory function and gastrin concentration in the blood serum were studied in 45 patients with Sjögren's disease. A sharp decrease in acid- and enzymoforming function of the stomach, disorder of the process of mucus formation and hypergastrinemia were detected in 80% of the patients. The relationship of stomach secretory function, gastrin concentration and the gravity of xerostomia was established. Morphology of the mucosa of the body and antral part of the stomach revealed chronic atrophic gastritis. Massive lymphohistiocytic infiltration of the mucous membrane with focal aggregations of lymphoid elements, atrophy and destruction of the glands were revealed. B-lymphocytes prevailed in the cellular infiltrate. T-lymphocytes were found in a small amount among the infiltrate cells and epithelial cells of the main gastric glands.
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Sixty patients with Sjogren's disease (SD) were examined. In all the patients--women aged 23 to 70, apart from the generalized "dry syndrome", there were signs of involvement of other organs and systems. Biopsy and autopsy material was studied histologically and histochemically, in some cases immunofluorescent and electron-microscopical study was performed. The most pronounced morphological and clinical manifestations of SD were linked with the damage to exocrine glands. Their alterations were represented by delayed type hypersensitivity and were similar in all exocrine glands, hence the exocrine tissue might be regarded as a target tissue in SD. One of the mechanisms of the exocrine tissue damage is connected with a mutual duct antigen of exocrine glands represented by the serum component IgA. The involvement of certain organs and systems with the development of chronic persistent hepatitis, fibrosing alveolitis, mesangioproliferative and tubulointerstitial nephritis, pronounced hyperplasia of lymphoid tissue with its plasmatization and generalized affection of the microcirculatory system of the immunocomplex nature, is noted in SD with various frequency.
Virus infection of organs and tissues in chronic active hepatitis (CAH) is generalized, therefore CAH may be considered to be a generalized viral infection in which liver involvement is only one but most important manifestation thereof. The involvement of both liver and other internal organs in CAH is underlain by delayed type hypersensitivity reaction supported by immune complexes containing hepatitis B virus antigens. The intensity of hypersensitivity reaction (immune inflammation) and autoimmunization is mediated genetically.
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Clinico-morphological examinations (repeated laparoscopies, histological and electron microscopic examinations of liver biopsies) were performed in 30 patients with chronic active hepatitis (CAH), in 20 of them in the time course of the disease. In 25 patients the viral etiology of CAH was established, in 5 patients the etiology remained obscure. In most cases of CAH there was a correlation between the intensity of clinico-laboratory and morphological manifestations of the disease activity. The following morphological variants of the CAH course were distinguished: progression of CAH with transition into liver cirrhosis (LC); decreasing activity of CAH under the influence of treatment; transition of chronic persisting hepatitis into CAH. Prognostically the most unfavourable form is CAH with pontile necrosis which rapidly terminates with LC. In patients with CAH of high activity with septal necroses the prognosis is more favourable and positive time course of the disease is possible. Patients with CAH treated with immunosuppressive drugs exhibited a decrease in the size of hepatocytic necroses and cell infiltration with increased sclerosis of the portal and lobular stroma up to the development of LC in some of them. The electron microscopic examinations specified the mechanisms of interaction of lymphocytes with hepatic cells in relation to the severity of the pathological process.
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The effect of frequency of administration of tetrachloride of carbon (CCl4) on synthesis of DNA by hepacytes and cells of the stroma, as well as on composition and magnitude of infiltrates in the liver of mice was studied. For this purpose autoradiographic and histological studies of the liver tissue in animals injected with poison once a week, twice a week and every day were carried out dayly. Periodic increases in number of hepacytes tagged with thymidin-H3 and an increase in the number of cells in infiltrates were observed. The rhythm of these changes corresponded to the frequency of administration of CCl4. With the rise in the frequency of injections of the poison the rate of increase in number of cells in infiltrates rose and synthesis of DNA in hepacytes became more intensive. The time interval, however, between the injection of the toxin and the rise of DNA synthesis in hepacytes remained constant irrespective of the frequency of exposure to the damaging factor.