[Morphological, functional and clinical aspects of the evolution of chronic hepatitis].
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Biomedical subjects
Publications and source records attributed to C Surrenti.
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The aim of this study was to determine the incidence of HBV markers in patients with alcoholic liver disease and to compare the results with those of patients with non-alcoholic liver disease and control subjects. We tried to determine whether the association between alcohol intake and HBV infection increases the risk of developing severe liver disease. The results showed an increased incidence of HBsAg in alcoholic patients when compared with controls as well as an increased incidence of severe chronic liver disease in HBV-positive groups when compared with HBV-negative groups. We conclude that HBV infection is an important additional risk factor for the development of severe liver disease in alcoholic patients.
BACKGROUND: In vitro studies showed that Helicobacter pylori strains carrying the cag pathogenicity island are able to induce epithelial secretion of Interleukin-8. AIMS: To evaluate the assessment of cag pathogenicity island and the expression of Interleukin-8 in the gastric mucosa of Helicobacter pylori-infected patients and correlate these data with the activity of gastritis and Helicobacter pylori density. METHODS: cag status was determined by polymerase chain reaction directly on gastric biopsies from 13 Helicobacter pylori+ patients with non-ulcer dyspepsia and 13 Helicobacter pylori+ with duodenal ulcer. Interleukin-8 gene transcription and protein expression were analysed by in situ hybridization and immunofluorescence, respectively. Gastritis activity and Helicobacter pylori density were also investigated. RESULTS: cag was present in 20/26 of Helicobacter pylori+ patients: in 7/13 non-ulcer dyspepsia (53.8%] and in 13/13 duodenal ulcer patients (100%), (p<0.05). Interleukin-8 mRNA and protein expression in epithelial and inflammatory cells was higher in cag+ than in cag- patients (p<0.005). Gastritis activity significantly correlated with cag (p<0.05) and Interleukin-8 expression (p<0.005]. Helicobacter pylori density was enhanced in cag+ [p<0.005] and correlated with Interleukin-8 expression (p<0.0051. CONCLUSIONS: The present study demonstrates that in Helicobacter pylori-infected human gastric mucosa, cag+ infection is associated with enhanced Interleukin-8 expression, higher levels of active gastritis and bacterial density, and presence of duodenal ulcer.
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Sera from cholestatic patients have been found to interfere with lymphocyte rosette formation (E rosettes). Lymphocytes from patients with cholestasis showed a lower percentage (42.36%) of cells binding sheep red blood cells in comparison with a control group (62%). In the presence of cholestatic serum the number of E rosettes formed by lymphocytes from normal subjects declined to 44.16%. This behaviour, however, can reverse, since lymphocytes from cholestatic patients previously incubated with normal serum, showed a nearly normal capability of forming E rosettes (57.90%). Therefore, it is conceivable that among the several factors which are present in sera from patients with either chronic or acute hepatitis and which are able to interfere with T-lymphocyte function, there may be included also the factor which is present in sera from cholestatic patients. The possible role of bile salts and hyperlipoproteinaemia present in those patients requires further investigation.