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dc.contributor.authorUrgancı, Nafiye
dc.contributor.authorÇullu, Fügen
dc.contributor.authorKıran, Bayram
dc.contributor.authorErkan, Tülay
dc.contributor.authorKutlu, Tufan
dc.contributor.authorTümay, Güngör
dc.contributor.authorÖzbay, Gülşen
dc.date.accessioned2016-06-14T06:50:51Z
dc.date.available2016-06-14T06:50:51Z
dc.date.issued2002
dc.identifier.urihttp://hdl.handle.net/11424/4699
dc.description.abstractObjective: An in-patient with portal hypertension PH was used in a trial conducted to determine the levels of vasoconstrictors endothelin-1 (ET- 1), Atrial natriuretic peptid (ANP), Angiotensin-ll, aldosterone and vasopressin, and to investigate the correlation between ET-1 and the other hormones. Methods: The trial included 40 patients with chronic active hepatitis B (CAH-B) ( n=10), cirrhosis with portal hypertension (PH ) (n=14), cirrhosis (n=6) and extrahepatic PH (n=10). The patients were followed up for one year in the pediatric clinic of the Cerrahpaşa School of Medicine in Istanbul, Turkey. Nineteen of them were female and 21 of them were male, with a mean age ± Standard deviation (sd) SD of 10.2 ± 6.2 years. The control group included 10 healthy children, all of whom were male with a mean age of 9.2 ± 6 years. Plasma ET-1, ANP, Angiotensin-ll, aldosterone and vasopressin levels were measured by radioimmunoassay (RIA) method in Istanbul University, Medical School, Experimental Research Institute (DETAM). Results : Plasma ET-1 levels in chronic liver patients were higher than in the healthy control group according to One Way Analysis of Variance (ANOVA) (p=0.0001). In chronic liver disease patients, there was a positive correlation between ET-1 and aldosterone, ANP and ADH respectively r=0.45 (p=0.003), r=0.37 (p=0.003), r=0.40 (p=0.0001 ). In the same group, there was No correlation between ET-1 and angiotensin-ll (r=0.22, p=0.07). Conclusion: In conclusion, we found that ET-1 levels were higher in group I and IV than in the control group. Plasma ET-1 levels increase in patients diagnosed as having chronic liver disease with an undefined mechanism. This could be explained by either an increase in production or decrease in metabolic clearances or probably by both of these mechanisms.en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectChronic liver disease, Endothelin-1, Childhooden_US
dc.titleEndothelın-1 levels ın chıldhood lıver dıseaseen_US
dc.typearticleen_US
dc.contributor.authorIDTR114776en_US
dc.contributor.authorIDTR101631en_US
dc.contributor.authorIDTR175332en_US
dc.relation.journalMarmara Medical Journalen_US
dc.identifier.volume15en_US
dc.identifier.issue3en_US
dc.identifier.startpage161en_US
dc.identifier.endpage168en_US


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