{"title":"Plasma iPGE2 and i6-keto PGF1α in the course of liver cirrhosis","authors":"Robert Flisiak, Danuta Prokopowicz","doi":"10.1016/S0090-6980(96)00137-2","DOIUrl":null,"url":null,"abstract":"<div><p>Plasma iPGE<sub>2</sub> and i6-keto PGF<sub>1α</sub> were measured with an EIA assay in twenty patients with alcohol-related liver cirrhosis (ALC group) and 13 patients with hepatitis B virus as an etiologic factor of liver cirrhosis (HLC group). Significant increase of both prostanoids was observed irrespectively of the etiology of liver cirrhosis. Their levels increased depending on the degree of liver insufficiency with the highest values in patients classified as Child-Pugh C class. A significant, positive correlation with Child-Pugh score was found regarding PGE<sub>2</sub> (r = 0,657; p < 0,001) as well as 6-keto PGF<sub>1α</sub> (r = 0, 736; p < 0,001). Correlation (r = 0, 789, p < 0,001) was also observed between levels of both prostaglandins. In conclusion we have shown that plasma iPGE<sub>2</sub> and i6-keto PGF<sub>1α</sub> arise simultaneously with the degree of liver insufficiency, that can be a result of activation of non-parenchymal liver cells accompanying hepatic fibrosis.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00137-2","citationCount":"15","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0090698096001372","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 15
Abstract
Plasma iPGE2 and i6-keto PGF1α were measured with an EIA assay in twenty patients with alcohol-related liver cirrhosis (ALC group) and 13 patients with hepatitis B virus as an etiologic factor of liver cirrhosis (HLC group). Significant increase of both prostanoids was observed irrespectively of the etiology of liver cirrhosis. Their levels increased depending on the degree of liver insufficiency with the highest values in patients classified as Child-Pugh C class. A significant, positive correlation with Child-Pugh score was found regarding PGE2 (r = 0,657; p < 0,001) as well as 6-keto PGF1α (r = 0, 736; p < 0,001). Correlation (r = 0, 789, p < 0,001) was also observed between levels of both prostaglandins. In conclusion we have shown that plasma iPGE2 and i6-keto PGF1α arise simultaneously with the degree of liver insufficiency, that can be a result of activation of non-parenchymal liver cells accompanying hepatic fibrosis.