肝硬化患者血浆iPGE2和i6-酮PGF1α的变化

Robert Flisiak, Danuta Prokopowicz
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引用次数: 15

摘要

采用EIA法检测20例酒精相关性肝硬化患者(ALC组)和13例乙肝病毒为肝硬化病因的患者(hcc组)血浆iPGE2和i6-酮PGF1α。与肝硬化病因无关,两种前列腺素均显著升高。它们的水平随着肝功能不全的程度而升高,Child-Pugh C级患者的值最高。PGE2与Child-Pugh评分显著正相关(r = 0.657;p & lt;0,001)和6-酮PGF1α (r = 0,736;p & lt;0001)。相关性(r = 0,789, p <0.001),两种前列腺素水平之间也存在差异。总之,我们已经表明血浆iPGE2和i6-酮PGF1α与肝功能不全的程度同时出现,这可能是伴随肝纤维化的非实质肝细胞活化的结果。
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Plasma iPGE2 and i6-keto PGF1α in the course of liver cirrhosis

Plasma iPGE2 and i6-keto PGF 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 PGF (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 PGF arise simultaneously with the degree of liver insufficiency, that can be a result of activation of non-parenchymal liver cells accompanying hepatic fibrosis.

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