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Demonstrates no correlation between iPF 2α -III levels and portal pressure in cirrhotic patients, suggesting different mechanisms for portal hypertension.
Background Isoprostane F 2α -III (iPF 2α -III), a recently described member of a family of prostaglandin F 2α isomers and a biologically active end-product of lipid peroxidation, has been reported to increase portal pressure in cirrhotic rats. We found that its urinary levels were elevated in cirrhotic patients. Methods To investigate whether portal levels of iPF 2α -III were elevated in cirrhotic patients and whether there was a relationship between these levels and the portal pressure in the same patients, peripheral and portal plasma from cirrhotic patients (n=18) undergoing elective transjugular intrahepatic portosystemic shunt and appropriate controls (n=18) were assayed for iPF 2α -III levels by using a gas chromatography/ mass spectrometry assay. Portal pressure was measured in all cirrhotic patients. Results Cirrhotic patients had higher peripheral plasma levels of iPF 2α -III [78 (27-150) pg/mL] than controls [18(10-30)pg/mL] (P< 0.001). Portal iPF 2α -III levels were higher than plasma peripheral levels [129(50-375) pg/mL; P< 0.0001]. No correlation was found between peripheral and portal levels of iPF 2α -III (Rho=0.17, P=0.5). Portal levels of iPF 2α -III and portal pressure did not correlate (Rho= 0.17, P= 0.49). Conclusions This study shows that peripheral and portal levels of iPF 2α -III, a marker of in vivo lipid peroxidation, are elevated in liver cirrhosis. There is no correlation between iPF 2α -III portal levels and the portal pressure observed in these patients. These findings suggest that this biologically active isoprostane does not directly contribute to the portal hypertension observed in hepatic cirrhosis.
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Praticò et al. (1998) studied this question.
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