We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cir-rhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, −0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and con-trols, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD40L (Spearman’s rank correlation coefficient [rs], −0.33; P < 0.001), sNox2-dp (rs, −0.57; P < 0.0001), and urinary excretion of isoprostanes (rs, −0.48; P < 0.0001) levels. The in vivo study showed a pro-gressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2α-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through inter-ference with mechanisms regulating platelet activation.

Serum Albumin Is Inversely Associated With Portal Vein Thrombosis in Cirrhosis

Cacciola Irene;
2019-01-01

Abstract

We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cir-rhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, −0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and con-trols, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD40L (Spearman’s rank correlation coefficient [rs], −0.33; P < 0.001), sNox2-dp (rs, −0.57; P < 0.0001), and urinary excretion of isoprostanes (rs, −0.48; P < 0.0001) levels. The in vivo study showed a pro-gressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2α-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through inter-ference with mechanisms regulating platelet activation.
2019
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3187504
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