TY - JOUR
T1 - ADAMTS-13/von Willebrand factor ratio: A prognostic biomarker for portal vein thrombosis in compensated cirrhosis. A prospective observational study
AU - Sacco, Monica
AU - Tardugno, Maira
AU - Lancellotti, Stefano
AU - Ferretti, Antonietta
AU - Ponziani, Francesca Romana
AU - Riccardi, Laura
AU - Zocco, Maria Assunta
AU - De Magistris, Antonio
AU - Santopaolo, Francesco
AU - Pompili, Maurizio
AU - De Cristofaro, Raimondo
PY - 2022
Y1 - 2022
N2 - Background and aims: In cirrhosis, decreased portal flow velocity, thrombophilia factors, and portal hyper-tension are considered risk factors for portal vein thrombosis (PVT). In cirrhosis, the transformation of the stellate cells causes a progressive decrease of ADAMTS-13, while VWF multimers secretion by endothelial cells is strongly enhanced. This imbalance leads to an accumulation of ultra-large VWF multimers that in sinusoidal circulation could favor PVT both in intra-and extra-hepatic branches, mostly in decompensated cirrhosis. This prospective study was aimed at identifying possible clinical, biochemical, and hemostatic factors predictive for non-tumoral PVT in a cohort of patients with compensated cirrhosis.Methods: Seventynine compensated cirrhosis patients were prospectively followed for 48 months, receiv-ing a periodic Doppler-ultrasound liver examination associated with an extensive evaluation of clinical, biochemical, and hemostatic profile.Results: Five patients developed PVT (cumulative prevalence = 6.3%), occurring 4-36 months after enroll-ment. In logistic regression analysis, the ADAMTS-13/VWF:GpIbR ratio < 0.4 was the only independent variable significantly associated with PVT (OR 14.6, 95% C.I.:1.36-157.2, p = 0.027). A Cox-regression -analysis confirmed this finding (HR = 7.7, p = 0.027).Conclusions: The ADAMTS-13/VWF ratio < 0.4 measured in compensated cirrhosis could be a reliable predictive biomarker for PVT development, paving the way to novel therapeutic strategies to prevent and treat PVT in this clinical setting.(c) 2022 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
AB - Background and aims: In cirrhosis, decreased portal flow velocity, thrombophilia factors, and portal hyper-tension are considered risk factors for portal vein thrombosis (PVT). In cirrhosis, the transformation of the stellate cells causes a progressive decrease of ADAMTS-13, while VWF multimers secretion by endothelial cells is strongly enhanced. This imbalance leads to an accumulation of ultra-large VWF multimers that in sinusoidal circulation could favor PVT both in intra-and extra-hepatic branches, mostly in decompensated cirrhosis. This prospective study was aimed at identifying possible clinical, biochemical, and hemostatic factors predictive for non-tumoral PVT in a cohort of patients with compensated cirrhosis.Methods: Seventynine compensated cirrhosis patients were prospectively followed for 48 months, receiv-ing a periodic Doppler-ultrasound liver examination associated with an extensive evaluation of clinical, biochemical, and hemostatic profile.Results: Five patients developed PVT (cumulative prevalence = 6.3%), occurring 4-36 months after enroll-ment. In logistic regression analysis, the ADAMTS-13/VWF:GpIbR ratio < 0.4 was the only independent variable significantly associated with PVT (OR 14.6, 95% C.I.:1.36-157.2, p = 0.027). A Cox-regression -analysis confirmed this finding (HR = 7.7, p = 0.027).Conclusions: The ADAMTS-13/VWF ratio < 0.4 measured in compensated cirrhosis could be a reliable predictive biomarker for PVT development, paving the way to novel therapeutic strategies to prevent and treat PVT in this clinical setting.(c) 2022 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
KW - ADAMTS-13
KW - Cirrhosis
KW - Portal vein thrombosis
KW - Von Willebrand factor
KW - ADAMTS-13
KW - Cirrhosis
KW - Portal vein thrombosis
KW - Von Willebrand factor
UR - http://hdl.handle.net/10807/231850
U2 - 10.1016/j.dld.2022.06.004
DO - 10.1016/j.dld.2022.06.004
M3 - Article
SN - 1590-8658
VL - 54
SP - 1672
EP - 1680
JO - Digestive and Liver Disease
JF - Digestive and Liver Disease
ER -