Predicting portal thrombosis in cirrhosis: A prospective study of clinical, ultrasonographic and hemostatic factors.
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BORIS DOI
Date of Publication
December 2021
Publication Type
Article
Division/Institute
Contributor
Turon, Fanny | |
Driever, Ellen G | |
Baiges, Anna | |
Cerda, Eira | |
García-Criado, Ángeles | |
Gilabert, Rosa | |
Bru, Concepció | |
Nuñez, Isabel | |
Orts, Lara | |
Reverter, Juan Carlos | |
Magaz, Marta | |
Camprecios, Genis | |
Olivas, Pol | |
Betancourt-Sanchez, Fabian | |
Perez-Campuzano, Valeria | |
Blasi, Annabel | |
Seijo, Susana | |
Reverter, Enric | |
Borràs, Roger | |
Hernandez-Gea, Virginia | |
Lisman, Ton | |
Garcia-Pagan, Juan Carlos |
Subject(s)
Series
Journal of hepatology
ISSN or ISBN (if monograph)
1600-0641
Publisher
Elsevier
Language
English
Publisher DOI
PubMed ID
34333101
Uncontrolled Keywords
Description
BACKGROUND & AIMS
Portal vein thrombosis (PVT) is a relatively frequent event in patients with cirrhosis. While different risk factors for PVT have been reported, such as decreased portal blood flow velocity (PBFV) and parameters related with severity of portal hypertension, these are based on retrospective studies assessing only a discrete number of parameters. The aim of the current study was to evaluate the incidence and risks factors for non-tumoral PVT development in a large prospective cohort of patients with cirrhosis.
METHODS
We performed an exhaustive evaluation of clinical, biochemical, inflammatory and acquired/hereditary hemostatic profiles in 369 patients with cirrhosis without PVT who were prospectively followed-up. Doppler ultrasound was performed at baseline and every 6 months or whenever clinically indicated. PVT development was always confirmed by computed tomography.
RESULTS
Twenty-nine patients developed non-tumoral PVT, with an incidence of 1.6%, 6% and 8.4% at 1, 3 and 5 years, respectively. Low platelet count, PBFV <15 cm/sec and history of variceal bleeding were factors independently associated with a high PVT risk. No relationship between PVT development and any other clinical biochemical, inflammatory and acquired or hereditary hemostatic parameter was found.
CONCLUSIONS
In patients with cirrhosis, the factors predictive of PVT development were mainly those related to the severity of portal hypertension. Our results do not support the role of hemostatic alterations (inherited or acquired) and inflammatory markers in the prediction of PVT in patients with cirrhosis.
LAY SUMMARY
Patients with cirrhosis and more severe portal hypertension are at higher risk of non-tumoral portal vein thrombosis development. Acquired or inherited hemostatic disorders, as well as inflammatory status, do not seem to predict the development of portal vein thrombosis in patients with cirrhosis.
Portal vein thrombosis (PVT) is a relatively frequent event in patients with cirrhosis. While different risk factors for PVT have been reported, such as decreased portal blood flow velocity (PBFV) and parameters related with severity of portal hypertension, these are based on retrospective studies assessing only a discrete number of parameters. The aim of the current study was to evaluate the incidence and risks factors for non-tumoral PVT development in a large prospective cohort of patients with cirrhosis.
METHODS
We performed an exhaustive evaluation of clinical, biochemical, inflammatory and acquired/hereditary hemostatic profiles in 369 patients with cirrhosis without PVT who were prospectively followed-up. Doppler ultrasound was performed at baseline and every 6 months or whenever clinically indicated. PVT development was always confirmed by computed tomography.
RESULTS
Twenty-nine patients developed non-tumoral PVT, with an incidence of 1.6%, 6% and 8.4% at 1, 3 and 5 years, respectively. Low platelet count, PBFV <15 cm/sec and history of variceal bleeding were factors independently associated with a high PVT risk. No relationship between PVT development and any other clinical biochemical, inflammatory and acquired or hereditary hemostatic parameter was found.
CONCLUSIONS
In patients with cirrhosis, the factors predictive of PVT development were mainly those related to the severity of portal hypertension. Our results do not support the role of hemostatic alterations (inherited or acquired) and inflammatory markers in the prediction of PVT in patients with cirrhosis.
LAY SUMMARY
Patients with cirrhosis and more severe portal hypertension are at higher risk of non-tumoral portal vein thrombosis development. Acquired or inherited hemostatic disorders, as well as inflammatory status, do not seem to predict the development of portal vein thrombosis in patients with cirrhosis.
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File | File Type | Format | Size | License | Publisher/Copright statement | Content | |
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1-s2.0-S0168827821019462-main.pdf | text | Adobe PDF | 754.73 KB | publisher | published |