Fanny Turon1, Ellen G Driever2, Anna Baiges1, Eira Cerda3, Ángeles García-Criado4, Rosa Gilabert4, Concepció Bru4, Annalisa Berzigotti5, Isabel Nuñez4, Lara Orts1, Juan Carlos Reverter6, Marta Magaz1, Genis Camprecios1, Pol Olivas3, Fabian Betancourt-Sanchez3, Valeria Perez-Campuzano3, Annabel Blasi7, Susana Seijo3, Enric Reverter1, Jaume Bosch8, Roger Borràs9, Virginia Hernandez-Gea1, Ton Lisman2, Juan Carlos Garcia-Pagan10. 1. Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain(†); Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. 2. Surgical Research Laboratory, Department of Surgery, University of Groningen, University Medical Center Groningen, The Netherlands. 3. Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain(†). 4. Centre de Diagnostic per l'Imatge, Hospital Clínic, Barcelona, Spain. 5. Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain(†); Centre de Diagnostic per l'Imatge, Hospital Clínic, Barcelona, Spain; Hepatologie, University Clinic for Visceral Surgery and Medicin, Inselspital, Bern, Switzerland. 6. Servei d'Hemoteràpia i hemostàsia, Hospital Clínic, Barcelona, Spain. 7. Servei d'Anestesiologia i reanimació, Hospital Clínic, Barcelona, Spain. 8. Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain(†); Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain; Hepatologie, University Clinic for Visceral Surgery and Medicin, Inselspital, Bern, Switzerland. 9. Arrhythmia Section, Cardiovascular Clinic Institute, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain. 10. Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain(†); Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. Electronic address: jcgarcia@clinic.cat.
Abstract
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.
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.
Authors: Maurice Michel; Alisha Wahl; Malena Anders; Saleh A Alqahtani; Wolfgang M Kremer; Peter R Galle; Christian Labenz; Daniel Grimm; Martin Sprinzl; Jörn M Schattenberg Journal: Qual Life Res Date: 2022-08-22 Impact factor: 3.440
Authors: Hannah McMurry; Jean M G Sabile; Benjamin Elstrott; Boris Chobrutskiy; Ajay Mohinani; Sarah Patel; Sonia Gowda; Kylee Martens; Joseph Shatzel Journal: Thromb Res Date: 2022-05-27 Impact factor: 10.407
Authors: Ellen G Driever; Marta Magaz; Jelle Adelmeijer; Fanny Turon; Anna Baiges; Pol Olivas; Valeria Pérez-Campuzano; Virginia Hernandez-Gea; Annabel Blasi; Juan-Carlos Garcia-Pagan; Ton Lisman Journal: J Thromb Haemost Date: 2022-07-11 Impact factor: 16.036