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- W3204753780 abstract "Predicting portal thrombosis in cirrhosis: A prospective study of clinical, ultrasonographic and hemostatic factorsJournal of HepatologyVol. 75Issue 6PreviewPortal 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. Full-Text PDF Open AccessMinor role of hemostatic alternation in portal vein thrombosis pathogenesis revealed by global measurementJournal of HepatologyVol. 76Issue 1PreviewWe read with great interest the article by Turon et al. recently published in Journal of Hepatology.1 The authors comprehensively evaluated the risk factors for portal vein thrombosis (PVT) in patients with cirrhosis, including clinical and ultrasonographic parameters, hemostatic alterations and inflammatory markers. Data indicated that only those factors related to the severity of portal hypertension were associated with PVT development. Full-Text PDF Predicting portal thrombosis in cirrhosis: Some issuesJournal of HepatologyVol. 76Issue 1PreviewWe read with great interest the excellent manuscript based on a prospective study recently published by Turon F et al.1 In the 369 patients with cirrhosis without portal vein thrombosis (PVT), 29 patients developed non-tumoral PVT with reported incidences of 1.6%, 6.0% and 8.4% at 1, 3 and 5 years, respectively. In evaluating the incidence and risk factors for PVT development, the authors have concluded that platelet count, decreased portal blood flow velocity (PBFV) (<15 cm/sec) and history of variceal bleeding, rather than acquired or inherited hemostatic disorders and inflammatory status, were factors independently associated with a high PVT risk. Full-Text PDF We thank Li et al.[1]Li B. He Q. Lu G. Hong C. Chen J. Minor role of hemostatic alternation in portal vein thrombosis pathogenesis revealed by global measurement.J Hepatol. 2022; 76: 225-227Abstract Full Text Full Text PDF Scopus (1) Google Scholar and Dai et al.[2]Dai C.-Y. Chuang W.-L. Yu M.-L. Predicting portal thrombosis in cirrhosis: some issues.J Hepatol. 2022; 76: 224-225Abstract Full Text Full Text PDF Scopus (1) Google Scholar for their interest in our recent publication in the Journal of Hepatology.[3]Turon F. Driever E.G. Baiges A. Cerda E. García-Criado Á. Gilabert R. et al.Predicting portal thrombosis in cirrhosis: a prospective study of clinical, ultrasonographic and hemostatic factors.J Hepatol. 2021; 75: 1367-1376Abstract Full Text Full Text PDF Scopus (50) Google Scholar Li et al. reported the results of a thromboelastography assay in 58 patients with cirrhosis undergoing transjugular intrahepatic portosystemic shunt, 12 of whom had portal vein thrombosis (PVT). No differences in thromboelastography were found between the 12 patients with PVT and the 46 without. Despite this being a different scenario from ours, their results reinforced our finding that hemostatic alterations are not the main risk factors for PVT. In addition, the authors report decreased platelet responses and propose that antiplatelet therapy would likely be ineffective in prevention or treatment of PVT. It has to be noted, however, that platelet function tests in thrombocytopenic blood likely underestimate true platelet reactivity, and that normal to enhanced platelet responses in patients with cirrhosis have been reported using different methodology.[4]Caldwell S. Lisman T. The cirrhotic platelet: shedding light on an enigma.Hepatology. 2017; 65: 407-410Crossref PubMed Scopus (16) Google Scholar We agree that mechanisms underlying PVT development require further exploration. Of note, we have recently demonstrated that the portal vein thrombus frequently does not consist of typical thrombus components such as platelets and fibrin. Rather, we showed the thrombus to consist, at least partly, of collagenous thickening of the portal vein intima. These results also suggest that the role of coagulation activation in PVT is more minor than previously thought.[5]Driever E.G. von Meijenfeldt F.A. Adelmeijer J. de Haas R.J. van den Heuvel M.C. Nagasami C. et al.Non-malignant portal vein thrombi in patients with cirrhosis consist of intimal fibrosis with or without a fibrin-rich thrombus.Hepatology. 2021; https://doi.org/10.1002/hep.32169Crossref Scopus (21) Google Scholar Dai et al. highlighted the relevance of plasma levels of Factor X as an independent significant factor for PVT. However, we would like to point out that the higher risk of PVT was in patients with lower levels of pro-coagulant Factor X, suggesting that this is a further sign of severity of liver disfunction more than a reflection of increased hypercoagulability. That is why we did not consider it appropriate to further explore Factor X in stratified groups as they suggested. Additionally, patients undergoing surgical procedures, such as splenectomy or devascularization for the treatment of portal hypertension were excluded from our study because these are extremely rare procedures in the setting of cirrhosis in western countries; these special sub-populations fall beyond the objective our study. The occurrence of PVT in these surgical settings is also frequently acute, whereas the development of ‘non-provoked’ PVT is usually more chronic. The pathogenesis of surgery-associated PVT in patients with cirrhosis may therefore be different from that of non-provoked PVT. The role of anticoagulant therapy in prevention of surgery-associated PVT remains to be established. Importantly, it has been demonstrated that surgery-associated PVT in patients without cirrhosis is efficiently reduced by anticoagulant therapy.[6]Yamashita Y.I. Bekki Y. Imai D. Ikegami T. Yoshizumi T. Ikeda T. et al.Efficacy of postoperative anticoagulation therapy with enoxaparin for portal vein thrombosis after hepatic resection in patients with liver cancer.Thromb Res. 2014; 134: 826-831Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar The authors received no financial support to produce this manuscript. All authors drafted and approved the final manuscript. JCGP is a consultant for GORE and research grants from NOVARTIS. Please refer to the accompanying ICMJE disclosure forms for further details. The following is the supplementary data to this article: Download .pdf (.17 MB) Help with pdf files Multimedia component 1" @default.
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- W3204753780 title "Reply to: Correspondence on “Predicting portal thrombosis in cirrosis: A prospective study of clinical, ultrasonographic and hemostatic factors”" @default.
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