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Nonmalignant portal vein thrombi in patients with cirrhosis consist of intimal fibrosis with or without a fibrin-rich thrombus

  • Ellen G. Driever
  • , Fien A. von Meijenfeldt
  • , Jelle Adelmeijer
  • , Robbert J. de Haas
  • , Marius C. van den Heuvel
  • , Chandrasekaran Nagasami
  • , John W. Weisel
  • , Constantino Fondevila
  • , Robert J. Porte
  • , Anabel Blasi
  • , Nigel Heaton
  • , Stephen Gregory
  • , Pauline Kane
  • , William Bernal
  • , Yoh Zen
  • , Ton Lisman*
  • *Corresponding author for this work
  • University Medical Centre Groningen
  • UPenn School of Medicine
  • University of Barcelona
  • King’s College Hospital

Research output: Contribution to journalArticleAcademicpeer-review

52 Citations (Scopus)
30 Downloads (Pure)

Abstract

Background and Aim: Portal vein thrombosis (PVT) is a common complication of cirrhosis. The exact pathophysiology remains largely unknown, and treatment with anticoagulants does not lead to recanalization of the portal vein in all patients. A better insight into the structure and composition of portal vein thrombi may assist in developing strategies for the prevention and treatment of PVT. Approach and Results: Sixteen prospectively and 63 retrospectively collected nonmalignant portal vein thrombi from patients with cirrhosis who underwent liver transplantation were included. Histology, immunohistochemistry, and scanning electron microscopy were used to assess structure and composition of the thrombi. Most recent CT scans were reanalyzed for thrombus characteristics. Clinical characteristics were related to histological and radiological findings. All samples showed a thickened, fibrotic tunica intima. Fibrin-rich thrombi were present on top of the fibrotic intima in 9/16 prospective cases and in 21/63 retrospective cases. A minority of the fibrotic areas stained focally positive for fibrin/fibrinogen (16% of cases), von Willebrand factor (VWF; 10%), and CD61 (platelets, 21%), while most of the fibrin-rich areas stained positive for those markers (fibrin/fibrinogen, 100%; VWF, 77%; CD61, 100%). No associations were found between clinical characteristics including estimated thrombus age and use of anticoagulants and presence of fibrin-rich thrombi. Conclusion: We demonstrate that PVT in patients with cirrhosis consists of intimal fibrosis with an additional fibrin-rich thrombus in only one-third of cases. We hypothesize that our observations may explain why not all portal vein thrombi in patients with cirrhosis recanalize by anticoagulant therapy.

Original languageEnglish
Pages (from-to)898-911
Number of pages14
JournalHepatology
Volume75
Issue number4
DOIs
Publication statusPublished - Apr 2022
Externally publishedYes

Bibliographical note

Funding Information:
Supported in part by the Dutch Thrombosis Foundation (Trombosestichting Nederland; 2018‐02).

Publisher Copyright:
© 2021 The Authors. Hepatology published by Wiley Periodicals LLC on behalf of American Association for the Study of Liver Diseases.

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