Von Willebrand and Factor VIII Portosystemic Circulation Gradient in Cirrhosis: Implications for Portal Vein Thrombosis

Clin Transl Gastroenterol. 2020 Feb;11(2):e00123. doi: 10.14309/ctg.0000000000000123.

Abstract

Objectives: Portal vein thrombosis seems to be dependent on local hypercoagulation and venous stasis; data regarding endothelial damage are lacking.

Methods: von Willebrad factor, a marker of endothelial damage/perturbation, factor VIII, and lipopolysaccharides (LPS) were studied in the portal and systemic circulation of 20 cirrhotic patients undergoing transjugular intrahepatic portosystemic procedure.

Results: von Willebrad factor, factor VIII, and LPS were higher in the portal compared with systemic circulation, with a significant correlation between LPS and the other 2 variables.

Discussion: Endothelial damage and hypercoagulation coexist in the portal tree of patients with cirrhosis, and both could contribute to portal vein thrombosis. LPS may be a potential trigger of endothelial damage.

Publication types

  • Observational Study

MeSH terms

  • Adult
  • Aged
  • Biomarkers / blood
  • Biomarkers / metabolism
  • Endothelium, Vascular / pathology
  • Enzyme-Linked Immunosorbent Assay
  • Factor VIII / analysis*
  • Factor VIII / metabolism
  • Female
  • Humans
  • Liver Cirrhosis / blood
  • Liver Cirrhosis / complications*
  • Male
  • Middle Aged
  • Portal Vein / pathology*
  • Portal Vein / surgery
  • Portasystemic Shunt, Transjugular Intrahepatic
  • Venous Thrombosis / blood
  • Venous Thrombosis / diagnosis*
  • Venous Thrombosis / etiology
  • Venous Thrombosis / surgery
  • von Willebrand Factor / analysis*
  • von Willebrand Factor / metabolism

Substances

  • Biomarkers
  • von Willebrand Factor
  • F8 protein, human
  • Factor VIII