title: Hypercoagulability in patients with chronic noncirrhotic portal vein thrombosis.
abstract: OBJECTIVE
  Although they have normal liver histology and function, patients with chronic noncirrhotic nontumoral portal vein thrombosis (NC-PVT) frequently have abnormal results from coagulation tests. We investigated the significance of these results.
  
  
  METHODS
  We analyzed blood samples collected from 50 stable patients with NC-PVT secondary to a thrombophilic disorder (32%) or local factor (32%), or that was idiopathic (36%). We measured endogenous thrombin potential (ETP) with and without thrombomodulin, prothrombin time, activated partial thromboplastin time, coagulation factors (I, II, V, VII, VIII, IX, X, XI, and XII), antithrombin, proteins C and S, von Willebrand factor (vWF) antigen, vWF ristocetin cofactor, a disintegrin and metalloprotease with thrombospondin type 1 motifs 13 antigen, D-dimer, plasmin-antiplasmin complex, prothrombin fragment F1+2, activated factor VII, and clot lysis time. Samples from 50 age- and sex-matched healthy individuals were evaluated as controls.
  
  
  RESULTS
  Compared with controls, patients with NC-PVT had significant increases in prothrombin time and activated partial thromboplastin time; they had significant reductions in levels of procoagulant factors II, V, VII, IX, X, XI, and XII, and the anticoagulants antithrombin, protein C, and protein S. The patients had increased levels of factor VIII and vWF antigen. Irrespective of etiology, patients with NC-PVT had a significant increase in ETP with thrombomodulin and higher levels of factor VIIa, prothrombin fragment F1+2, D-dimer, and plasmin-antiplasmin complex than controls, indicating in vivo activation of coagulation and fibrinolysis.
  
  
  CONCLUSIONS
  Patients with NC-PVT have hypercoagulability that is independent of the underlying etiology, based on in vitro analyses of thrombin-generation capacity and increased levels of biomarkers in blood samples. Further studies are required to determine if activation of hemostasis increases the risk for thrombotic events.
authors.affiliation: Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona and Centro de Investigación Biomédica en red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain.
authors.forename: Sebastián
authors.initials: S
authors.lastname: Raffa
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Reverter
authors.forename: Susana
authors.initials: S
authors.lastname: Seijo
authors.forename: Dolors
authors.initials: D
authors.lastname: Tassies
authors.forename: Juan G
authors.initials: JG
authors.lastname: Abraldes
authors.forename: Jaume
authors.initials: J
authors.lastname: Bosch
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: García-Pagán
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001779:Blood Coagulation Factors / Q000032:analysis; D002908:Chronic Disease; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010314:Partial Thromboplastin Time; D011169:Portal Vein / Q000473:pathology*; D011517:Prothrombin Time; D019851:Thrombophilia / Q000175:diagnosis*; D013927:Thrombosis / Q000150:complications* / Q000473:pathology; D055815:Young Adult
chemical_list: D001779:Blood Coagulation Factors