Impaired fibrinolysis as a risk factor for Budd-Chiari syndrome

Blood

Volumn 115, Issue 2, 2010, Pages 388-395

  Hoekstra, Jildou ^a   Guimarães, Ana H C ^a   Leebeek, Frank W G ^a   Murad, Sarwa Darwish ^a   Malfliet, Joyce J M C ^a   Plessier, Aurelie ^b   Hernandez Guerra, Manuel ^c   Langlet, Philippe ^d   Elias, Elwyn ^e   Trebicka, Jonel ^f   Primignani, Massimo ^g   Garcia Pagan, Juan Carlos ^c   Valla, Dominique C ^b   Rijken, Dingeman C ^a   Janssen, Harry L A ^a  

^a ERASMUS MEDICAL CENTER   (Netherlands)

^b ASSISTANCE PUBLIQUE HÔPITAUX DE PARIS   (France)

^c INSTITUT D INVESTIGACIONS BIOMÈDIQUES AUGUST PI I SUNYER IDIBAPS   (Spain)

^d BRUGMANN UNIVERSITY HOSPITAL   (Belgium)

^e QUEEN ELIZABETH HOSPITAL   (United Kingdom)

^f UNIVERSITY HOSPITAL BONN   (Germany)

^g FONDAZIONE IRCCS CA GRANDA OSPEDALE MAGGIORE POLICLINICO   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

PLASMIN INHIBITOR; PLASMINOGEN ACTIVATOR INHIBITOR 1; THROMBIN ACTIVATABLE FIBRINOLYSIS INHIBITOR; ANTIFIBRINOLYTIC AGENT;

ADOLESCENT; ADULT; AGED; ARTICLE; BLOOD CLOT LYSIS; BUDD CHIARI SYNDROME; CONTROLLED STUDY; ENZYME BLOOD LEVEL; FEMALE; FIBRINOLYSIS; HUMAN; MAJOR CLINICAL STUDY; MALE; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; RISK ASSESSMENT; RISK FACTOR; SINGLE NUCLEOTIDE POLYMORPHISM; BLOOD; BLOOD CLOTTING TEST; CLINICAL TRIAL; GENETICS; INFERIOR CAVA VEIN; METABOLISM; METHODOLOGY; MIDDLE AGED; MULTICENTER STUDY; PROSPECTIVE STUDY;

ADOLESCENT; ADULT; AGED; AGED, 80 AND OVER; ANTIFIBRINOLYTIC AGENTS; BLOOD COAGULATION TESTS; BUDD-CHIARI SYNDROME; CARBOXYPEPTIDASE U; FEMALE; FIBRINOLYSIS; HUMANS; MALE; MIDDLE AGED; PLASMINOGEN ACTIVATOR INHIBITOR 1; POLYMORPHISM, SINGLE NUCLEOTIDE; PROSPECTIVE STUDIES; RISK FACTORS; VENA CAVA, INFERIOR;

EID: 75649107875     PISSN: 00064971     EISSN: 15280020     Source Type: Journal    
DOI: 10.1182/blood-2009-03-211557     Document Type: Article

References (53)

1. Janssen HL, Garcia-Pagan JC, Elias E, Mentha G, Hadengue A, Valla DC. Budd-Chiari syndrome: a review by an expert panel. J Hepatol. 2003;38(3):364-371.
2. Deltenre P, Denninger MH, Hillaire S, et al. Factor V: Leiden related Budd-Chiari syndrome. Gut. 2001;48(2):264-268.
3. Janssen HL, Meinardi JR, Vleggaar FP, et al. Factor V: Leiden mutation, prothrombin gene mutation, and deficiencies in coagulation inhibitors associated with Budd-Chiari syndrome and portal vein thrombosis: results of a case-control study. Blood. 2000;96(7):2364-2368.
4. Smalberg JH, Murad SD, Braakman E, Valk PJ, Janssen HL, Leebeek FW. Myeloproliferative disease in the pathogenesis and survival of Budd-Chiari syndrome. Haematologica. 2006;91(12):1712-1713.
5. Denninger MH, Chait Y, Casadevall N, et al. Cause of portal or hepatic venous thrombosis in adults: the role of multiple concurrent factors. Hepatology. 2000;31(3):587-591.
6. Murad SD, Plessier A, Hernandez-Guerra M, et al. Etiology, management, and outcome of the Budd-Chiari syndrome. Ann Intern Med. 2009;151(3):167-175.
7. Hadengue A, Poliquin M, Vilgrain V, et al. The changing scene of hepatic vein thrombosis: recognition of asymptomatic cases. Gastroenterology. 1994;106(4):1042-1047.
8. Valla D, Casadevall N, Lacombe C, et al. Primary myeloproliferative disorder and hepatic vein thrombosis: a prospective study of erythroid colony formation in vitro in 20 patients with Budd-Chiari syndrome. Ann Intern Med. 1985;103(3):329-334.
9. Rijken DC. Plasminogen activators and plasminogen activator inhibitors: biochemical aspects. Baillieres Clin Haematol. 1995;8(2):291-312.
10. Cesarman-Maus G, Hajjar KA. Molecular mechanisms of fibrinolysis. Br J Haematol. 2005;129(3):307-321.
11. Eichinger S, Schonauer V, Weltermann A, et al. Thrombin-activatable fibrinolysis inhibitor and the risk for recurrent venous thromboembolism. Blood. 2004;103(10):3773-3776.
12. Erickson LA, Fici GJ, Lund JE, Boyle TP, Polites HG, Marotti KR. Development of venous occlusions in mice transgenic for the plasminogen activator inhibitor-1 gene. Nature. 1990;346(6279):74-76.
13. Folsom AR, Cushman M, Heckbert SR, Rosamond WD, Aleksic N. Prospective study of fibrinolytic markers and venous thromboembolism. J Clin Epidemiol. 2003;56(6):598-603.
14. Nilsson IM, Ljungner H, Tengborn L. Two different mechanisms in patients with venous thrombosis and defective fibrinolysis: low concentration of plasminogen activator or increased concentration of plasminogen activator inhibitor. Br Med J (Clin Res Ed). 1985;290(6480):1453-1456.
15. van Tilburg NH, Rosendaal FR, Bertina RM. Thrombin activatable fibrinolysis inhibitor and the risk for deep vein thrombosis. Blood. 2000;95(9):2855-2859.
16. Lisman T, de Groot PG, Meijers JC, Rosendaal FR. Reduced plasma fibrinolytic potential is a risk factor for venous thrombosis. Blood. 2005;105(3):1102-1105.
17. Meltzer ME, Lisman T, Doggen CJ, de Groot PG, Rosendaal FR. Synergistic effects of hypofibrinolysis and genetic and acquired risk factors on the risk of a first venous thrombosis. PLoS Med. 2008;5(5):e97.
18. Murad SD, Valla DC, de Groen PC, et al. Determinants of survival and the effect of portosystemic shunting in patients with Budd-Chiari syndrome. Hepatology. 2004;39(2):500-508.
19. Clauss A. [Rapid physiological coagulation method in determination of fibrinogen.] Acta Haematol. 1957;17(4):237-246.
20. Brunner J, Skrabal P, Hauser H. Single bilayer vesicles prepared without sonication: physicochemical properties. Biochim Biophys Acta. 1976;455(2):322-331.
21. Van Wijnen M, Stam JG, Chang GT, et al. Characterization of mini-protein S, a recombinant variant of protein S that lacks the sex hormone binding globulin-like domain. Biochem J. 1998;330(1):389-396.
22. Thomas A, Lamlum H, Humphries S, Green F. Linkage disequilibrium across the fibrinogen locus as shown by five genetic polymorphisms, G/A-455 (HaeIII), C/T-148 (HindIII/AluI), T/G+689 (AvaII), and BclI (beta-fibrinogen) and TaqI (alpha-fibrinogen), and their detection by PCR. Hum Mutat. 1994;3(1):79-81.
23. Dawson S, Hamsten A, Wiman B, Henney A, Humphries S. Genetic variation at the plasminogen activator inhibitor-1 locus is associated with altered levels of plasma plasminogen activator inhibitor-1 activity. Arterioscler Thromb. 1991;11(1):183-190.
24. Mikkola H, Syrjala M, Rasi V, et al. Deficiency in the A-subunit of coagulation factor XIII: two novel point mutations demonstrate different effects on transcript levels. Blood. 1994;84(2):517-525.
25. Brouwers GJ, Vos HL, Leebeek FW, et al. A novel, possibly functional, single nucleotide polymorphism in the coding region of the thrombinactivatable fibrinolysis inhibitor (TAFI) gene is also associated with TAFI levels. Blood. 2001;98(6):1992-1993.
26. Henry M, Aubert H, Morange PE, et al. Identification of polymorphisms in the promoter and the 3′ region of the TAFI gene: evidence that plasma TAFI antigen levels are strongly genetically controlled. Blood. 2001;97(7):2053- 2058.
27. Ladenvall P, Wall U, Jern S, Jern C. Identification of eight novel single-nucleotide polymorphisms at human tissue-type plasminogen activator (t-PA) locus: association with vascular t-PA release in vivo. Thromb Haemost. 2000;84(2):150-155.
28. Bombeli T, Jutzi M, De Conno E, Seifert B, Fehr J. In patients with deep-vein thrombosis elevated levels of factor VIII correlate only with von Willebrand factor but not other endothelial cell-derived coagulation and fibrinolysis proteins. Blood Coagul Fibrinolysis. 2002;13(7):577-581.
29. Schulman S, Wiman B. The significance of hypo-fibrinolysis for the risk of recurrence of venous thromboembolism: Duration of Anticoagulation (DURAC) Trial Study Group. Thromb Haemost. 1996;75(4):607-611.
30. Jorgensen M, Bonnevie-Nielsen V. Increased concentration of the fast-acting plasminogen activator inhibitor in plasma associated with familial venous thrombosis. Br J Haematol. 1987;65(2):175-180.
31. Crowther MA, Roberts J, Roberts R, et al. Fibrinolytic variables in patients with recurrent venous thrombosis: a prospective cohort study. Thromb Haemost. 2001;85(3):390-394.
32. Ridker PM, Vaughan DE, Stampfer MJ, et al. Baseline fibrinolytic state and the risk of future venous thrombosis: a prospective study of endogenous tissue-type plasminogen activator and plasminogen activator inhibitor. Circulation. 1992;85(5):1822-1827.
33. Booth NA. Fibrinolysis and thrombosis. Baillieres Best Pract Res Clin Haematol. 1999;12(3):423-433.
34. Chandler WL, Trimble SL, Loo SC, Mornin D. Effect of PAI-1 levels on the molar concentrations of active tissue plasminogen activator (t-PA) and t-PA/PAI-1 complex in plasma. Blood. 1990;76(5):930-937.
35. Leebeek FW, Kluft C, Knot EA, de Maat MP, Wilson JH. A shift in balance between profibrinolytic and antifibrinolytic factors causes enhanced fibrinolysis in cirrhosis. Gastroenterology. 1991;101(5):1382-1390.
36. Dayal S, Pati HP, Sharma MP. Tissue plasminogen activator and plasminogen activator inhibitor status in Budd-Chiari syndrome. Haemostasis. 1996;26(5):284-287.
37. Posan E, Ujj G, Kiss A, Telek B, Rak K, Udvardy M. Reduced in vitro clot lysis and release of more active platelet PAI-1 in polycythemia vera and essential thrombocythemia. Thromb Res. 1998;90(2):51-56.
38. Cancelas JA, Garcia-Avello A, Garcia-Frade LJ. High plasma levels of plasminogen activator inhibitor 1 (PAI-1) in polycythemia vera and essential thrombocythemia are associated with thrombosis. Thromb Res. 1994;75(5):513-520.
39. Schafer AI. Bleeding and thrombosis in the myeloproliferative disorders. Blood. 1984;64(1):1-12.
40. Takahashi H, Hattori A, Shibata A. Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders. Tohoku J Exp Med. 1982;138(1):71-80.
41. Anwar R, Miloszewski KJ. Factor XIII deficiency. Br J Haematol. 1999;107(3):468-484.
42. Van Hylckama Vlieg A, Komanasin N, Ariens RA, et al. Factor XIII Val34Leu polymorphism, factor XIII antigen levels and activity and the risk of deep venous thrombosis. Br J Haematol. 2002;119(1):169-175.
43. Lisman T, Leebeek FW. Hemostatic alterations in liver disease: a review on pathophysiology, clinical consequences, and treatment. Dig Surg. 2007;24(4):250-258.
44. Simpson AJ, Booth NA, Moore NR, Bennett B. Distribution of plasminogen activator inhibitor (PAI-1) in tissues. J Clin Pathol. 1991;44(2):139-143.
45. Kruithof EK, Gudinchet A, Bachmann F. Plasminogen activator inhibitor 1 and plasminogen activator inhibitor 2 in various disease states. Thromb Haemost. 1988;59(1):7-12.
46. Martini CH, Brandts A, de Bruijne EL, et al. The effect of genetic variants in the thrombin activatable fibrinolysis inhibitor (TAFI) gene on TAFIantigen levels, clot lysis time and the risk of venous thrombosis. Br J Haematol. 2006;134(1):92-94.
47. Tsantes AE, Nikolopoulos GK, Bagos PG, et al. Association between the plasminogen activator inhibitor-1 4G/5G polymorphism and venous thrombosis: a meta-analysis. Thromb Haemost. 2007;97(6):907-913.
48. Wells PS, Anderson JL, Scarvelis DK, Doucette SP, Gagnon F. Factor XIII Val34Leu variant is protective against venous thromboembolism: a HuGE review and meta-analysis. Am J Epidemiol. 2006;164(2):101-109.
49. de Bruijne EL, Murad SD, de Maat MP, et al. Genetic variation in thrombin-activatable fibrinolysis inhibitor (TAFI) is associated with the risk of splanchnic vein thrombosis. Thromb Haemost. 2007;97(2):181-185.
50. Ladenvall P, Johansson L, Jansson JH, et al. Tissue-type plasminogen activator -7,351C/T enhancer polymorphism is associated with a first myocardial infarction. Thromb Haemost. 2002;87(1):105-109.
51. Lim BC, Ariens RA, Carter AM, Weisel JW, Grant PJ. Genetic regulation of fibrin structure and function: complex gene-environment interactions may modulate vascular risk. Lancet. 2003;361(9367):1424-1431.
52. Boekholdt SM, Sandhu MS, Wareham NJ, Luben R, Reitsma PH, Khaw KT. Fibrinogen plasma levels modify the association between the factor XIII Val34Leu variant and risk of coronary artery disease: the EPIC-Norfolk prospective population study. J Thromb Haemost. 2006;4(10):2204-2209.
53. Vossen CY, Rosendaal FR. The protective effect of the factor XIII Val34Leu mutation on the risk of deep venous thrombosis is dependent on the fibrinogen level. J Thromb Haemost. 2005;3(5):1102-1103.