medigraphic.com

2012, Número 1

<< Anterior Siguiente >>

Rev Hematol Mex 2012; 13 (1)


Tromboscopia calibrada automatizada en el estudio de los trastornos de la hemostasia

Coenraad HH, Jaloma CAR

Idioma: Español
Referencias bibliográficas: 34
Paginas: 25-31
Archivo PDF: 120.96 Kb.


RESUMEN

Por sus múltiples funciones, la trombina es la molécula “clave” del mecanismo hemostático que incluye actividades pro y anticoagulantes y efectos pro-inflamatorios. La generación de trombina es una prueba de la capacidad hemostática de la sangre como órgano aislado (el plasma). A diferencia de los tiempos de coagulación (TP, TTPa, TCST), también detecta la hiperfunción o tendencia trombótica, clínicamente mucho más relevante que la tendencia hemorrágica. La capacidad del plasma para generar trombina se refleja en la curva de generación de trombina (trombograma) y particularmente en el potencial de trombina endógeno (PTE), que corresponde al área bajo la curva de generación de trombina y medida directa de su “trabajo enzimático”. El ensayo actualmente disponible, la trombografía calibrada automatizada (CAT), permite una prueba rutinaria cuantitativamente correcta (imprecisión 2.5 - 4%) de la medición de la curva de generación de trombina a bajo costo y alto rendimiento. Las aplicaciones alternativas son semicuantitativas o requieren de inhibidores de la polimerización de la fibrina con fuerte influencia en la generación normal de trombina.
El monitorieo del trombograma permite: i)detectar una trombosis en curso; ii) detectar riesgo incrementado de trombosis; iii) monitorear el tratamiento antitrombótico; iv) detectar trastornos hemorrágicos y monitorear su profilaxis y terapia. A pesar de que las trombosis arteriales y venosas muestran diferencias importantes, la generación de trombina puede cubrir todas estas indicaciones. Especialmente cuando el ensayo se realiza no solamente en plasma pobre en plaquetas, sino con plasma rico en plaquetas o sangre total, que es una técnica en desarrollo.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Eikelboom JW, Hirsh J. Monitoring unfractionated heparin with the aPTT: time for a fresh look. Thromb Haemost 2006;96:547-552.

  2. Al Dieri R, Alban S, Béguin S, Hemker HC. Thrombin generation for the control of heparin treatment, comparison with the activated partial thromboplastin time. J Thromb Haemost 2004;2:1395-1401.

  3. Kessels H, Kester AD, Hemker HC. Intrinsic and methodinduced variation of the bleeding time and related parameters [letter]. Thromb Haemost 1994;71:798-799.

  4. Bohn RL, Schramm W, Bullinger M, van den Berg M, Blanchette V. Outcome measures in haemophilia: more than just factor levels. Haemophilia 2004;10 Suppl 1:2-8.

  5. Beltran-Miranda CP, Khan A, Jaloma-Cruz AR, Laffan MA. Thrombin generation and phenotypic correlation in haemophilia A. Haemophilia 2005;11:326-334.

  6. Biggs R, Macfarlane RG. Human Blood Coagulation and its Disorders. Blackwell, Oxford, 1953.

  7. Béguin S, Lindhout T, Hemker HC. The mode of action of heparin in plasma. Thromb Haemost 1988;60(3): 457-62.

  8. Béguin S, Mardiguian J, Lindhout T, Hemker HC. The mode of action of low molecular weight heparin preparation (PK10169) and two of its major components on thrombin generation in plasma. Thromb Haemost 1989; 61(1):30-34.

  9. Hemker HC. Recollections on thrombin generation. J Thromb Haemost 2008;6:219-226.

  10. Hemker HC, Willems GM, Béguin S. A computer assisted method to obtain the prothrombin activation velocity in whole plasma independent of thrombin decay processes. Thromb Haemost 1986;56(1):9-17.

  11. Béguin S, Lindhout T, Hemker HC. The effect of trace amounts of tissue factor on thrombin generation in platelet rich plasma, its inhibition by heparin. Thromb Haemost 1989;61(1):25-29.

  12. Hemker HC, Wielders S, Kessels H, Béguin S. Continuous registration of thrombin generation in plasma, its use for the determination of the thrombin potential. Thromb Haemost 1993;70(4):617-624.

  13. Hemker HC, Giesen PLA, Ramjee M, Wagenvoord R, Béguin S. The Thrombogram: monitoring thrombin generation in platelet rich plasma. Thromb Haemost 2000;83(4):589-591.

  14. Hemker HC, Giesen P, Al Dieri R, et al. Calibrated automated thrombin generation measurement in clotting plasma. Pathophysiol Haemost Thromb 2003;33:4-15.

  15. Bertina RM, Koeleman BP, Koster T, et al. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature 1994;369:64-67.

  16. Rosing J, Tans G, Nicolaes GA, et al. Oral contraceptives and venous thrombosis: different sensitivities to activated protein C in women using second- and third-generation oral contraceptives. Br J Haematol 1997;97:233-238.

  17. Béguin S, Keularts I, Al Dieri R, Bellucci S, Caen J, Hemker HC. Fibrin polymerization is crucial for thrombin generation in plateletrich plasma in a VWF-GPIb-dependent process, defective in Bernard-Soulier syndrome. J Thromb Haemost 2004;2:170-176.

  18. Wielders S, Mukherjee M, Michiels J, et al. The routine determination of the endogenous thrombin potential, first results in different forms of hyper- and hypocoagulability. Thromb Haemost 1997;77:629-636.

  19. Hron G, Kollars M, Binder BR, Eichinger S, Kyrle PA. Identification of patients at low risk for recurrent venous thromboembolism by measuring thrombin generation. JAMA 2006;296:397-402.

  20. Besser M, Baglin C, Luddington R, van Hylckama Vlieg A, Baglin T. High rate of unprovoked recurrent venous thrombosis is associated with high thrombin-generating potential in a prospective cohort study. J Thromb Haemost 2008;6:1720-1725.

  21. ten Cate-Hoek AJ, Dielis AW, Spronk HM, et al. Thrombin generation in patients after acute deep-vein thrombosis. Thromb Haemost 2008;100:240-245.

  22. Tripodi A, Legnani C, Chantarangkul V, Cosmi B, Palareti G, Mannucci PM. High thrombin generation measured in the presence of thrombomodulin is associated with an increased risk of recurrent venous thromboembolism. J Thromb Haemost 2008;6:1327-1333.

  23. Orbe J, Zudaire M, Serrano R, et al. Increased thrombin generation after acute versus chronic coronary disease as assessed by the thrombin generation test. Thromb Haemost 2008;99:382-387.

  24. Puccetti L, Bruni F, Bova G, et al. Effect of diet and treatment with statins on platelet-dependent thrombin generation in hypercholesterolemic subjects. Nutr Metab Cardiovasc Dis 2001;11:378-387.

  25. Al Dieri R, Peyvandi F, Santagostino E, et al. The thrombogram in rare inherited coagulation disorders: its relation to clinical bleeding, Thromb Haemost 2002;88:576-582.

  26. Dargaud Y, Béguin S, Lienhart A, et al. Evaluation of thrombin generating capacity in plasma from patients with haemophilia A and B. Thromb Haemost 2005;93:475-480.

  27. Dargaud Y, Bordet JC, Lienhart A, Negrier C. Use of the thrombin generation test to evaluate response to treatment with recombinant activated factor VII. Semin Hematol 2008;45:S72-73.

  28. Schols SE, van der Meijden PE, van Oerle R, Curvers J, Heemskerk JW, van Pampus EC. Increased thrombin generation and fibrinogen level after therapeutic plasma transfusion: relation to bleeding. Thromb Haemost 2008;99:64-70.

  29. Giesen PL, Rauch U, Bohrmann B, et al. Blood-borne tissue factor: another view of thrombosis. Proc Natl Acad Sci USA 1999;96:2311-2315.

  30. Furie B, Furie BC. Mechanisms of thrombus formation. N Engl J Med 2008;359:938-949.

  31. Hacquard M, Perrinhttp://www.sciencedirect.com/science/article/pii/S0049384810004330 - af0010#af0010 J, Lelievre N, Vigneron C, Lecompte T. Inter-individual variability of effect of 7 low molecular weight antithrombin-dependent anticoagulants studied in vitro with Calibrated Automated Thrombography. Thrombosis Research 2011; 127(1):29-34.

  32. Bostrom SL, Hansson GF, Kjaer M, Sarich TC. Effects of melagatran, the active form of the oral direct thrombin inhibitor ximelagatran, and dalteparin on the endogenous thrombin potential in venous blood from healthy male subjects. Blood Coagul Fibrinolysis 2003;14:457-462.

  33. Al Dieri R, Béguin S, Hemker HC. The ionic contrast medium ioxaglate interferes with thrombin-mediated feedback activation of factor V, factor VIII and platelets. J Thromb Haemost 2003;1:269-274.

  34. Rosing J, Middeldorp S, Curvers J, et al. Low-dose oral contraceptives and acquired resistance to activated protein C: a randomised cross-over study. Lancet 1999;354:2036-2040.




2020     |     www.medigraphic.com