Unchanged global fibrinolytic capacity during the course of hematopoietic stem cell transplantation


Aksu S., BEYAZIT Y., Haznedaroglu I., Goker H., KEKİLLİ M., Karakaya J., ...Daha Fazla

BLOOD COAGULATION & FIBRINOLYSIS, cilt.17, sa.1, ss.47-51, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 17 Sayı: 1
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1097/01.mbc.0000200521.71046.d6
  • Dergi Adı: BLOOD COAGULATION & FIBRINOLYSIS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.47-51
  • Anahtar Kelimeler: hematopoietic stem cell transplantation, hematopoietic, fibrinolysis, global fibrinolytic capacity, global fibro cap, BONE-MARROW-TRANSPLANTATION, HEPATIC VENOOCCLUSIVE DISEASE, ACTIVATOR INHIBITOR PAI-1, PLASMINOGEN-ACTIVATOR, ENDOTHELIAL MARKERS, COAGULATION PROFILE, PROTHROMBOTIC STATE, BEHCETS-DISEASE, HOST-DISEASE, PROTEIN-C
  • Gazi Üniversitesi Adresli: Hayır

Özet

Hemostatic changes due to vascular endothelial damage are seen during the course of hematopoietic stem cell transplantation (HSCT). The fibrinolytic response to ongoing hemostatic activation in HSCT remains to be elucidated. Global fibrinolytic capacity (GFC) is a novel method, which reflects the amount of generated D-dimer when fibrinolysis of a freeze-dried fibrin clot is stopped by introducing aprotinin. GFC is sensitive to all the factors involved in the process of fibrinolysis. The aim of this study was to serially assess GFC at certain critical time points (days -1, +7, +14, +21 prior to and following stem cell infusion) during the course of HSCT. The study group comprised 16 patients with hematological malignancies (11 women, five men; median age 32 +/- 9 years) in whom HSCT had been performed. Thirty healthy adults (21 women, nine men; median age 31 +/- 7 years) served as controls. In this study, global fibrinolytic response, as reflected by GFC, was unchanged despite ongoing hemostatic activation, as indicated by D-dimer, moreover GFC remained stable, despite the development of thrombocytopenia associated with HSCT prior to platelet engraftment. Our results indicate that a global fibrinolytic response was impaired as a compensatory response to endothelial activation and to other hemostatic changes seen in HSCT. Further studies in larger HSCT populations are warranted to better understand the implications of these findings.