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Haemostatic function and biomarkers of endothelial damage before and after platelet transfusion in patients with acute myeloid leukaemia
Author(s) -
Larsen A. M.,
Leinøe E. B.,
Johansson P. I.,
Larsen R.,
Wantzin P.,
Birgens H.,
Ostrowski S. R.
Publication year - 2015
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1111/tme.12209
Subject(s) - thromboelastography , platelet , medicine , thrombomodulin , hematology , endothelium , whole blood , immunology , platelet transfusion , hemostasis , von willebrand factor , platelet activation , gastroenterology , thrombin
SUMMARY Objectives The beneficial effect of platelet transfusion on haemostasis is well established, but there is emerging evidence that platelet transfusion induces an inflammatory response in vascular endothelial cells. Background We investigated haemostatic function and endothelial biomarkers before and after platelet transfusion in patients with acute myeloid leukaemia. Materials and Methods Blood was sampled before, 1 and 24 h after platelet transfusion. Primary and secondary haemostasis was evaluated by whole blood aggregometry (Multiplate) and thromboelastography ( TEG ). Endothelial biomarkers (sICAM‐1, syndecan‐1, sThrombomodulin, sVE‐Cadherin) and platelet activation biomarkers (sCD40L, TGF‐beta) were investigated along with haematology/biochemistry analyses. Results Twenty‐two patients were included. Despite continued low platelet counts, platelet transfusion normalised the median values of most TEG parameters and slightly increased platelet aggregation (all P  < 0·05). Endothelial biomarkers were not significantly affected by transfusion. The 1 h sCD40L level correlated positively with Syndecan‐1 and soluble thrombomodulin delta values, biomarkers of endothelial damage (both P  = 0·005). Conclusion Platelet transfusion improved haemostasis, whereas post‐transfusion increases in sCD40L were associated with endothelial damage, indicating that transfused platelets and platelet‐derived pro‐inflammatory mediators may have opposite effects on the endothelium.

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