4.6 Article

Thromboelastography characterized CD36 null subjects as slow clot formation and indicative of hypocoagulability

期刊

THROMBOSIS RESEARCH
卷 178, 期 -, 页码 79-84

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.thromres.2019.04.006

关键词

CD36; Thromboelastography (TEG); Platelet-monocyte aggregate (PMA)

资金

  1. National Taiwan University Hospital [NTUH.100-S1611]
  2. Taiwan Blood Services Foundation [PM-98-TP-046]

向作者/读者索取更多资源

Background: Platelet CD36 is the receptor for oxidized low-density lipoprotein and collagen. The conventional platelet test cannot distinguish CD36-null subjects from normal expression subjects. Thromboelastography (TEG) testing can analyze global hemostasis. TEG testing data on CD36-null subjects are not available. Methods: Our subjects were 40 apheresis platelet donors, including 8 CD36-null individuals. We grouped the donors according to the platelet CD36 expression levels to assess the effects of platelet CD36 expression levels on TEG measurement variables. Results: The whole blood TEG test revealed that CD36-null subjects had prolonged reaction time of fibrin formation (TEG R time) and a slower rate to build up cross-linked fibrin (TEG a angle). The final maximal amplitudes of clot formation showed little difference between CD36-null individuals and normal expression individuals. Correlation analysis showed that CD36 expression levels were negatively correlated with TEG R time (r=-0.342, p= 0.031) and positively correlated with the TEG a angle (0.379, p= 0.016). TEG testing on apheresis platelet samples with diminished heterocellular interaction did not reveal differences between CD36null and normal expression individuals. A subanalysis of the data of a group of healthy subjects showed that platelet CD36 levels correlated positively with platelet-monocyte aggregates (PMAs). Low PMA can diminish heterocellular interaction and likely explain the abnormal TEG results observed in CD36-null individuals. Conclusion: TEG distinguishes CD36-null subjects from normal CD36 expression subjects as having a slower rate of fibrin formation and reassessment of TEG-based diagnostic monitoring is necessary for CD36 null subjects.

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