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Editorial
. 2008 Jan;93(1):1-3.
doi: 10.3324/haematol.12318.

Hemolysis-associated hypercoagulability in sickle cell disease: the plot (and blood) thickens!

Mark T Gladwin, Gregory J Kato
Editorial

Hemolysis-associated hypercoagulability in sickle cell disease: the plot (and blood) thickens!

Mark T Gladwin et al. Haematologica. 2008 Jan.
No abstract available

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Figures

Figure 1
Figure 1. Hemolysis-associated hemostatic activation
Intravascular hemolysis releases hemoglobin into plasma which quenches NO and generates reactive oxygen species (directly via Fenton chemistry or via induction of xanthine oxidase and NADPH oxidase). In addition, arginase I is released from the red blood cell during hemolysis and metabolizes arginine, the substrate for NO synthesis, further impairing NO homeostasis. The depletion of NO is associated with pathological platelet activation and tissue factor expression. Hemolysis and splenectomy are also associated with phosphatidylserine exposure on red cells which can activate tissue factor and form a platform for coagulation.
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Comment on

References

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