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. 2020 Feb 20;8:38. doi: 10.3389/fped.2020.00038

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Copyright © 2020 Ochocinski, Dalal, Black, Carr, Lew, Sullivan and Kissoon.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hemolysis-associated hemostatic activation. Intravascular hemolysis releases hemoglobin into plasma which quenches nitric oxide (NO) and generates reactive oxygen species (directly via fenton chemistry or via induction of xanthine oxidase and NADP 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. Used with permission from Gladwin MT, Kato GJ. Hemolysis-associated hypercoagulability in sickle cell disease: the plot (and blood) thickens! Haematologica (2008) 93:1-3.