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Hematocrit and thrombotic risk in erythrocytosis
tifying and developing novel targeted therapies for these disorders. The evidence we have presented here points to favoring the use of myelosuppressive therapy for intermediate- and high-risk PV, as this approach has been proven to decrease the risk of thrombosis in PV. Furthermore, we trust that the urge to correct any abnor- mal laboratory data by a therapeutic intervention should be tempered by consideration of the risk-benefit ratio of any such intervention. The routine practice of phleboto- my for elevated hematocrit, with its inevitable iron defi- ciency (which leads to inhibition of PHD2, increased HIF, and increased erythropoietin) and potential detrimental thrombotic effects, should be re-evaluated. We hope that this review will encourage more studies to pursue the
challenge of defining the specific molecular basis of thrombosis in diverse types of polycythemia and ery- throcytosis. Improved knowledge of the pathophysiolo- gy of these entities should be extended to the develop- ment of targeted approaches for the prevention and ther- apy of thrombotic complications. A review of potential molecular mechanisms contributing to thrombosis in myeloproliferative neoplasms was published at the time of the submission of this manuscript.87
Acknowledgments
This work was supported in part by a grant from the National Institutes of Health, R01HL137991 (to JP), and institutional funds from the University of Illinois at Chicago.
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