Genetic Underpinnings of Splanchnic Vein Thrombosis in Myeloproliferative Neoplasms May Provide New Insights

Researchers examined the clinical and molecular risk factors for MPN-associated SVT and reported that both environmental and host genetic factors appear to be involved.
Researchers examined the clinical and molecular risk factors for MPN-associated SVT and reported that both environmental and host genetic factors appear to be involved.

A greater understanding of the pathophysiology and molecular mechanisms of splanchnic vein thrombosis (SVT) may lead to better treatment of SVT in patients with myeloproliferative neoplasms (MPNs), a study published in Therapeutic Advances in Hematology has shown.

The researchers report that MPNs are the most common underlying prothrombotic disorder found in patients with SVT, and their development appears to be multifactorial.


In this study, the researchers examined the clinical and molecular risk factors for MPN-associated SVT and report that both environmental and host genetic factors appear to be involved. They found that the JAK2 V617F mutation, young age, female sex, and the presence of concomitant hypercoagulable disorders appear to be risk factors for the development of SVT in patients with MPN.

The team reports that intrinsic characteristics of the splanchnic venous bed may lay the groundwork for thrombotic interactions with atypical blood cells. In addition, these atypical blood cells may be modified by the JAK2 V617F mutation or other mutations. The researchers were unable to identify any other specific genetic alterations involved in SVT, even when they considered CALR, MPL, or the JAK2 46/1 haplotype — known genetic alterations implicated in MPN pathogenesis.

The researchers theorize that a better characterization of patients with MPN with and without SVTs is warranted, as well as the development of a database of such phenotypes.

Reference

1. How J, Zhou A, Oh ST. Splanchnic vein thrombosis in myeloproliferative neoplasms: pathophysiology and molecular mechanisms of disease. Ther Adv Hematol. 2017;8(3):107-118.

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