Explores thrombosis management in polycythemia vera and essential thrombocythemia, indicating new therapeutic potentials.
This paper explores emerging therapies in polycythemia vera and essential thrombocythemia, focusing on thrombosis as a driver of disease progression leading to myelofibrosis, blast phase, second cancers, and mortality. While the thrombosis rate in high-risk patients has declined, it remains persistently high in low-risk individuals, with most events being arterial. Inflammation driven by JAK2 V617F mutation plays a primary role in pathogenesis, and mounting evidence suggests arterial thrombosis itself can fuel a self-sustaining cycle of inflammation, thereby accelerating hematologic and systemic complications. Early intervention with cytoreductive and anti-inflammatory drugs may not only prevent incidental thrombosis but also disrupt this inflammatory circuit.
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Barbui et al. (2025) studied this question.
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