Case reports in hematology · 2026
Pacritinib-Based Salvage Therapy in High-Risk Polycythaemia Vera With Recurrent Arterial and Venous Thrombosis After Hydroxyurea and Ruxolitinib: A Case Report.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Al-Rasheed Muna
Аннотация
OBJECTIVES: Polycythaemia vera (PV) is associated with substantial arterial and venous thrombotic risk, particularly in patients with prior thrombosis and inadequate haematocrit (HCT) control. Although ruxolitinib is an established second-line treatment after hydroxyurea failure or intolerance, some patients remain difficult to manage. We report a case of highly thrombotic, treatment-challenging PV in which pacritinib-based salvage therapy was used after inadequate disease control with hydroxyurea and ruxolitinib.
CASE PRESENTATION: A 44-year-old man was referred with portal vein thrombosis and a history of premature myocardial infarction and cerebrovascular accident. Investigations demonstrated JAK2V617F-positive PV with borderline low erythropoietin and bone marrow panmyelosis. Despite antiplatelet therapy, anticoagulation, hydroxyurea and subsequent ruxolitinib, the patient experienced further thrombotic complications, including recurrent cerebrovascular events, bilateral limb ischaemia and left ventricular thrombosis. Ruxolitinib was escalated to 25 mg twice daily and combined with low-dose hydroxyurea; however, HCT control remained suboptimal, with recurrent need for venesection. In February 2025, ruxolitinib was replaced with pacritinib 200 mg twice daily while hydroxyurea and warfarin were continued. During follow-up, the patient achieved improved HCT control, no longer required venesection and had no further documented thrombotic events. Pacritinib was well tolerated.
CONCLUSION: This case describes a patient with high-risk, refractory PV and recurrent arterial and venous thrombosis in whom pacritinib-based salvage therapy was associated with improved HCT control, cessation of venesection and absence of further thrombosis during follow-up. Although off-label and hypothesis-generating, this experience supports further evaluation of pacritinib in selected patients with treatment-challenging PV.
CASE PRESENTATION: A 44-year-old man was referred with portal vein thrombosis and a history of premature myocardial infarction and cerebrovascular accident. Investigations demonstrated JAK2V617F-positive PV with borderline low erythropoietin and bone marrow panmyelosis. Despite antiplatelet therapy, anticoagulation, hydroxyurea and subsequent ruxolitinib, the patient experienced further thrombotic complications, including recurrent cerebrovascular events, bilateral limb ischaemia and left ventricular thrombosis. Ruxolitinib was escalated to 25 mg twice daily and combined with low-dose hydroxyurea; however, HCT control remained suboptimal, with recurrent need for venesection. In February 2025, ruxolitinib was replaced with pacritinib 200 mg twice daily while hydroxyurea and warfarin were continued. During follow-up, the patient achieved improved HCT control, no longer required venesection and had no further documented thrombotic events. Pacritinib was well tolerated.
CONCLUSION: This case describes a patient with high-risk, refractory PV and recurrent arterial and venous thrombosis in whom pacritinib-based salvage therapy was associated with improved HCT control, cessation of venesection and absence of further thrombosis during follow-up. Although off-label and hypothesis-generating, this experience supports further evaluation of pacritinib in selected patients with treatment-challenging PV.