Splenic Artery Aneurysm Associated with Myelofibrosis Managed by Coil Embolization.
Key claim: Ruxolitinib-induced splenomegaly reduction in a JAK2 V617F-positive secondary myelofibrosis patient facilitated safe spleen-preserving coil embolization of a splenic artery aneurysm, suggesting JAK inhibitor therapy may optimize hemodynamic conditions for endovascular intervention in MF-associated vascular complications.
Abstract
Myelofibrosis (MF) is a myeloproliferative neoplasm frequently complicated by splenomegaly, with vascular abnormalities, such as splenic artery aneurysm (SAA), rarely reported. We herein report a 74-year-old woman with secondary MF harboring a JAK2 V617F mutation who developed SAA requiring intervention because of its potential risk of rupture. Ruxolitinib therapy markedly reduced splenomegaly and improved constitutional symptoms, thereby optimizing hemodynamic conditions and overall status for safe spleen-preserving coil embolization. This case highlights the potential relationship between MF and aneurysm formation while demonstrating that concomitant Janus kinase inhibitor therapy may facilitate safe endovascular treatment in select patients.
Why this matters
This case expands the recognized vascular complications of MPN-related splenomegaly beyond thrombotic events to include splenic artery aneurysm, and introduces a novel clinical use of JAK inhibitors as hemodynamic bridging therapy before endovascular intervention. For symptom management, it reframes ruxolitinib’s spleen-shrinking effect as potentially enabling spleen-preserving procedures rather than splenectomy, which carries substantial post-operative morbidity in MF.