Polycythemia vera (PV) is associated with high morbidity and mortality for thrombosis. We hypothesized that in PV altered sensitivity to aspirin might be related to dysfunction of the endothelial repair and/or of the nitric oxide (NO) system. Urinary thromboxane (TX) A 2 metabolite (TXM). endothelial colony-forming cells (ECFCs), plasma asymmetric dimethyl- arginine (ADMA) and von Willebrand factor (VWF) were measured in 37 PV patients on low-dose aspirin and 12 healthy controls. Patients showed an approximately 2-fold increase in median TXM and plasma ADMA levels (P2 = 0.39). Serum TXB 2, measured in 22 patients, was approximatly 10-fold higher than aspirin-treated controls. PV patients appear to have an unbalanced ECFC/NO axis, and an apparent altered sensitivity of platelet TXA 2 production, all potentially contributing to aspirin- insensitive TXM formation. Thus, additional antithrombotic strategies may be beneficial in PV.
ASJC Scopus subject areas
- Cell Biology