A novel vascular thrombophilia Comment

In this issue of Blood, Fassel et al(1) report a higher frequency of reduced plasminogen-activating capacity by peripheral blood mononuclear cells (PBMCs) from patients with thrombosis and a positive family history, but not a known inherited thrombophilia, compared with either patients without a family history of thrombosis or patients with a family history accompanied by an inherited thrombophilia (see figure). Deficient cell surface plasmin generation by PBMCs, used in this study as a surrogate for endothelial cells, was caused by decreased expression of annexin A2. This report extends previous studies, primarily in animal models, suggesting an important role for annexin A2-mediated plasmin generation on the vascular wall in the maintenance of blood fluidity and suggests that deficient annexin A2 expression may represent a novel variant of thrombophilia that is independent of altered levels and/or mutations in circulating coagulation proteins or their inhibitors.

Automated summary

The study found a novel variant of thrombophilia independent of circulating coagulation proteins or their inhibitors, which is associated with deficient annexin A2 expression. This variant may play an important role in maintaining blood fluidity, suggesting a potential therapeutic target for thrombosis.