Angiogenic and prothrombotic markers in extensive slow-flow vascular malformations: implications for antiangiogenic/antithrombotic strategies
P. Redondo, L. Aguado, M. Marquina, J.A. Paramo,* A. Sierra, ** A. Martínez-Cuesta,*** J. Cabrera
Unit of Vascular Malformations. Departments of Dermatology, Hematology*, Immunology**, and Radiology***, University Clinic of Navarra, Pamplona, Spain
Venous and combined malformations are slow-flow hemodynamically inactive lesions that are present at birth and worsen slowly with advancing age, showing no tendency toward involution.
The pathogenesis of vascular anomalies has not been fully elucidated, but their formation and progression are closely related to angiogenesis. Localized intravascular coagulation associated with venous or combined malformations is characterized by low fibrinogen, high D-dimers, and normal platelet count.
To assess the relationship of angiogenic factors with prothrombotic and endothelial damage/dysfunction markers in patients with extensive slow-flow vascular malformations.
A two-year study (2005-2007) included 31 consecutive patients with extensive slow-flow vascular malformations from one center.
Serum levels of TIE-2, MMP-9, Ang-2 and plasma levels of D-dimer, PAI, tPA, and vWf were significantly increased in patients compared with healthy controls, whereas serum levels of VEGF-C, VEGF-D, MMP-2, Ang-1, PDGF-AB, and PDGF-BB were significantly decreased in patients than in controls. A strong positive correlation was present between Ang-1 and PDGF-AB levels (r=0.63, p<0.001), between PDGF-AB and PDGF-BB levels (r=0.67, p<0.001), and between fibrinogen and PAI levels (r=0.41, p=0.031). A strong negative correlation was present between Ang-1 and vWF levels (r=-0.48, p=0.006), between D-dimer and fibrinogen levels (r=-0.71, p<0.001), and between PDGF-AB and vWF levels (r=-0.42, p=0.017).
These findings suggest that angiogenic, coagulation and endothelial damage/dysfunction markers are possibly linked in pathogenesis of extensive slow-flow vascular malformations, what might have therapeutic implications.
CITATION Br J Dermatol. 2010 Feb 1;162(2):350-6.