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Editorial |

The Hidden Face of Venous Malformations A Multidisciplinary Therapeutic Approach

Pedro Redondo, MD
Arch Dermatol. 2008;144(7):922-926. doi:10.1001/archderm.144.7.922.
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Venous malformations (VMs) are ectatic vessels that are morphologically and histologically similar to veins and have a low blood flow. The thin-walled vascular channels are composed of a deficient layer of smooth-muscle cells and are lined by quiescent endothelium. The TIE2 signaling pathway is critical for endothelial cell–smooth muscle cell communication in venous morphogenesis.1 Venous malformations represent approximately one-half to two-thirds of all vascular malformations, and the majority of them are sporadic anomalies. The skin or mucosa that covers VMs varies in color according to the depth and degree of ectasia of the lesion. More superficial malformations are purple and deeper ones are blue, green, or even imperceptible. The lesions are soft to the touch, can have a nodular appearance, and empty with compression. Highly ectatic vessels sometimes contain small venous thromboses, producing pain and inflammation. Phleboliths, which are used as radiological markers of this type of malformation, can be present from an early age.

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Figure 1.

Anticoagulant and antiangiogenic actions of heparins. Low-molecular-weight heparin (LMWH) binds to antithrombin and inhibits thrombin and factor Xa by different binding mechanisms. LMWH has been shown to inhibit vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-mediated angiogenesis in vivo, inhibiting the binding of these growth factors to their receptors. R indicates receptor.

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Figure 2.

Schematic representation of the relationship between fibrinolytic system and angiogenesis. Interactions among vascular endothelial growth factor (VEGF)-activated endothelial cells, local/distant fibrinolysis, and angiogenic stimulus. α2-AP indicates α2-antiplasmin; bFGF, basic fibroblast growth factor; ECM, extracellular matrix; FDP, fibrin degradation product; MMPs, matrix metalloproteinases; PAI-1, plasminogen activator inhibitor type 1; t-PA, tissue plasminogen activator; U-PA, urokinase plasminogen activator; and U-PAR, urokinase plasminogen activator receptor.

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