The horizon for treating cutaneous vascular lesions

Abstract

Dermatologists encounter a wide range of cutaneous vascular lesions, including infantile hemangiomas, port-wine stain birthmarks, arteriovenous malformations, venous malformations, Kaposi sarcomas, angiosarcomas, and angiofibromas. Current treatment modalities to reduce these lesions include topical and/or intralesional steroids, laser therapy, surgical resection, and endovascular therapy. However, each method has limitations owing to recurrence, comorbidities, toxicity, or lesion location. Photodynamic therapy, antiangiogenic therapy, and evolving methods of sclerotherapy are promising areas of development that may mitigate limitations of current treatments and offer exciting options for patients and their physicians.

Figure 1

Proposed mechanism of action of beta-blockers in the treatment of IH. A CD34⁺ population of ICC found in IH are thought to express ACE in addition to the angiotensin II receptor. Local angiotensin I (A1) is converted by ACE to angiotensin II (A2). A2 presumably promotes: (a) the release of VEGF from MSC within IH, and (b) a paracrinelike proliferation of ICC. It is thought that VEGF not only prevents the terminal differentiation of MSC into fibrofatty tissue, but also facilitates the maturation of ICC into endothelial cells. Beta-blockers inhibit the upstream release of renin, thereby blocking the entire sequence of events illustrated previously. Note that in this proposed schematic, inhibition of VEGF release would lead to normal terminal differentiation of MSC into fibrofatty tissue, the clinically observed endpoint of IH. ACE, angiotensin-converting enzyme; IH, infantile hemangioma; ICC, immature capillary cells; VEGF, vascular endothelial growth factor; MSC, mesenchymal stem cells.