Infantile hemangioma (IH) is the most common tumor of infancy ranging from a tiny red papule to a giant mass. Its typical natural history is characterized by an early rapid growth following birth and a slow spontaneous involution which is complete before puberty but almost complete within the first 3-6 years of life. The cause underlying IH is still unknown, but the role of fetal hypoxic stress is strongly suggested as a triggering signal. A different hypothesis suggests that IH can be derived from embolized placental progenitor cells that lodge in privileged sites of the developing embryo. Alternatively, IH has been reported as an aberrant proliferation and differentiation of a primitive mesoderm-derived hemogenic endothelium regulated by the renin-angiotensin system (RAS) leading to propose angiotensin-converting enzyme (ACE) as a potential therapeutic target. While some angiogenic factors have been identified (e.g., mast cells, heparin), there are no data demonstrating a hereditary component. Immunohistochemical studies of IH confirm their vascular origin. During the proliferative phase, IH shows a high expression of cell proliferation nuclear antigen, vascular endothelial growth factor (VEGF), type IV collagen, urokinase, basic fibroblast growth factor (bFGF), and von Willebrand factor. These data demonstrate active angiogenesis and are not observed in vascular malformations.
Beta-blockers for hemangiomas / C. Gelmetti, R. Cavalli - In: European Handbook of Dermatological Treatments / [a cura di] A.D. Katsambas, T.M. Lotti, C. Dessinioti, A.M. D’Erme. - Riedizione. - Berlin : Springer, 2015. - ISBN 9783662451380. - pp. 1393-1402 [10.1007/978-3-662-45139-7_135]
Beta-blockers for hemangiomas
C. GelmettiPrimo
;
2015
Abstract
Infantile hemangioma (IH) is the most common tumor of infancy ranging from a tiny red papule to a giant mass. Its typical natural history is characterized by an early rapid growth following birth and a slow spontaneous involution which is complete before puberty but almost complete within the first 3-6 years of life. The cause underlying IH is still unknown, but the role of fetal hypoxic stress is strongly suggested as a triggering signal. A different hypothesis suggests that IH can be derived from embolized placental progenitor cells that lodge in privileged sites of the developing embryo. Alternatively, IH has been reported as an aberrant proliferation and differentiation of a primitive mesoderm-derived hemogenic endothelium regulated by the renin-angiotensin system (RAS) leading to propose angiotensin-converting enzyme (ACE) as a potential therapeutic target. While some angiogenic factors have been identified (e.g., mast cells, heparin), there are no data demonstrating a hereditary component. Immunohistochemical studies of IH confirm their vascular origin. During the proliferative phase, IH shows a high expression of cell proliferation nuclear antigen, vascular endothelial growth factor (VEGF), type IV collagen, urokinase, basic fibroblast growth factor (bFGF), and von Willebrand factor. These data demonstrate active angiogenesis and are not observed in vascular malformations.File | Dimensione | Formato | |
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