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If there is involvement of the papillary dermis, the cutaneous surface is often bright red and thus classified as a superficial and deep IH.
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They present as a localized, firm, rubbery subcutaneous mass that can be slightly raised with a bluish color or with telangiectasias involving the overlying skin, or they may be deep enough that the overlying skin is completely flat and of normal hue. Deep IH proliferate in the lower dermis and subcutaneous tissue without penetration of the papillary dermis ( Fig. + +Ītypical presentations of IH include deep hemangiomas and those with minimal to no proliferation. Though the exact number is somewhat arbitrary, the presence of more than five hemangiomas confers a risk of extracutaneous hemangiomas. 14 Multifocal hemangiomas are usually multiple localized hemangiomas. The patterns of facial segmental IH have been found to correspond to neural-crest-derived facial prominences, and a new map for them has recently been proposed. Those hemangiomas not clearly identifiable as localized or segmental are termed indeterminate (see Fig. 33 They are often plaque-like in nature with a linear or geographic configuration. Segmental hemangiomas (similar to other segmental dermatologic disease such as vitiligo and neurofibromatosis) correspond to a portion of a developmental segment or broad anatomic territory ( Fig. 31, 32 Localized hemangiomas exhibit clear spatial containment as if arising from one central focus ( Fig. In addition to this clinical appearance, IH can be classified as localized, segmental, or indeterminate. Those involving both superficial and deeper skin structures, so-called mixed hemangiomas, have both features. Hemangiomas which involve the upper dermis (so-called superficial hemangiomas) have a bright strawberry red color whereas those with deep dermal and subcutaneous location are skin color to blue in color. Some children have normal skin after involution whereas the remainder has telangiectasias, atrophy, fibrofatty residuum, or scarring. Most IH complete their course by the age of 7–10 years. 29 Smaller hemangiomas typically involute sooner than very large ones, but there are exceptions. Evidence of involution (change to a dull red, then gray or milky-white color, followed by flattening and softening) is usually apparent by 1 year of age. 30 This growth phase is followed by a slower involution phase which is more variable in length, lasting for months to years ( Fig. Large, segmental, deep, and parotid gland hemangiomas may continue to enlarge slowly for months to years longer. 29 Deep hemangiomas may be noted at a somewhat later age, on average 1 month later than superficial IH and uncommonly are not appreciated until a few months of life. The period of most rapid growth typically occurs within the first 5 months of life, with 80% of growth being completed by 5 months of age. Though IH are not present at birth as fully formed tumors, superficial IH almost always become apparent within the first month of life. 23 While not a perfect replica of IH growth, this model merits attention and additional study. 21, 22 Implantation into immunodeficient mice of CD133 + cells isolated from IH gives rise to GLUT1+ vessels that later diminish and are replaced by adipocytes. They have features similar to an early embryologic vessel, the cardinal vein 20 and express CD133, a primitive cell marker, during proliferation. 19 Further investigations into the cellular origin of hemangioma endothelial cells have demonstrated that these cells have features of immature mesenchymal cells. 18 In addition, a recent study determined that hemangioma endothelial cells are of fetal, not maternal origin. 16, 17 IH lack a villous architecture and do not express known placental trophoblastic markers suggesting that they are not placental emboli. This, together with other immunohistochemical markers shared by IH and human placenta (FcγRII, merosin, and LeY), and the similar gene expression profiles found on DNA-based microarrays led to speculation that these tumors are of placental origin from either embolized placental cells or invading angioblasts that have differentiated toward a placental phenotype. 15, 16 GLUT1 expression in absent in the normal cutaneous vasculature but is found in placental blood vessels as well as in other so-called barrier tissues such as the blood–brain barrier. The recognition that a glucose transporter protein, GLUT1, is expressed in all stages of hemangioma maturation spurred new hypotheses on the pathogenesis of IH.