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Melanocytic lesions are extremely
common in pediatric patients. At least 1 melanocytic nevus develops
by early childhood in more than 95% of fair-skinned individuals.1 Dermal
melanocytosis and other pigmented lesions such as freckles, lentigines,
café au lait macules, and Becker nevi are also frequently
observed in children and adolescents. In addition, a variety of
disorders characterized by increased or decreased cutaneous pigmentation
can present in childhood, ranging from postinflammatory hyperpigmentation
and hypopigmentation to vitiligo to patterned pigmentation reflecting
cutaneous mosaicism. Genetic diseases with pigmentary manifestations
(eg, oculocutaneous albinism, piebaldism, Waardenburg syndrome,
tuberous sclerosis, neurofibromatosis) are reviewed in Chapter 360. It is important for pediatricians to be aware of the clinical
spectrum and natural history of benign melanocytic lesions and self-limited disorders
of pigmentation in children as well as of findings that should raise
concern.
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Melanocytic nevi (moles) are benign proliferations of a type
of melanocyte. The 2 major differences between ordinary melanocytes
that reside in the basal layer of the epidermis and nevus cells are
that (1) nevus cells cluster as nests within the lower epidermis and/or
dermis, whereas epidermal melanocytes are evenly dispersed as single
cells; and (2) nevus cells do not have dendritic processes (with
the exception of those within blue nevi). Like ordinary melanocytes,
nevus cells are capable of producing the pigment melanin. Melanocytic
nevi can be acquired or congenital, banal or atypical (dysplastic).
There are several variants, such as halo, blue, and Spitz nevi,
that have specific clinical and histologic characteristics.2
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Acquired Melanocytic
Nevi
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Acquired melanocytic nevi begin to appear after the first 6 months
of life and increase in number during childhood and adolescence,
typically reaching a peak count during the third decade and then
slowly regressing with age.3-5 Both environmental and genetic factors
play a role in the development of acquired melanocytic nevi. Sun
exposure is the primary environmental influence (eTable
361.1); hereditary components include pigmentary phenotype
as well as a particular predisposition to “moliness.”
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