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. 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 355. 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.
MELANOCYTIC NEVI AND OTHER PIGMENTED LESIONS
Melanocytic nevi (moles) are benign proliferations of a type of melanocyte known as a nevus cell. 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 and banal or atypical (dysplastic). There are several variants, such as halo, blue, and Spitz nevi, that have specific clinical and histologic characteristics.
ACQUIRED MELANOCYTIC NEVI
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 by the third decade; they then slowly regress with age. Both environmental and genetic factors play a role in the development of acquired melanocytic nevi. Sun exposure is the primary environmental influence (Table 356-1), and hereditary components include pigmentary phenotype as well as a predisposition to “moliness.”
TABLE 356-1ENVIRONMENTAL TRIGGERS FOR THE DEVELOPMENT AND GROWTH OF MELANOCYTIC NEVI IN CHILDREN AND ADOLESCENTS |Favorite Table|Download (.pdf) TABLE 356-1ENVIRONMENTAL TRIGGERS FOR THE DEVELOPMENT AND GROWTH OF MELANOCYTIC NEVI IN CHILDREN AND ADOLESCENTS
Sun exposure leading to multiple or severe sunburnsa
Intermittent intense sun exposure (eg, on sunny holidays)
Chronic moderate sun exposure (eg, residence at lower latitudes)
Tanning bed use
Possibly neonatal phototherapy (associated with nevus development in some but not all studies)
Blistering Processes (Other Than Severe Sunburns)
Toxic epidermal necrolysis/Stevens-Johnson syndromea
Epidermolysis bullosa: junctional (particularly the generalized intermediate type) > recessive dystrophic > recessive simplexa
Childhood bullous pemphigoid
Chemotherapy, particularly for childhood hematologic malignanciesa,b,c
Allogeneic hematopoietic stem cell transplantationc
Solid-organ transplantation, particularly renala,c
Human immunodeficiency ...