Academic journal article International Journal of Child Health and Human Development

Skin Pigmentation

Academic journal article International Journal of Child Health and Human Development

Skin Pigmentation

Article excerpt


Melanin is the pigment responsible for the color of the hair and skin. Melanin present in the epidermis of the skin serves a protective function against ultraviolet radiation-induced changes that may lead to skin cancer. Melanin is synthesized in the melanocytes, which are embyrogenically derived from the neural crest (1, 2). Melanin is formed from the amino acid tyrosine. Tyrosine is converted to dihyrdoxyphenylalanine (DOPA) by tyrosinase. DOPA is then oxidized to dopaquinone and finally to melanin (2). In addition to the presence of melanin in the epidermis, other factors contribute to the color of the skin that include the thickness of the stratum corneum and local blood flow (2-4).

Skin pigmentation largely depends on the formation and packaging of melanin in the melanosomes of the epidermal cells. The intensity of the skin pigmentation depends on the size and number or density of melanosomes present in the keratinocytes, the rate of melanin synthesis, and the rate of transport of melanin within keratinocytes (2). Sex steroids (estrogen and progesterone) and peptide hormones (alpha- and beta-melanocyte stimulating hormone (MSH), and adrenocorticorophic hormone (ACTH)) also affect skin pigmentation. Skin pigmentation is also influenced by genetic factors. Typically the dorsal and extensor surfaces are relatively darker than the ventral surfaces. Numerous conditions can cause either hypopigmentation (Tables 1 and 2) or hyperpigmentation of the skin (Table 3) (1-6).

Disorders of hypopigmentation


Vitiligo is characterized by loss of skin pigmentation typically resulting in oval or irregular ivory-white patches of skin with well-demarcated convex borders (1, 2, 7). The underlying cause of vitiligo is genetically determined - autosomal dominant trait of variable penetrance - and its prevalence is estimated to be 2% in the population (2). Approximately 30% of individuals with vitiligo have a positive family history of vitiligo, halo nevi, traumatic depigmentation of the skin or markedly premature graying of the scalp hair (2).

Although the onset of vitiligo is most common during young adult age, it can begin at any age, and approximately half of the cases are reported to have onset before age 20 years (1, 2, 3). About 20% of cases have been reported with onset before age 10 years (1). Rare cases of congenital vitiligo have been reported.

In three quarters of the cases the initial lesions at presentation are noted on the exposed areas such as dorsal surfaces of the hands, face, and neck. Other sites that are relatively more prone to develop depigmentation include the axillae, groin, around the eyes, nostrils, mouth, navel, areolae, genitals, perinanal regions, and bony prominences around joints of the extremities (3-6). The lesions vary in size and shape and can be partially or fully depigmented. Individual depigmented areas can be just few millimeters in size to total body involvement.

The patient typically presents with concerns about hypopigmented areas of the skin following a recent sun exposure. Often the patient initially attributes the lesion to effects of sunburn. Some patients present following a period of severe psychological or physical stress. The diagnosis of vitiligo is clinical based on the history and characteristic morphology of the skin lesions. Wood light examination may help differentiate normal skin from depigmented lesions, especially in fair skinned individuals.

Lesions of vitiligo should be differentiated from other common conditions. These include post-inflammatory hypopigmentation, albinism, hypo-popigmented macules seen in tuberous sclerosis, pityriasis alba, and tinea versicolor. The mainstay of differentiation is the morphologic characteristics of the lesions in different conditions.

There is no cure for vitiligo. The clinical course of vitiligo is variable with intermittent periods of exacerbations and partial improvement. …

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