First, determine whether the disorder is hyperpigmentation or hypopigmentation, ie, an increase or decrease in skin pigment from the patient’s baseline. Each may be considered to be primary or to be secondary to other disorders. Depigmentation, the absence of all pigment, should also be differentiated from hypopigmentation, in which the affected skin is lighter than baseline skin color, but not completely devoid of pigment.
The evaluation of pigmentary disorders is helped by Wood light, which accentuates epidermal pigmentation in hyperpigmented disorders and highlights complete loss of pigment in depigmentating disorders. Depigmentation, as seen in vitiligo, enhances with Wood light examination, whereas postinflammatory hypopigmentation does not.
A. Primary Pigmentary Disorders
The disorders in this category are nevoid, congenital, or acquired. Nevoid and congenital disorders include pigmented nevi, mosaic hyperpigmentation, ephelides (juvenile freckles), and lentigines (senile freckles). Hyperpigmentation due to systemic diseases may be seen in in association with Addison disease, vitamin B12 deficiency, hemochromatosis, and Wilson disease. Melasma (chloasma) occurs as patterned hyperpigmentation of the face, most commonly as a direct effect of estrogens. It may occur during pregnancy, exposure to oral contraceptives, or be idiopathic. Although more common in women, melasma affects both sexes and all races.
2. Hypopigmentation and depigmentation
Depigmenting disorders in this category are vitiligo, albinism, and piebaldism. In vitiligo, pigment cells (melanocytes) are destroyed (Figure 6–39) (eFigure 6–38). Vitiligo, present in approximately 1% of the population, may be associated with other autoimmune disorders, such as autoimmune thyroid disease, pernicious anemia, diabetes mellitus, and Addison disease.
Depigmented—vitiligo. (Used, with permission, from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 3rd ed. McGraw-Hill, 2019.)
B. Secondary Pigmentary Disorders
Any damage to the skin (irritation, allergy, infection, excoriation, burns, or dermatologic therapy, such as chemical peels and freezing with liquid nitrogen) may result in hyperpigmentation or hypopigmentation. Several disorders of clinical importance are described below.
The most common type of secondary hyperpigmentation occurs after another inflammatory dermatologic condition, such as acne, lichen planus, or eczema, and is most commonly seen in moderately complexioned persons (Asians, Hispanics, and light-skinned black individuals). It is called post-inflammatory hyperpigmentation. Hemosiderin deposition, as in stasis dermatitis, may lead to hyperpigmentation that is red-brown in color.
Pigmentation may be produced by certain medications, eg, chloroquine, chlorpromazine, minocycline (Figure 6–40), and amiodarone. Fixed drug eruptions to phenolphthalein (in laxatives), TMP-SMZ, NSAIDs, and tetracyclines also lead to hyperpigmentation, typically in annular patches.
Minocycline hyperpigmentation. (Used, with permission, from Lindy Fox, MD.)
Hypopigmentation may complicate atopic dermatitis, lichen planus, psoriasis, discoid lupus, and lichen simplex chronicus. It may also be posttraumatic or iatrogenic (eg, due to the use of superpotent topical corticosteroids) or both. Clinicians must exercise special care in using liquid nitrogen on any patient with olive or darker complexions, since doing so may result in hypopigmentation or depigmentation, at times permanent. Intralesional or intra-articular injections of high concentrations of corticosteroids may also cause localized temporary hypopigmentation.