Melasma is an acquired disorder of hyperpigmentation that most commonly presents as symmetrically distributed brown to gray macules and coalescent reticulated patches that have a predilection for the face (Figure 1a). It can rarely present on the neck, upper chest, upper back, and extensor forearms. Based upon the depth of melanin deposition, melasma can be classified into 4 subtypes—epidermal, dermal, mixed, or indeterminate—which are delineated by Wood’s lamp examination. Epidermal melanin is anticipated to accentuate on exam, while dermal melanin does not, though some clinicopathologic studies have demonstrated that this does not always hold true.1,2 There may also be a vascular contribution to melasma, as an increase in erythema in telangiectasias have been demonstrated in lesional skin.3
The prevalence of melasma is not precisely known, and published estimates have varied widely, ranging from around 1–40%.4,5 Populations in whom a higher prevalence is observed include pregnant women, individuals with darker skin types (namely Fitzpatrick skin types [FST] III – VI who are of Hispanic, Asian, and African descent), and those who receive abundant and intense sun exposure as a function of geography, occupation, or both. Although less common, men are also affected by melasma, with prevalence estimates similarly broad. One study of Indian men found a prevalence as high as 25.8%.6 The pathogenesis of melasma is both multifactorial and incompletely understood. In addition to the aforementioned factors observed in higher risk populations, genetics and hormonal influences are believed to contribute to the development of melasma. It is not uncommon for melasma patients to be in a state of estrogen or progesterone excess, or to report having family members who are similarly affected. In recent years, the contributory role that various signaling molecules, growth factors, and reactive oxygen species may be playing in the pathogenesis of melasma has increasingly come to light, though their detailed discussion is beyond the scope of this review.
Histologically, there is an increase in epidermal and dermal melanin that is generally believed to be unaccompanied by an increase in the number of melanocytes,1,2 though one case that demonstrated increased epidermal melanocytes that protruded into the dermis has been reported.7 Melanocytes present in melasma lesions are typically enlarged, and have elongated dendrites to facilitate transfer of increased numbers of melanosomes to neighboring keratinocytes. An increase in mast cells, dermal blood vessels, and solar elastosis may also be present.1,2 Melasma can cause significant psychosocial distress and quality of life impairments in those affected. Melasma patients have reported lower levels of self-esteem, decreased freedom, and annoyance at costly treatments, which negatively impact their social life, leisure time, and emotional well-being.8,9 In some cases, a poor correlation between disease severity and quality of life has been observed, suggesting that the patient may