Melasma is a common acquired pigmentary disorder characterized by light to dark brown hyperpigmented macules and patches with irregular circumscribed borders and confetti-like islands of normal appearing skin, resulting from increased melanin in the epidermis, dermis, or both. The term “melasma” is derived from a Greek word meaning “a black spot” and is synonymous with “chloasma,” meaning “a green spot.”1
This condition favors the face, but occasionally can involve the extensor forearms and trunk in what is termed extrafacial melasma. This condition is seen primarily in young to middle-aged women; however, men can also develop the same troublesome hyperpigmentation. It has been reported that at least 90% of patients are women, and it is often referred to as chloasma, or the “mask of pregnancy.”2
However, this rate may be closer to 75% when the rates of men in Southeast Asia and India are taken into account. The negative impact of melasma on quality of life is well known. It contends a phenotype of photodamaged skin and can be quite psychologically distressing for some patients.
Normal skin color is determined by a mixture of four biochromes in the skin, specifically, reduced hemoglobin (blue), oxyhemoglobin (red), carotenoids (yellow), and melanin (brown).1
Melanin is the main determinant of skin color. It is genetically determined by constitutive melanin pigmentation
and can be increased in response to stimulants such as UV radiation or hormones, through inducible melanin pigmentation
Increased melanin in the epidermis, or hypermelanosis
, reflects an increased number of melanocytes as in solar lentigines, or an increase in the production of melanin with no increase in the number of melanocytes, or melanotic hypermelanosis
, as is marked by melasma.1
Irregularities in the appearance of skin pigmentation due to hypermelanosis, hypomelanosis, or a combination of both can be viewed or interpreted as a failure to present an attractive appearance. This is both a conscious and subconscious part of human nature.
Many chronic diseases, including pigmentary disorders, affect the way patients view and feel about themselves and the way they are perceived in society. This has significant psychosocial impacts for patients suffering from visible chronic skin diseases. Pigmentary disorders can cause great turmoil and grief for many patients. The psychosocial repercussions can be especially marked in populations with naturally darker skin phototypes, or where dyspigmentation of the skin may be viewed as hereditary or confused with Hansen disease. Of the many different pigmentary disorders that affect the appearance of the skin, melasma and vitiligo predominate. The anxiety and extraordinary distress attributed to melasma has been well documented. The impact can be profound, and patients may be willing to go to great lengths, even to reallocate money for necessities to the treatment in the appearance of melasma.
Patients typically present in child-bearing years or per-imenopausal years with complaints of dark spots on the face. They will sometimes give a history of having been prescribed oral contraceptives, a recent pregnancy, a sunny vacation, or a laser treatment followed by sun exposure precipitating its appearance.
Melasma is multifactorial in etiology. It appears to mostly affect adult women of child-bearing age with Fitzpatrick phototype III to VI skin. It has a genetic and racial predilection for individuals of Asian, Hispanic/Latino, and African American descent. Although the etiology is not completely known, several factors have been implicated. Common etiologic factors include a genetic predisposition, ultraviolet (UV) radiation and visible light, specifically blue light exposure, barrier abnormalities, hormone sensitivities relating to pregnancy, and exogenous hormones from oral contraceptives, or hormone replacement therapy. UV light both precipitates and exacerbates melasma. Endogenous and exogenous estrogen, combined with progesterone and sunlight, can lead to significant darkening of pigmentation in melasma. Less common risk factors include thyroid disorders, photosensitizing medications, and type 4 hypersensitivity reactions to common allergens found in cosmeceuticals and topical preparations.10
A pilot study examining the role of cosmetic contact allergy found that a significant portion of melasma patients had positive results when patch tested to the Indian Cosmetic and Fragrance Series, the Indian Sunscreen Series, p-phenylenediamine, and some of the patients’ own cosmetic products. Nearly half (43.3%) had positive patch test results to the Indian Cosmetics and Fragrance Series, with cetrimide (52%), gallate mix (31%), and thiomersal (24%) being the most common contact allergens tested.14
The role of contact dermatitis
should not be overlooked in melasma, and products containing these allergens should be avoided. Although melasma has many associated triggers, it can also be termed idiopathic when no clear predisposing factors can be identified. Melasma tends to be more persistent in more darkly pigmented skin types and tends to fade over the winter months in northern latitudes where there is less daytime UV exposure.
In pregnancy, up to 90% of women develop some form of hyperpigmentation, which can manifest as hyperpigmented areolae, linea nigra, and/or melasma.2
These skin lesions arise from the quality and quantity of the physiologic hormone changes in pregnancy, specifically elevated serum levels of melanocyte stimulating hormone (MSH), estrogen, and possibly progesterone.2
In pregnancy, pituitary enlargement is accompanied by an increase in the blood level of MSH, in addition to an increased output of gonadotropins, and corticotrophin.15
Moreover, cortisol levels are increased from increased adrenocortical activity, which is thought to weaken and rupture dermal elastic fibers as seen in striae distensae, and high levels of circulating estrogen lead to the vascular changes seen in pregancy.15
Up to 70% of pregnant women may develop melasma, which either first appears or becomes noticed by the patient during pregnancy.16
It is estimated that between 5% and 34% of nonpregnant women taking oral contraceptives may also develop melasma.2
The onset often follows or may be exacerbated by UV exposure. This “mask of pregnancy” often fades or even disappears after parturition in more lightly pigmented skin types but can persist following pregnancy and discontinuation of oral contraceptives in more darkly pigmented individuals.2
The pathogenesis of melasma is complex and, although not entirely known, is thought to be related to hyperfunctional melanocytes, which can be stimulated by various factors, with concomitant angiogenesis. Ongoing research has led to an increased understanding of the complex pathogenesis of this disorder. Melanocytes, keratinocytes, and even dermal cells including mast cells and fibroblasts have all been described as playing a role in the pathogenesis. Advancements in molecular techniques have allowed for the identification of certain genes, cytokines, chemokines, angiogenic factors, and defects in the structural integrity of affected skin.
It is believed that following exposure to an inciting agent, such as UV radiation, hyperfunctional melanocytes in the skin produce increased amounts of melanin.4
On histology, increased melanin is always seen, often with overlying solar elastosis. This suggests a role of UV radiation and dermal damage in the pathogenesis.3
The role of UV radiation is further supported by relative fading of the lesions during the winter months in northern latitudes and sparing of sun-protected sites such as the philtrum. The expression of KIT within lesional epidermis, and stem cell factor within lesional dermis, is increased.
Defects in the basement membrane may facilitate the fall or migration of melanin, and active melanocytes into the dermis.17
This can be exacerbated by aggressive treatments, which may disrupt the basement membrane, trigger dermal inflammation and destruction of melanocytes, upregulate stem cell factors, and increase vascularity, which effectively promotes melanogenesis and causes PIH, worsening the appearance of melasma.18
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Angiogenesis also plays a role in the pathogenesis of melasma. Lesions of melasma display an increased number and size of blood vessels, and vascular endothelial growth factor (VEGF) appears to be upregulated.19
VEGF receptors are found on human melanocytes.20
VEGF stimulates the release of arachidonic acid, in addition to the phosphorylation and activation of cytosolic phospholipase A2.21
There appears to be a complex link between the VEGF and arachidonic acid pathways with inflammatory cytokines induced by the effects of UV on cutaneous blood vessels in the melanogenesis seen in melasma.19
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