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Melasma is an acquired hypermelanosis of sun-exposed areas. Melasma presents as symmetrically distributed hyperpigmented macules, which can be confluent or punctate. Areas that receive excessive sun exposure, including the cheeks, the upper lip, the chin, and the forehead, are the most common locations; however, melasma can occasionally occur in other sun-exposed locations. Note the images below.

Chloasma is a synonymous term sometimes used to describe the occurrence of melasma during pregnancy. Chloasma is derived from the Greek word chloazein, meaning “to be green.” Melas, also Greek, means “black.” Because the pigmentation is never green in appearance, melasma is the preferred term.

See Diagnosing Dermatoses in Pregnant Patients: 8 Cases to Test Your Skills, a Critical Images slideshow, for help identifying several types of cutaneous eruptions associated with pregnancy.

The pathophysiology of melasma is uncertain. A direct relationship with female hormonal activity appears to be present, because melasma occurs more frequently in females than in males and commonly develops or worsens during pregnancy and with the use of oral contraceptive pills. Indeed, one half of melasma cases present initially during pregnancy. Additionally, the expression of estrogen receptors appears to be up-regulated in melasma lesions. [1] Whether hormone levels play a role in male melasma development is still a topic of debate. Other factors implicated in the pathogenesis of melasma are photosensitizing medications, mild ovarian or thyroid dysfunction, and certain cosmetics.

The most important factor in the development of melasma is exposure to sunlight. Ultraviolet (UV) radiation is known to induce increased production of alpha-melanocyte–stimulating hormone and corticotropin, as well as interleukin 1 and endothelin 1, all of which contribute to increased melanin production by intraepidermal melanocytes. Fibroblasts located in the dermal layer of the skin may also contribute to the development of melasma; overexpression of the tyrosine kinase receptor c-kit and certain stem cell factors have been identified in melasma lesions, and these are believed to increase melanogenesis. [2] Without the strict avoidance of sunlight, potentially successful treatments for melasma are doomed to fail.

A genetic predisposition is a major factor in the development of melasma. Melasma is much more common in women than in men. Persons with light-brown skin types from regions of the world with intense sun exposure are much more prone to the development of melasma. . In a global study of 324 women with melasma, 48% reported a positive family history of the condition. [3] Identical twins have been reported to develop melasma, [4] while other siblings under similar conditions did not.

Another major factor in melasma is exposure to sunlight. Ultraviolet radiation can cause peroxidation of lipids in cellular membranes, leading to generation of free radicals, which could stimulate melanocytes to produce excess melanin. Sunscreens that primarily block UV-B radiation (290-320 nm) are unsatisfactory because longer wavelengths (UV-A and visible radiation, 320-700 nm) also stimulate melanocytes to produce melanin.

Hormonal influences play a role in some individuals. The mask of pregnancy is well known to obstetric patients. The exact mechanism by which pregnancy affects melasma is unknown. Estrogen, progesterone, and melanocyte-stimulating hormone (MSH) levels are normally increased during the third trimester of pregnancy. Nulliparous patients with melasma have no increased levels of estrogen or MSH, but they may show elevated levels of estrogen receptors within lesions. In addition, the occurrence of melasma with estrogen- and progesterone-containing oral contraceptive pills and diethylstilbestrol treatment for prostate cancer has been reported. [5] The observation that postmenopausal woman who are given progesterone develop melasma, while those who are given only estrogen do not, implicates progesterone as playing a critical role in the development of melasma.

One study found a four-fold increase in thyroid disease in patients with melasma when compared with matched controls. A case report of two women who developed melasma after sudden and profound emotional stress implicated the release of MSH by the hypothalamus as a cause. Additionally, one study demonstrated an association between the development of melasma and the presence of melanocytic nevi and lentiginous nevi; patients with melasma showed a significantly higher number of both types of nevi than a control population. This would indicate a relationship between the development of melasma and the overall presence of pigmentation. [6]

Exactly which hormones and what mechanisms are involved in the development of melasma are yet to be determined. Genetic and hormonal influences in combination with ultraviolet radiation are the two most important causes of melasma, yet phototoxic and photoallergic medications and certain cosmetics have been reported to cause melasma in rare instances.

Melasma is very common, affecting over 5 million people in the United States. [7] Prevalence rates range from 8.8% among females of Latino descent living in the southern United States to up to 40% in some females of southeast Asian populations. [8, 9]

Persons of any race can be affected by melasma. However, melasma is much more common in constitutionally darker skin types than in lighter skin types, and it may be more common in light brown skin types, especially Latinos and Asians, from areas of the world with intense sun exposure.

Melasma is much more common in women than in men. Women are affected in 90% of cases. When men are affected, the clinical and histologic picture is identical.

Melasma is rare before puberty and most commonly occurs in women during their reproductive years. Melasma is present in 15-50% of pregnant patients.

Melasma has no associated mortality or morbidity. There have been no reported cases of malignant transformation, and it has not been associated with an increased risk of melanoma or other malignancies. In fact, patients with melasma are considered to be at decreased risk for melanoma. This is likely secondary to lower rates of skin malignancies in patients with a dark complexion.

Dermal pigment may take longer to resolve than epidermal pigment because no effective therapy is capable of removing dermal pigment. However, treatment should not be withheld simply because of a preponderance of dermal pigment. The source of the dermal pigment is the epidermis, and, if epidermal melanogenesis can be inhibited for long periods, the dermal pigment will not replenish and will slowly resolve.

Resistant cases or recurrences of melasma occur often and are certain if strict avoidance of sunlight is not rigidly heeded.

Strict sun avoidance is essential for resolution and to prevent recurrence of melasma. Patients with melasma should apply bleaching creams to areas of darkening only. Resolution with strict sun avoidance and topical bleaching creams can take months; caution patients to expect slow but gradual lightening.

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Willis Hughes Lyford, ENS Medical Corps, United States Navy; Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

John G Albertini, MD Private Practice, The Skin Surgery Center; Clinical Associate Professor (Volunteer), Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine; President-Elect, American College of Mohs Surgery

John G Albertini, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: QualDerm Partners; Novascan<br/>Have a 5% or greater equity interest in: QualDerm Partners – North Carolina.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.

Andrew D Montemarano, DO Consulting Staff, The Skin Cancer Surgery Center

Andrew D Montemarano, DO is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery, MedChi The Maryland State Medical Society

Disclosure: Nothing to disclose.


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