Melasma Clinical Presentation

  • Author: Andrew D Montemarano, DO; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 14, 2012
 

History

Patients may inquire about progressive hyperpigmentation of the face, which may be temporally related to pregnancy or to the use of oral contraceptive pills.

Intense or chronic exposure to sunlight worsens the condition and may precipitate melasma, but because the development of pigmentation is often insidious, patients may not recognize the association.

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Physical

The macular hyperpigmentation of melasma is commonly tan to brown. Blue or black may be evident in patients with dermal melasma. The distribution is 1 of 3 patterns: centrofacial, malar, or mandibular. A rare pattern confined to the forearms is seen in women receiving exogenous progesterone and in Native American Indians.

The excess melanin can be visually localized to the epidermis or the dermis by use of a Wood lamp (wavelength, 340-400 nm). Epidermal pigment is enhanced during examination with a Wood light, whereas, dermal pigment is not. Clinically, a large amount of dermal melanin is suspected if the hyperpigmentation is bluish black. In individuals with dark-brown skin, examination with a Wood light does not localize pigment, and these patients are thus classified as indeterminate.

The Melasma Area and Severity Index (MASI) is common outcome measure used to assess melasma patients; however, it previously had not been validated. The goal of a 2010 study was to determine the reliability and validity of the MASI. The authors report that the MASI is a reliable tool for measuring the severity of melasma when compared with the melasma severity scale, mexameter scores, and area measurements.[1]

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Causes

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. More than 30% of patients have a family history of melasma. Identical twins have been reported to develop melasma,[2] 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. However, nulliparous patients with melasma have no increased levels of estrogen or MSH. In addition, the occurrence of melasma with estrogen- and progesterone-containing oral contraceptive pills and diethylstilbestrol treatment for prostate cancer has been reported.[3] 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 4-fold increase in thyroid disease in patients with melasma when compared with matched controls. A case report of 2 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.[4]

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 2 most important causes of melasma, yet phototoxic and photoallergic medications and certain cosmetics have been reported to cause melasma in rare instances.

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Contributor Information and Disclosures
Author

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 Micrographic Surgery and Cutaneous Oncology, American Society for Dermatologic Surgery, and MedChi

Disclosure: Nothing to disclose.

Coauthor(s)

Hugh Lyford  Surgical Technician, The Skin Cancer Surgery Center

Disclosure: Nothing to disclose.

Specialty Editor Board

James Fulton Jr, MD, PhD  Center for Cosmetic Dermatology; Consultant, Vivant Pharmaceuticals, LLC

James Fulton Jr, MD, PhD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, American Society for Laser Medicine and Surgery, Dermatology Foundation, International Society of Cosmetic and Laser Surgeons, and Skin Cancer Foundation

Disclosure: Vivant Pharmaceuticals Grant/research funds Consulting

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, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

John G Albertini, MD  Consulting Staff, Dermatologic Surgery, The Skin Surgery Center; Program Director, ACGME Accredited Fellowship in Procedural Dermatology

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

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

References

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Confluent hyperpigmented macules in a malar distribution.
Melasma in a man.
 
 
 
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