eMedicine Specialties > Dermatology > Diseases of Pigmentation

Melasma

Author: Andrew D Montemarano, DO, Consulting Staff, The Skin Cancer Surgery Center
Coauthor(s): Hugh Lyford,, Surgical Technician, The Skin Cancer Surgery Center
Contributor Information and Disclosures

Updated: Dec 16, 2009

Introduction

Background

Melasma is an acquired hypermelanosis of sun-exposed areas. Melasma presents as symmetric hyperpigmented macules, which can be confluent or punctate. The cheeks, the upper lip, the chin, and the forehead are the most common locations, as shown in the images below, but melasma can occasionally occur in other sun-exposed locations.

Confluent hyperpigmented macules in a malar distr...

Confluent hyperpigmented macules in a malar distribution.

Confluent hyperpigmented macules in a malar distr...

Confluent hyperpigmented macules in a malar distribution.


Melasma in a man.

Melasma in a man.

Melasma in a man.

Melasma in a man.


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.

Pathophysiology

The pathophysiology of melasma is uncertain. In many cases, a direct relationship with female hormonal activity appears to be present because melasma occurs with pregnancy and with the use of oral contraceptive pills. Other factors implicated in the etiopathogenesis 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. Without the strict avoidance of sunlight, potentially successful treatments for melasma are doomed to fail.

Race

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 Hispanics and Asians, from areas of the world with intense sun exposure.

Sex

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.

Age

Melasma is rare before puberty and most commonly occurs in women during their reproductive years.

Clinical

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.

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.

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,1 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.2 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.3

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.

More on Melasma

Overview: Melasma
Differential Diagnoses & Workup: Melasma
Treatment & Medication: Melasma
Follow-up: Melasma
Multimedia: Melasma
References

References

  1. Hughes BR. Melasma occurring in twin sisters. J Am Acad Dermatol. Nov 1987;17(5 Pt 1):841. [Medline].

  2. Resnik S. Melasma induced by oral contraceptive drugs. JAMA. Feb 27 1967;199(9):601-5. [Medline].

  3. Adalatkhah H, Sadeghi-bazargani H, Amini-sani N, Zeynizadeh S. Melasma and its association with different types of nevi in women: a case-control study. BMC Dermatol. Aug 5 2008;8:3. [Medline].

  4. Aloi F, Solaroli C, Giovannini E. Actinic lichen planus simulating melasma. Dermatology. 1997;195(1):69-70. [Medline].

  5. Tabata H, Yamakage A, Yamazaki S. Bandlike melasma mimicking linear morphea ("en coup de sabre" type). Cutis. Apr 1998;61(4):225-6. [Medline].

  6. Lawrence N, Cox SE, Brody HJ. Treatment of melasma with Jessner's solution versus glycolic acid: a comparison of clinical efficacy and evaluation of the predictive ability of Wood's light examination. J Am Acad Dermatol. Apr 1997;36(4):589-93. [Medline].

  7. Kopera D, Hohenleutner U. Ruby laser treatment of melasma and postinflammatory hyperpigmentation. Dermatol Surg. Nov 1995;21(11):994. [Medline].

  8. Taylor CR, Anderson RR. Ineffective treatment of refractory melasma and postinflammatory hyperpigmentation by Q-switched ruby laser. J Dermatol Surg Oncol. Sep 1994;20(9):592-7. [Medline].

  9. Nouri K, Bowes L, Chartier T, Romagosa R, Spencer J. Combination treatment of melasma with pulsed CO2 laser followed by Q-switched alexandrite laser: a pilot study. Dermatol Surg. Jun 1999;25(6):494-7. [Medline].

  10. Salem A, Gamil H, Ramadan A, Harras M, Amer A. Melasma: treatment evaluation. J Cosmet Laser Ther. Sep 2009;11(3):146-50. [Medline].

  11. Kanwar AJ, Dhar S, Kaur S. Treatment of melasma with potent topical corticosteroids. Dermatology. 1994;188(2):170. [Medline].

  12. Burke H, Carmichael AJ. Reversible melasma associated with tretinoin. Br J Dermatol. Nov 1996;135(5):862. [Medline].

  13. Kimbrough-Green CK, Griffiths CE, Finkel LJ, et al. Topical retinoic acid (tretinoin) for melasma in black patients. A vehicle-controlled clinical trial. Arch Dermatol. Jun 1994;130(6):727-33. [Medline].

  14. Kang WH, Chun SC, Lee S. Intermittent therapy for melasma in Asian patients with combined topical agents (retinoic acid, hydroquinone and hydrocortisone): clinical and histological studies. J Dermatol. Sep 1998;25(9):587-96. [Medline].

  15. Chan R, Park KC, Lee MH, et al. A randomized controlled trial of the efficacy and safety of a fixed triple combination (fluocinolone acetonide 0.01%, hydroquinone 4%, tretinoin 0.05%) compared with hydroquinone 4% cream in Asian patients with moderate to severe melasma. Br J Dermatol. Sep 2008;159(3):697-703. [Medline].

  16. Balina LM, Graupe K. The treatment of melasma. 20% azelaic acid versus 4% hydroquinone cream. Int J Dermatol. Dec 1991;30(12):893-5. [Medline].

  17. Breathnach AS. Melanin hyperpigmentation of skin: melasma, topical treatment with azelaic acid, and other therapies. Cutis. Jan 1996;57(1 Suppl):36-45. [Medline].

  18. Garcia A, Fulton JE Jr. The combination of glycolic acid and hydroquinone or kojic acid for the treatment of melasma and related conditions. Dermatol Surg. May 1996;22(5):443-7. [Medline].

  19. Wolf R, Wolf D, Tamir A, Politi Y. Melasma: a mask of stress. Br J Dermatol. Aug 1991;125(2):192-3. [Medline].

  20. Grimes PE. Melasma. Etiologic and therapeutic considerations. Arch Dermatol. Dec 1995;131(12):1453-7. [Medline].

  21. Grimes PE, Stockton T. Pigmentary disorders in blacks. Dermatol Clin. Apr 1988;6(2):271-81. [Medline].

  22. Grimes PE, Stockton T. Pigmentary disorders in blacks. Dermatol Clin. Apr 1988;6(2):271-81. [Medline].

  23. Hassan I, Kaur I, Sialy R, Dash RJ. Hormonal milieu in the maintenance of melasma in fertile women. J Dermatol. Aug 1998;25(8):510-2. [Medline].

  24. Pathak MA, Fitzpatrick TB, Kraus EW. Usefulness of retinoic acid in the treatment of melasma. J Am Acad Dermatol. Oct 1986;15(4 Pt 2):894-9. [Medline].

  25. Perez M, Sanchez JL, Aguilo F. Endocrinologic profile of patients with idiopathic melasma. J Invest Dermatol. Dec 1983;81(6):543-5. [Medline].

  26. Sialy R, Hassan I, Kaur I, Dash RJ. Melasma in men: a hormonal profile. J Dermatol. Jan 2000;27(1):64-5. [Medline].

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Further Reading

Keywords

melasma, chloasma, the mask of pregnancy, hypermelanosis

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.

Medical Editor

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 Ownership interest Consulting

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University 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.

Managing Editor

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.

CME Editor

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, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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