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Copyright © 2005, Can Fam Physician Brown macules on the cheeks Can you identify this condition? A 38-year-old Asian woman presented with brown macules on both cheeks that she had
had for several years. She began to notice the macules with the birth of her first
child 6 years ago. She currently takes no medications, and her medical history was
unremarkable. The most likely diagnosis is:
1. Melasma Melasma, the Greek term for “a brown spot,” is a common hypermelanosis that typically
occurs on sun-exposed areas of the face. Chloasma, the Greek term for “a green
spot,” is a synonymous term that describes melasma during pregnancy (the “mask of
pregnancy”). Melasma is characterized by symmetrically distributed macules with
irregular borders ranging from light brown to dark brown to gray-brown.1 Pigmentation can be guttate or confettilike,
linear, or confluent. Three common clinically distinct distributions include
centrofacial (ie, forehead, nose, chin, upper lip), malar (ie, cheeks), and
mandibular (ie, lower jaw).2-4 Pigmentation usually evolves slowly over weeks
or months. Melasma is not exclusive to any sex, age, or race. Melasma is rarely reported before
puberty and is more common in women of reproductive age. Men comprise only 10% of
the affected population.5 The condition is
more prevalent among people with darker complexions (skin types IV to VI), including
those of Hispanic, Middle Eastern, Asian, and Indian descent who live in areas of
the world that receive high-intensity ultraviolet radiation.2 Investigations Wood’s light (wavelength 340 to 400 nm) examination is useful in diagnosis and can
help classify melasma into epidermal, dermal, and mixed types.4 Epidermal pigmentation is the most common type of melasma;
pigmentation is accentuated under Wood’s light examination. Dermal pigmentation
disappears under Wood’s light examination, and mixed types show areas with increased
(epidermal), absent, or decreased (dermal) pigmentation.4 On dark-brown skin (skin type VI), Wood’s light is unable to
locate hyperpigmentation; hence, the classification is indeterminate.3,4 These
classifications are valuable indicators of prognosis. While epidermal pigmentation
tends to respond better and faster to hypopigmenting agents (eg, hydroquinone),
dermal pigmentation responds variably and often unsatisfactorily.3 Histologic studies indicate an increase in the number and activity of melanocytes,
which enhance formation and transfer of melanosomes (pigment-containing granules) to
the layers of the epidermis and dermis.4
Epidermal and dermal classification of melasma is determined by the location of
melanocyte deposition. Although epidermal melanin is usually found in keratinocytes
of basal and suprabasal areas, dermal melanin is found in macrophages of the
superficial and deep layers.3 Mixed types
present with the histologic characteristics of both epidermal and dermal types.
Melanocyte-stimulating hormone does not have a role in melasma.6 While most cases are idiopathic, melasma can also be associated with genetics,
exposure to ultraviolet radiation, pregnancy, oral contraceptives, hormone
replacement therapies, mild endocrine disturbances (ie, ovarian or thyroid
dysfunction), cosmetics, antiepileptic medications, and other photosensitizing
drugs.2,6,7 Melasma is commonly reported
in women using estrogen-progesterone oral contraceptives, hormone replacement
therapy for prevention of osteoporosis, and in men using an estrogen derivative for
treatment of prostate cancer.3 An
endocrinologic study of women with melasma who had never been pregnant nor used oral
contraceptives reported increased serum concentrations of luteinizing hormone, which
could implicate mild ovarian dysfunction as a possible cause of idiopathic cases of
melasma.6 Sun exposure tends to be the
most important causative factor in all patients, so management options for melasma
must always include protection from the sun and avoidance of excessive exposure to
sunlight. Treatment Melasma is a cosmetic problem that is difficult to treat. Current treatments include
hypopigmenting compounds, exfoliative agents, and lasers.3,7,8 Hypopigmenting agents, such as hydroquinone (2% to 5%),
tretinoin cream (0.1%), azelaic acid (15% to 20%), kojic acid (2% to 4%), mild
cortisone, and combinations of these agents are effective at attenuating the
formation, decreasing the stability, and promoting the destruction of
melanocytes.3,8 Exfoliative agents, such as alpha-hydroxy and glycolic acid,
used in superficial chemical peels are more commonly used to treat
light-complexioned people. Complications of hypopigmentation are occasionally seen
on darker complexions.7 In recent years, attempts have been made to use pigmented lesion dye, Q-switched
Nd:YAG, Q-switched ruby, and argon and carbon dioxide lasers; however, studies using
these instruments have achieved only moderate success.3,7,8 Lasers are typically used after hypopigmenting and exfoliative
therapeutic options have been considered. In some cases, melasma spontaneously
disappears several months postpartum or after cessation of oral contraceptives. If
appropriate, discontinuation of causative medications is indicated. Treatment and
prevention of melasma should always include avoiding excessive exposure to the sun
and daily application of broad-spectrum sunscreens, preferably those containing
opaque physical blockers, such as titanium dioxide and zinc oxide. Consultation with
a dermatologist for therapeutic options is recommended. Biographies
References 1. Sams MW, Lynch PJ. Principles and practice of dermatology. 2nd ed. New York, NY: Churchill Livingstone Inc; 1996. 2. Pandya AG, Guevara IL. Disorders of hyperpigmentation. Dermatol Clin. 2000;18:91–98. [PubMed] 3. Perez-Bernal A, Munoz-Perez MA, Camacho F. Management of facial hyperpigmentation. Am J Clin Dermatol. 2000;1:261–268. [PubMed] 4. Sanchez NP, Pathak MA, Sato S, Fitzpatrick TB, Sanchez JL, Mihm MC., Jr Melasma: a clinical, light microscopic, ultrastructural, and
immunofluorescence study. J Am Acad Dermatol. 1981;4:698–710. [PubMed] 5. Vazquez M, Maldonado H, Benmaman C, Sanchez JL. Melasma in men. A clinical and histologic study. Int J Dermatol. 1988;27:25–27. [PubMed] 6. Perez M, Sanchez JL, Aguilo F. Endocrinologic profile of patients with idiopathic melasma. J Invest Dermatol. 1983;81:543–545. [PubMed] 7. Grimes PE. Melasma. Etiologic and therapeutic considerations. Arch Dermatol. 1995;131:1453–1457. [PubMed] 8. Piamphongsant T. Treatment of melasma: a review with personal experience. Int J Dermatol. 1998;37:897–903. [PubMed] |
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Dermatol Clin. 2000 Jan; 18(1):91-8, ix.
[Dermatol Clin. 2000]J Am Acad Dermatol. 1981 Jun; 4(6):698-710.
[J Am Acad Dermatol. 1981]Int J Dermatol. 1988 Jan-Feb; 27(1):25-7.
[Int J Dermatol. 1988]Dermatol Clin. 2000 Jan; 18(1):91-8, ix.
[Dermatol Clin. 2000]J Am Acad Dermatol. 1981 Jun; 4(6):698-710.
[J Am Acad Dermatol. 1981]Am J Clin Dermatol. 2000 Sep-Oct; 1(5):261-8.
[Am J Clin Dermatol. 2000]J Am Acad Dermatol. 1981 Jun; 4(6):698-710.
[J Am Acad Dermatol. 1981]Am J Clin Dermatol. 2000 Sep-Oct; 1(5):261-8.
[Am J Clin Dermatol. 2000]J Invest Dermatol. 1983 Dec; 81(6):543-5.
[J Invest Dermatol. 1983]Dermatol Clin. 2000 Jan; 18(1):91-8, ix.
[Dermatol Clin. 2000]J Invest Dermatol. 1983 Dec; 81(6):543-5.
[J Invest Dermatol. 1983]Arch Dermatol. 1995 Dec; 131(12):1453-7.
[Arch Dermatol. 1995]Am J Clin Dermatol. 2000 Sep-Oct; 1(5):261-8.
[Am J Clin Dermatol. 2000]Am J Clin Dermatol. 2000 Sep-Oct; 1(5):261-8.
[Am J Clin Dermatol. 2000]Arch Dermatol. 1995 Dec; 131(12):1453-7.
[Arch Dermatol. 1995]Int J Dermatol. 1998 Dec; 37(12):897-903.
[Int J Dermatol. 1998]Am J Clin Dermatol. 2000 Sep-Oct; 1(5):261-8.
[Am J Clin Dermatol. 2000]Arch Dermatol. 1995 Dec; 131(12):1453-7.
[Arch Dermatol. 1995]Int J Dermatol. 1998 Dec; 37(12):897-903.
[Int J Dermatol. 1998]