Dermatology · Pigmentary Disorders
The facts most likely to be tested
Melasma presents as symmetric, hyperpigmented macules and patches typically involving the malar cheeks, forehead, and chin.
The primary risk factors for melasma include ultraviolet (UV) light exposure, pregnancy, and the use of oral contraceptives.
Melasma is most commonly seen in women of reproductive age with Fitzpatrick skin types IV-VI.
Wood’s lamp examination is used to classify melasma into epidermal, dermal, or mixed types based on the enhancement of pigment.
The first-line treatment for melasma is strict photoprotection with broad-spectrum sunscreen and avoidance of sun exposure.
Triple therapy consisting of hydroquinone, a topical retinoid, and a topical corticosteroid is the gold standard pharmacological treatment.
Melasma is frequently referred to as the mask of pregnancy due to its strong association with hormonal fluctuations.
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A 32-year-old female G1P0 at 24 weeks gestation presents to the clinic for a routine prenatal visit. She reports the development of dark, blotchy skin patches on her face over the last two months. Physical examination reveals symmetric, hyperpigmented, light-to-dark brown macules distributed across her malar cheeks and forehead. She denies any pruritus, scaling, or recent changes in her skincare routine. She works as a lifeguard and spends significant time outdoors.
What is the most likely diagnosis?
Melasma
The patient's presentation of symmetric hyperpigmentation on the face during pregnancy is classic for melasma, which is triggered by hormonal changes and UV exposure.
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Etiology / Epidemiology
Common in reproductive-age women with Fitzpatrick skin types IV-VI. Triggered by UV exposure and estrogen.
Clinical Manifestations
Symmetric, hyperpigmented macules on the face. Mask of pregnancy is the classic chloasma presentation.
Diagnosis
Primarily clinical diagnosis. Wood's lamp examination helps determine depth of pigment.
Treatment
Triple therapy (hydroquinone, tretinoin, fluocinolone) is first-line. Strict sun protection is mandatory.
Prognosis
Chronic, relapsing condition. UV avoidance is the most critical factor for long-term control.
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Epidemiology & Etiology
Prevalence is highest in individuals with darker skin tones exposed to intense sunlight. Primary triggers include UV radiation, pregnancy, and oral contraceptives. Genetic predisposition is noted in approximately 30-50% of cases.
Pertinent Anatomy
Melasma involves the epidermis and/or dermis of the face. The distribution is typically centrofacial, malar, or mandibular, sparing the eyelids and submental area.
Pathophysiology
Increased melanocyte activity leads to excessive melanin production. Estrogen and progesterone receptors on melanocytes stimulate pigment synthesis. Chronic UV-induced oxidative stress exacerbates the hyperpigmentation process.
Clinical Manifestations
Presents as symmetric, brown-to-gray hyperpigmented patches. The mask of pregnancy, or chloasma, is a classic presentation. Rule out systemic endocrine disorders if distribution is atypical or sudden in onset.
Diagnosis
Diagnosis is clinical. A Wood's lamp examination is used to classify pigment as epidermal (accentuated), dermal (no change), or mixed. Dermoscopy may be used to visualize pigment patterns in complex cases.
Treatment
Triple therapy (hydroquinone, tretinoin, fluocinolone) is the gold standard. Hydroquinone can cause exogenous ochronosis with long-term use. Strict sun protection with broad-spectrum SPF 50+ is required to prevent recurrence.
Prognosis
Condition is chronic and often refractory. Recurrence is common upon sun re-exposure. Long-term maintenance requires consistent photoprotection and intermittent topical therapy.
Differential Diagnosis
Post-inflammatory hyperpigmentation: history of preceding skin trauma or acne
Solar lentigines: discrete, non-symmetric sun spots
Drug-induced hyperpigmentation: history of minocycline or amiodarone use
Addison's disease: generalized hyperpigmentation with systemic symptoms
Riehl's melanosis: contact dermatitis-related pigmentary change