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melasma

DermatologyIntegumentary (Skin)Endocrine/Reproductive (hormonal association)

Summary

Melasma is an acquired, symmetric hyperpigmentary disorder of sun-exposed skin, especially the face (cheeks, forehead, upper lip), caused by increased melanin production/deposition. It is classically associated with pregnancy ("mask of pregnancy"/chloasma), oral contraceptives/estrogen, and UV exposure, and is most common in women with Fitzpatrick skin types III–V.

Detail

**Definition:** Chronic, acquired hypermelanosis presenting as symmetric, irregular tan-to-brown (or gray-brown) macules and patches on the face. Also called chloasma or "mask of pregnancy."

**Epidemiology/risk factors:** - Women >> men (about 90% of cases); reproductive-age adults - Fitzpatrick skin types III–V (Hispanic, Asian, Middle Eastern, African descent) - Pregnancy (often 2nd–3rd trimester), estrogen/progesterone exposure (OCPs, HRT) - UV and visible light exposure (the main trigger and cause of relapse) - Genetic predisposition; thyroid disease association; certain drugs (phenytoin, photosensitizing agents); cosmetics

**Pathophysiology:** - Melanocytes are normal in number but hyperfunctional, causing increased melanin synthesis and transfer to keratinocytes (increased tyrosinase activity) - Hormonal influence (estrogen and progesterone receptors, MSH stimulation) - UV light stimulates melanogenesis; also involves vascular and dermal changes - Histologic location of pigment: - Epidermal: melanin in basal/suprabasal layers; accentuated under Wood's lamp - Dermal: melanophages in the dermis; not accentuated under Wood's lamp - Mixed: most common

**Clinical patterns:** - Centrofacial (most common): forehead, cheeks, nose, upper lip, chin - Malar: cheeks and nose - Mandibular: jawline - Typically asymptomatic and not preceded by inflammation. Cosmetic and psychosocial impact is significant.

**Diagnosis:** Clinical. Wood's lamp can help determine depth. Dermoscopy or biopsy is rarely needed. Differential includes post-inflammatory hyperpigmentation, drug-induced pigmentation, lentigines, Riehl melanosis, acquired bilateral nevus of Ota-like macules (Hori nevus), and lupus (malar rash is erythematous, not purely pigmented).

**Management:** - Prevention: daily broad-spectrum sunscreen (ideally tinted/iron oxide-containing to block visible light), photoprotection, and stopping or changing hormonal triggers - First-line topical: triple combination cream (hydroquinone + tretinoin + topical corticosteroid, e.g., Tri-Luma) - Other topicals: hydroquinone alone (tyrosinase inhibitor), azelaic acid, kojic acid, tranexamic acid, cysteamine, vitamin C - Oral tranexamic acid is an option for refractory cases (caution with thrombotic risk) - Procedures: chemical peels, and lasers with caution (risk of post-inflammatory hyperpigmentation and rebound) - Pregnancy-related melasma often fades postpartum but may persist or recur; the condition is chronic and relapsing. - Adverse effects to know: hydroquinone can cause exogenous ochronosis (blue-black pigmentation) with prolonged high-concentration use; topical steroids can cause atrophy.

**High-yield board points:** - "Mask of pregnancy" + OCP use + sun exposure = melasma - Benign, with no malignant potential - Treatment is sun protection + hydroquinone (tyrosinase inhibitor) - Not to be confused with the malar rash of SLE (spares nasolabial folds, erythematous, photosensitive) or the linea nigra and areolar darkening of pregnancy (also hormonally driven)

Sources

  • First Aid for the USMLE Step 1 (Dermatology section)
  • Bolognia: Dermatology (Disorders of Hyperpigmentation)
  • Fitzpatrick's Dermatology
  • UpToDate: Melasma
  • AAD (American Academy of Dermatology) Melasma clinical resources
  • Robbins & Cotran Pathologic Basis of Disease (Skin: pigmentary disorders)

Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.