# Melasma (기미) --- ## 1. Definition - **Melasma (기미)** is an **acquired hyperpigmentation disorder**, characterized by symmetric, irregular, brown-to-gray macules and patches. - Typically appears on **sun-exposed areas**: face (malar, forehead, upper lip, nose, chin), and sometimes forearms. - Chronic, relapsing, and strongly influenced by hormonal and environmental factors. --- ## 2. Epidemiology & Prevalence - Common in women of reproductive age, especially **20–40 years**. - Strong prevalence in darker phototypes (Fitzpatrick III–V). - Female:male ratio ~9:1. - More common in Asian, Hispanic, and Middle Eastern populations. - Incidence increases during pregnancy (“mask of pregnancy”). --- ## 3. Pathophysiology ![Mayo Clinic Q and A: Treating melasma - Mayo Clinic News Network](https://newsnetwork.mayoclinic.org/n7-mcnn/7bcc9724adf7b803/uploads/2019/11/a-medical-illustration-of-melasma-original-1.jpg) ### A. Cellular and Molecular Basis - **Melanocyte hyperactivity** (not hyperplasia): melanocytes produce more melanin. - **Melanin deposition** in epidermis, dermis, or both. - Key drivers: - **UV radiation** → upregulates melanogenesis via melanocortin-1 receptor and α-MSH. - **Hormones** → estrogen and progesterone increase melanocyte activity. - **Genetic predisposition**. ### B. Pigment Distribution Types - **Epidermal Melasma**: melanin in basal and suprabasal keratinocytes → brown, more responsive to treatment. - **Dermal Melasma**: melanophages in dermis → blue-gray, resistant to therapy. - **Mixed**: combination of both, most common. ### C. Vascular and Inflammatory Contributions - Increased dermal vascularity may play a role. - Disrupted basement membrane may allow melanin leakage into dermis. --- ## 4. Clinical Features - **Presentation**: - Symmetrical, irregular hyperpigmented patches. - Face: centrofacial (forehead, nose, upper lip, chin), malar, mandibular. - **Wood’s lamp examination**: - Epidermal melasma → pigment enhancement. - Dermal melasma → no enhancement. - **Dermoscopic features**: - Brown reticular network (epidermal). - Bluish-gray granules (dermal). - Mixed patterns common. --- ## 5. Histopathology - Epidermal: basal hyperpigmentation, elongated rete ridges. - Dermal: dermal melanophages, solar elastosis. - Often accompanied by **increased vascularity**. --- ## 6. Risk Factors - UV exposure. - Pregnancy, oral contraceptives, HRT. - Genetic predisposition (family history). - Thyroid disease associations (controversial). - Medications (e.g., phenytoin). --- ## 7. Management ### A. General Principles - **Chronic and relapsing** → requires long-term control, not cure. - Sun protection is cornerstone. ### B. First-line: Topical Agents - **Hydroquinone** (HQ, 2–4%) → gold standard, inhibits tyrosinase. - **Triple combination cream** (HQ + tretinoin + corticosteroid). - **Alternative depigmenting agents**: azelaic acid, kojic acid, arbutin, tranexamic acid. ### C. Procedures - **Chemical peels**: glycolic acid, salicylic acid (superficial). - **Lasers/light therapy**: - Low-fluence Q-switched Nd:YAG (1064 nm, “laser toning”). - Fractional lasers. - Risks: rebound hyperpigmentation, PIH, especially in darker skin. - **Microneedling + tranexamic acid**: emerging therapy. ### D. Systemic Agents - **Oral tranexamic acid** (off-label): reduces melanogenesis via plasmin inhibition. - Caution: thromboembolic risk. --- ## 8. Prognosis & Patient Counseling - Chronic, often recurs with UV or hormonal triggers. - Requires **lifelong photoprotection**. - Set realistic expectations: “Improvement and control” rather than complete cure. --- ## 9. Clinical Pearls 1. Melasma (기미) = melanocyte hyperactivity, not proliferation. 2. Epidermal type responds best to topical/laser; dermal type resistant. 3. Strict sun protection = most effective long-term therapy. 4. Oral tranexamic acid is promising but not without risk. 5. Always differentiate from post-inflammatory hyperpigmentation (PIH), drug-induced pigmentation, and lentigines. Melasma (기미) is a chronic, hormonally and UV-driven acquired hyperpigmentation disorder. Histologically, it is due to melanocyte hyperactivity, with melanin deposition in epidermis and/or dermis. Clinically, it presents as symmetrical brown patches on sun-exposed skin. Management requires multimodal therapy (sun protection, topical agents, procedural treatments), with realistic counseling due to its relapsing nature.