Notes · Dermatology · 29 October 2026

Melasma

Definition

• Melasma is a chronic, acquired hyperpigmentation disorder characterized by symmetric, irregularly shaped brown to gray‑brown macules and patches on sun‑exposed skin, most commonly the face.
• The condition is benign but often causes significant cosmetic concern and psychosocial distress.

Epidemiology

• Melasma affects up to 10 % of the general population, with higher prevalence (up to 30 %) in women of reproductive age.
• It is more common in individuals with Fitzpatrick skin types III–VI, particularly in South‑Asian, Hispanic, Middle‑Eastern, and African‑American groups.
• The peak incidence occurs between 20 and 40 years, and pregnancy‑related melasma (the “mask of pregnancy”) accounts for about 20 % of cases.

Aetiology

• Hormonal factors: Oral contraceptives, hormone replacement therapy, and pregnancy increase estrogen and progesterone levels, which stimulate melanocyte activity.
• Ultraviolet (UV) radiation: Chronic sun exposure induces melanogenesis and oxidative stress, acting as the primary environmental trigger.
• Genetic predisposition: A positive family history is reported in 40–60 % of patients, suggesting polygenic inheritance.
• Medications and cosmetics: Photosensitizing drugs (e.g., antiepileptics, tetracyclines) and certain cosmetics can exacerbate melasma.
• Thyroid disease: Subclinical hyperthyroidism has been associated with increased melasma prevalence, though causality remains unclear.

Pathophysiology

• Melanocyte hyperactivity: UV radiation and hormonal stimulation up‑regulate melanogenic enzymes (tyrosinase, TRP‑1, TRP‑2) leading to excess melanin synthesis.
• Melanosome transfer: Increased transfer of melanosomes from melanocytes to keratinocytes results in visible pigmentation.
• Dermal involvement: In chronic melasma, melanophages (melanin‑laden macrophages) accumulate in the upper dermis, producing a “dermal” component that is less responsive to topical therapy.
• Vascular component: Histologic studies show increased dermal blood vessels and up‑regulation of VEGF, contributing to erythema and possibly pigment persistence.
• Oxidative stress: UV‑induced reactive oxygen species damage keratinocytes and melanocytes, perpetuating melanogenesis.

Clinical Features

• Distribution: Symmetrical lesions on the malar region, forehead, chin, and upper lip; less commonly on the neck, forearms, and décolletage.
• Pattern types:
  • Malar (most common) – confined to the cheeks and nose.
  • Centrofacial – involves forehead, cheeks, upper lip, and chin.
  • Mandibular – limited to the jawline, more frequent in men and darker skin types.
• Color: Varies from light brown to gray‑brown; darker shades suggest deeper dermal melanin.
• Texture: Lesions are flat, non‑scaly, and non‑pruritic.
• Worsening factors: Sun exposure, hormonal fluctuations, heat, and certain cosmetics.

Investigations

• Clinical diagnosis: Primarily based on history and physical examination; Wood’s lamp examination helps differentiate epidermal (enhanced fluorescence) from dermal (no fluorescence) melasma.
• Dermatoscopy: Shows brown reticular network and gray‑blue granules indicating dermal pigment.
• Skin biopsy: Rarely required; histology reveals increased melanin in basal keratinocytes (epidermal type) or melanophages in the papillary dermis (dermal type).
• Laboratory tests: Thyroid function tests may be ordered if clinical suspicion exists; otherwise, routine labs are not indicated.

Management (Guideline 2024)

• General measures:
  • Strict photoprotection with broad‑spectrum sunscreen SPF 50+ applied 15 minutes before sun exposure and reapplied every 2 hours.
  • Physical barriers (wide‑brimmed hats, UV‑protective clothing).
  • Avoidance of known triggers (e.g., hormonal contraceptives, irritating cosmetics).
• Topical therapy (first‑line):
  • Hydroquinone 4 % cream nightly for 8–12 weeks (gold standard).
  • Combination creams (Kligman’s formula) containing hydroquinone 4 %, tretinoin 0.05 % and a mild steroid (fluocinolone acetonide 0.01 %) applied alternately to reduce irritation.
  • Azelaic acid 15–20 % gel twice daily – useful in patients intolerant to hydroquinone.
  • Tranexamic acid 5 % topical formulation – inhibits melanocyte‑stimulating pathways.
• Procedural options (second‑line or adjunct):
  • Chemical peels (glycolic acid 30 %, trichloroacetic acid 15 %) performed at 4‑week intervals.
  • Laser therapy – Q‑switched Nd:YAG 1064 nm for dermal melasma; low‑fluence laser resurfacing for epidermal type.
  • Intense pulsed light (IPL) – effective for vascular component; requires multiple sessions.
  • Microneedling combined with topical depigmenting agents – emerging evidence supports modest improvement.
• Systemic therapy (selected cases):
  • Oral tranexamic acid 250 mg twice daily for 8–12 weeks – recommended by the 2023 Indian Dermatology Association (IDA) guideline for refractory melasma; monitor for thromboembolic risk.
  • Polypodium leucotomos oral antioxidant 240 mg daily – adjunctive role in reducing UV‑induced oxidative stress.
• Follow‑up: Assess response every 4 weeks; taper or rotate agents to minimize irritation and tachyphylaxis.

Complications

• Post‑inflammatory hyperpigmentation (PIH): Aggressive procedures can trigger PIH, especially in darker skin types.
• Hydroquinone‑induced ochronosis: Long‑term high‑dose hydroquinone may cause paradoxical hyperpigmentation resembling ochronosis; avoid use beyond 6 months without a break.
• Psychological impact: Persistent cosmetic disfigurement can lead to anxiety, depression, and reduced quality of life; counseling may be required.

High‑Yield Exam Points

• Melasma is a hormone‑sensitive and UV‑exacerbated hyperpigmentation disorder.
• The three clinical patterns are malar, centrofacial, and mandibular.
• Wood’s lamp helps differentiate epidermal (enhanced fluorescence) from dermal (no fluorescence) melasma.
• First‑line topical therapy is hydroquinone 4 %; Kligman’s combination is the next step.
• Strict photoprotection (SPF 50+, broad‑spectrum) is essential for both treatment and prevention of recurrence.
• Oral tranexamic acid is indicated for refractory melasma per 2023 IDA guidelines; monitor for thrombotic risk.
• Avoid prolonged hydroquinone use to prevent ochronosis.
• Dermal melasma responds better to Q‑switched Nd:YAG laser than to topical agents alone.

Practice questions

1. A 28‑year‑old woman presents with symmetric brown patches on her cheeks that worsen after sun exposure. Wood’s lamp examination shows accentuation of the lesions. Which of the following is the most appropriate first‑line therapy?

• A) Oral tranexamic acid
• B) Hydroquinone 4 % cream
• C) Q‑switched Nd:YAG laser
• D) Topical retinoid alone

Answer: B — hydroquinone 4 % cream is the gold‑standard first‑line topical agent for epidermal melasma.

2. Which of the following statements about melasma is FALSE?

• A) It is more common in Fitzpatrick skin types I–II.
• B) Pregnancy can precipitate melasma.
• C) Dermal melasma shows little fluorescence under Wood’s lamp.
• D) Strict photoprotection is a cornerstone of management.

Answer: A — melasma is more prevalent in darker skin types (III–VI), not in types I–II.

3. A patient with refractory melasma is started on oral tranexamic acid. Which precaution is essential before initiating therapy?

• A) Baseline liver function tests
• B) Screening for hypercoagulable states
• C) Serum calcium level measurement
• D) Allergy testing for tranexamic acid

Answer: B — tranexamic acid carries a thromboembolic risk; screening for hypercoagulable conditions is necessary.

More in Dermatology

AI-assisted study material for exam revision. Always confirm with standard textbooks and current guidelines; not medical advice.