Melasma

Meet the patient

A 34-year-old woman with olive skin, six months postpartum, returns from a beach holiday to find symmetrical brown patches across her cheeks, forehead and upper lip — a mask she cannot wash off. Her mother had the same thing in pregnancy. She wants to know whether it will ever go.[5][6]

Two questions decide her management and her expectations: how deep is the pigment? — Wood's lamp answers that, and depth predicts everything — and what is driving it? — sun, hormones and skin type, all of which she has. Hold those two and the whole plan writes itself.[5][6]

One disease, two lights, two depths — the whole puzzle

Melasma is not excess melanin alone; it is hyperactive melanocytes fired by light and hormones, and where the pigment lands decides whether creams can reach it. Ultraviolet A and B and — increasingly recognised — visible light stimulate keratinocytes to release stem cell factor, which switches on melanocytes through the c-KIT receptor, MITF and tyrosinase, the rate-limiting enzyme of melanin synthesis.[5][7]

Oestrogen and progesterone (pregnancy, the oral contraceptive pill, hormone replacement) amplify that same response through receptors on the melanocyte — which is why melasma is roughly nine women to one man and why the mask of pregnancy is the textbook presentation.[5][6]

The depth is the bit that earns marks. In melasma the basement membrane is disrupted, so melanin can fall through gaps into the dermis and be swallowed by melanophages. Pigment trapped in the epidermis is within reach of creams; pigment sequestered in dermal melanophages is not. The Wood's lamp tells you which you are dealing with.[5][7]

Etymology for viva gold: chloasma, the old name, is from the Greek khloos, "greenish" — a colour the lesions never actually are, which is exactly why the modern term melasma (from melas, "black") replaced it. The "mask of pregnancy" is the lay name that has outlived every textbook edition.[1]

The three patterns — and where they sit

Melasma sorts by anatomical distribution and by Wood's lamp depth, and both classifications are examinable. Distribution is the easy one to spot at the bedside.[1][6]

• Centrofacial — forehead, cheeks, nose, upper lip, chin; the commonest pattern and the most cosmetically distressing. (Note the spared upper-lip skin above the vermillion in those who shave — a clue it is light-driven, not hormonal alone.)[5]
• Malar — cheeks and nose only, a butterfly mask often mistaken for early rosacea before the colour settles.[5]
• Mandibular — jawline; more common in older patients, often more dermal and more resistant.[5][6]

Wood's lamp depth — the classification that predicts treatment

The Wood's lamp is the single most useful bedside test in melasma: it separates the pigment that creams can reach from the pigment they cannot. It emits long-wave UVA at about 365 nm; epidermal melanin absorbs it and the patch darkens and sharpens, while dermal melanin, shielded by overlying skin, does not change.[6]

[1] [6]

The discriminator line: brown and accentuated is epidermal and treatable; slate-grey and not accentuated is dermal and stubborn; set the patient's expectations to match the depth on day one.[1]

How common, who, and the seven triggers

[5] [6]

The strongest risk factors run together: female sex, Fitzpatrick III-IV skin, pregnancy, the oral contraceptive pill or HRT, ultraviolet and visible light, and family history. Patients with darker skin have melanocytes that fire more readily and transfer pigment more efficiently, so once triggered the pigmentation is more conspicuous and more prone to post-inflammatory darkening from over-aggressive treatment.[5][6]

[5] [6]

Why it happens — the cascade, in one paragraph

UV (and visible light) hits the keratinocyte, which releases stem cell factor; SCF binds c-KIT on the melanocyte; MITF rises; tyrosinase fires; eumelanin is made and shipped to keratinocytes. Hormones amplify the same pathway; a leaky basement membrane lets pigment drop into the dermis; mast cells and new vessels sustain the inflammation. Every treatment you will name attacks a node on that cascade — tyrosinase, turnover, transfer, vascularity, plasmin.[5][7]

The depth mechanism — why dermal melasma resists creams

Basement membrane disruption (thinning, duplication, gap formation) lets melanin fall through into the dermis, where dermal melanophages engulf it. That pigment sits below the reach of any topical, which is why dermal and mixed melasma need oral tranexamic acid or procedures rather than cream alone. Increased VEGF and mast-cell mediators add a vascular and inflammatory component that oral tranexamic acid — anti-plasmin and anti-angiogenic — is uniquely placed to address.[5][7]

Read the patch like the Wood's lamp does

Symmetrical, poorly defined, brown to grey-brown patches on sun-exposed face, asymptomatic but for mild stinging after sun, are melasma until disproven. The colour is the depth clue: brown is epidermal, slate-grey is dermal, brown-grey is mixed.[6]

• Centrofacial is commonest and most distressing; malar is the butterfly; mandibular favours older patients and runs deeper.[5]
• Extra-facial melasma (neck, forearms) marks severe cumulative sun exposure.[5]
• A subtle erythematous or brown-pink undertone signals the vascular component and predicts a weaker response to topicals alone.[7]

The classic trap: a unilateral lesion, a violaceous hue, marked scale, mucosal involvement, palmar-crease darkening or systemic symptoms is not melasma — reach for the differential and the cortisol/ACTH before reaching for hydroquinone.[1][6]

Face-off — melasma versus its closest mimics

[1] [6]

The mimics not to miss: exogenous ochronosis — paradoxical blue-black darkening from hydroquinone overuse, with banana-shaped ochre dermal deposits on histology, that does not improve with more hydroquinone; drug-induced pigmentation (minocycline slate-grey, amiodarone blue-grey, antimalarials, heavy metals), often diffuse and involving sclerae or nails; Riehl melanosis (reticulated brown-grey from cosmetic contact allergy); and Addison's disease — generalised pigmentation with palmar creases, mucosa, scars, fatigue, weight loss and postural drop.[2][3][6]

Assessment and investigation — clinical first, biopsy last

Melasma is a clinical diagnosis. History (onset, pregnancy, hormones, sun, family, cosmetics, drugs, prior hydroquinone and any paradoxical darkening), examination under ambient light, then Wood's lamp in a darkened room 10-15 cm from the skin — that is the assessment. Photograph with standard lighting for monitoring, because improvement is gradual and patients miss incremental change.[1][6]

Investigations exist to exclude mimics, not to confirm melasma. TSH if thyroid symptoms (autoimmune thyroid disease is over-represented); cortisol and ACTH or a short synacthen test if there is generalised pigmentation, mucosal involvement, postural drop or hyponatraemia (Addison's); skin biopsy only for atypical features, failure to respond, or to confirm ochronosis, lichen planus pigmentosus or drug pigmentation — and not lightly on the face, where biopsy itself can post-inflammatory-darken in darker skin.[1][6]

Management — photoprotection first, always, for everyone

Every patient starts with strict photoprotection, regardless of depth or severity, because without it no topical, oral or procedural therapy holds. This is the non-negotiable foundation and the single most effective intervention in the whole disease.[1][6]

• Sunscreen broad-spectrum SPF 50 or higher with PA++++, applied generously 15-30 minutes before exposure and reapplied every two hours outdoors; a tinted iron-oxide formulation is preferred because iron oxide blocks visible light, a major driver especially in darker skin.[2][6]
• Physical measures — wide-brimmed hats, sunglasses, shade, avoiding midday sun, UV film on car and home windows for long commuters.[1]
• Trigger review — the oral contraceptive pill, HRT and photosensitising drugs; switch where practical. Pregnant patients avoid hydroquinone and tretinoin entirely and rely on photoprotection and azelaic acid.[6]

The stepwise ladder — triple combination, then the rest

Kligman's triple combination is the most evidence-based first-line topical: hydroquinone 2-4 percent, tretinoin 0.05 percent and fluocinolone acetonide 0.01 percent, applied nightly for 8-12 weeks. Hydroquinone blocks tyrosinase, tretinoin speeds keratinocyte turnover and hydroquinone penetration, and the mild steroid dampens the irritation that would otherwise cause post-inflammatory darkening. The 2022 systematic review and 2025 network meta-analysis both confirm triple combination beats any single agent.[1][6][8]

• Azelaic acid 15-20 percent is the safe alternative — tyrosinase inhibition and anti-proliferative, the agent of choice in pregnancy, where hydroquinone and tretinoin are avoided.[1][6]
• Second-line topicals — hydroquinone monotherapy 2-4 percent in short courses, tretinoin 0.025-0.05 percent, kojic acid, arbutin, cysteamine (a potent emerging agent with a sulphurous odour), niacinamide (blocks melanosome transfer) and topical tranexamic acid.[2][3]
• Oral tranexamic acid 250 mg two to three times daily for refractory, mixed or dermal disease — anti-plasmin and anti-angiogenic; contraindicated in thromboembolic disease, active malignancy, severe renal impairment and pregnancy.[2]

[1] [6]

Procedures — last, and cautious, in darker skin

Procedures are third-line and dangerous in Fitzpatrick IV-VI, where they can cause post-inflammatory hyperpigmentation and paradoxical worsening. Chemical peels (glycolic 30-70 percent, salicylic 20-30 percent, mandelic — safer in darker skin for its larger molecule and slower penetration, Jessner's), low-fluence Q-switched Nd:YAG 1064 nm laser toning, picosecond lasers (less thermal damage), fractional non-ablative lasers, and microneedling (enhancing topical delivery) — all only in experienced hands, at conservative settings, with test patches, under strict photoprotection. Intense pulsed light is generally avoided in Fitzpatrick IV-VI.[1][4][6][8]

How patients with melasma come to harm (the preventable list)

• Exogenous ochronosis from hydroquinone pushed beyond six months — the paradoxical darkening that more hydroquinone only deepens[2][6]
• Post-inflammatory hyperpigmentation from an aggressive peel or laser in darker skin that was never test-patched[4][6]
• Missed Addison's disease labelled melasma while the patient loses weight and drops her blood pressure[1]
• Thromboembolism from oral tranexamic acid given without a clotting-risk history[2]
• Teratogenic exposure — hydroquinone or tretinoin in pregnancy instead of azelaic acid[6]
• Frustration and non-adherence because no one set the expectation that this is chronic, relapsing and controllable, not curable[5][6]

Special populations

Pregnancy and lactation: management is photoprotection and azelaic acid 15-20 percent only — hydroquinone and tretinoin avoided, oral tranexamic acid contraindicated. Much postpartum melasma fades; reassure and defer the full ladder until after breastfeeding.[6]

Darker skin (Fitzpatrick IV-VI): highest risk of melasma and of treatment-related post-inflammatory hyperpigmentation. Start gentle, avoid aggressive procedures, use tinted iron-oxide sunscreen, and monitor hydroquinone courses.[2][6]

Men: less hormonally driven, more sun- and thyroid-linked; the same ladder applies but response is more variable.[5]

Older patients: often mandibular and more dermal; differentiate from solar lentigines, actinic bronzing and drug pigmentation, and biopsy if atypical before long-term therapy.[1]

Prognosis, prevention and the counselling that matters

Melasma is chronic and relapsing; complete permanent cure is uncommon, and the disease is best framed as a lifelong tendency to pigment in response to light and hormones. Epidermal disease does best with topicals; mixed is intermediate; dermal is the most resistant and may need oral tranexamic acid or procedures for substantial — not complete — improvement.[1][6]

Prevention is maintenance: daily broad-spectrum SPF 50 plus tinted iron oxide, reapplied outdoors, with hats and shade, indefinitely — even after apparent clearance, because relapse with the next holiday or pregnancy is the rule. Regional regulation of hydroquinone varies (restricted to prescription in the EU and Japan, available over the counter in parts of the US), but the principle is constant: short courses, monitoring, no continuous long-term use.[1][6]

Counselling is as important as the drug. At the first visit say melasma is controllable, not curable, that the aim is lightening and stability, that 8-12 weeks is the realistic timeline for a topical to show, and that visible light and heat — not just sunburn — reactivate pigment. Demonstrate sunscreen quantity; address cost and the white-cast problem; review at 8-12 weeks and escalate or reconsider the diagnosis if the plateau is unsatisfactory.[5][6]

The mantra, and the memory device

[1] [6]

The mantra: photoprotection first, Wood's lamp for depth, triple combination for epidermal, tranexamic acid for dermal, and never push hydroquinone past six months.[1][6]

Ward-round test — three stems, thirty seconds each

Stem 1 — the postpartum mask (answer)

A 34-year-old with olive skin, six months postpartum, has symmetrical brown patches on cheeks, forehead and upper lip after a beach holiday; Wood's lamp accentuates them. What is it, and what is the first prescription? Model: Epidermal melasma, light- and hormone-driven. First prescription is strict photoprotection — broad-spectrum SPF 50 plus tinted iron-oxide sunscreen, hats, shade — then Kligman's triple combination (hydroquinone 2-4 percent, tretinoin 0.05 percent, fluocinolone 0.01 percent) nightly for 8-12 weeks. Set the expectation: controllable, not curable; 8-12 weeks to judge response. Reassure that postpartum disease often improves but recurs with sun and future pregnancies.[1][5][6]

Stem 2 — paradoxical darkening after a year of creams (answer)

A 45-year-old has used over-the-counter hydroquinone continuously for 14 months and her cheek patches are now blue-black and worsening. What happened? Model: Exogenous ochronosis — paradoxical darkening from prolonged hydroquinone, with dermal deposition of homogentisic-acid-like pigment (banana-shaped ochre deposits on histology) that does not improve with more hydroquinone. Stop hydroquinone immediately, switch to azelaic acid or cysteamine, intensify photoprotection, and consider laser only in experienced hands. The prevention is the lesson: cap hydroquinone at 8-12 weeks, then break.[2][6]

Stem 3 — melasma that is not melasma (answer)

A 50-year-old has facial pigmentation plus fatigue, weight loss, postural light-headedness and darkening of her palmar creases and oral mucosa. Is this melasma? Model: No — this is Addison's disease until proven otherwise, and the discriminators are the systemic symptoms, the mucosal and palmar-crease pigmentation, and the generalised rather than purely sun-exposed distribution. Check morning cortisol and ACTH and arrange a short synacthen test; treat the adrenal failure, not the pigment. Reaching for hydroquinone here would be a serious and delay-causing error.[1][6]

References

1. [1]Neagu N, Conforti C, Agozzino M, et al. Melasma treatment: a systematic review J Dermatolog Treat, 2022.PMID 33849384
2. [2]Gan C, Rodrigues M. An Update on New and Existing Treatments for the Management of Melasma Am J Clin Dermatol, 2024.PMID 38896402
3. [3]Thawabteh AM, Jibreen A, Karaman D, et al. Skin Pigmentation Types, Causes and Treatment-A Review Molecules, 2023.PMID 37375394
4. [4]Tan MG, Jo CE, Chapas A, et al. Radiofrequency Microneedling: A Comprehensive and Critical Review Dermatol Surg, 2021.PMID 33577211
5. [5]Ali L, Al Niaimi F. Pathogenesis of Melasma Explained Int J Dermatol, 2025.PMID 40022484
6. [6]McKesey J, Tovar-Garza A, Pandya AG. Melasma Treatment: An Evidence-Based Review Am J Clin Dermatol, 2020.PMID 31802394
7. [7]Gu D, Pan R, Meng X, et al. What lies behind melasma: a review of the related skin microenvironment Int J Dermatol, 2025.PMID 39212112
8. [8]Leung JH, Leung HWC, Wang SY, et al. Efficacy and Safety of Different Treatments for Melasma: Network Meta-Analysis of Updated Data Diseases, 2025.PMID 41149049