Melasma guide: causes, treatment options, and why it always comes back

Melasma is one of the most challenging pigmentation conditions to treat — not because effective treatments don't exist, but because relapse is near-universal without sustained maintenance. Here is the complete evidence-based guide.

What melasma is

Definition and distribution

Melasma is a chronic acquired hypermelanosis — a condition of excess melanin production in the epidermis and dermis, driven by UV exposure and hormonal triggers, producing symmetrical hyperpigmented patches on:
Centrofacial pattern (most common): cheeks, forehead, nose, upper lip, chin
Malar pattern: cheeks and nose only
Mandibular pattern: jawline (least common; often associated with hormonal fluctuation)

The symmetrical distribution and characteristic locations are diagnostic — melasma almost never presents as isolated single spots.

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Triggers and pathophysiology

UV exposure: the primary driver

Melasma is a UV-triggered condition — even brief UV exposure significantly worsens it. The mechanism:

UV activates keratinocytes → release of stem cell factor (SCF), endothelin-1, and prostaglandins
These keratinocyte-derived signals stimulate adjacent melanocytes via c-Kit receptor and PAR-2 pathways
Tyrosinase is upregulated → increased DOPA and dopaquinone production → increased melanin
Abnormally increased vascularization in melasma lesions (evident on dermoscopy) further enhances the keratinocyte-melanocyte signaling

UVA is particularly implicated: UVA (320–400 nm) reaches the dermis, and melasma lesions show dermal melanophage involvement alongside epidermal melanin excess. This is why UVA-blocking (PA++++ rated, zinc oxide or avobenzone/tinosorb) sunscreens are specifically important for melasma.

Visible light also triggers melasma in darker skin types — a significant finding because standard sunscreens (mineral and chemical) do not block visible light. Iron oxide-containing tinted sunscreens are required to block HEV/visible light.

Hormonal triggers

Estrogen and progesterone upregulate melanocyte-stimulating hormone receptors and increase tyrosinase expression. Melasma commonly appears or worsens during:
Pregnancy ("mask of pregnancy" — chloasma)
Combined oral contraceptive pill use
Hormone replacement therapy

Stopping the hormonal trigger (discontinuing the OCP, postpartum) often results in partial improvement but rarely complete clearance — UV exposure perpetuates melasma even after hormonal triggers are removed.

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Evidence-based treatments

Kligman triple therapy (gold standard)

*Kligman AM, Willis I. (1975). A new formula for depigmenting human skin. Archives of Dermatology, 111(1), 40–44.*

The original Kligman formula: hydroquinone 5% + tretinoin 0.1% + dexamethasone 0.1% in a cream base. Modern adaptations:

Tri-Luma cream (FDA-approved): fluocinolone acetonide 0.01% + hydroquinone 4% + tretinoin 0.05% — the most studied combination for melasma.

Mechanism of the triple combination:
Hydroquinone: Tyrosinase substrate analog + melanocyte cytotoxicity → reduces melanin production
Tretinoin: Accelerates epidermal cell turnover → removes melanin-containing keratinocytes faster; also improves HQ penetration
Mild corticosteroid: Reduces post-inflammatory stimulation from the other two actives (HQ and tretinoin can cause mild irritation → inflammation → new melanin stimulus); the steroid breaks this cycle

Triple therapy at 8 weeks produces significantly greater improvement than any single or dual agent in controlled trials. Tri-Luma RCTs show 70–80% of patients achieving good to excellent improvement at 8 weeks.

Long-term steroid caution: Topical steroids on the face should not be used indefinitely — skin atrophy, telangiectasia, and steroid-induced acne develop with prolonged use. Triple therapy is used in 8–12 week cycles with maintenance on the other two agents (HQ + tretinoin) without the steroid.

Topical tranexamic acid (2–5%)

Inhibits keratinocyte-derived plasminogen activators → reduces PAR-2 activation → less SCF and prostaglandin release → reduced melanocyte stimulation. Multiple RCTs demonstrate meaningful improvement comparable to hydroquinone with substantially better tolerability.

Particularly useful for:
Maintenance phase after initial triple therapy (TXA + tretinoin)
Patients who cannot use hydroquinone (allergy, preference, or extended use concern)

Oral tranexamic acid (250 mg twice daily)

Zhu JW meta-analysis (2019): Oral TXA was consistently superior to topical TXA for melasma in the studies analyzed. It addresses the systemic hormonal and photobiological triggers that topical application cannot fully counteract.

Requires prescriber oversight — screening for thrombotic risk factors. 8–12 week courses are standard; many patients require maintenance dosing.

Azelaic acid 20%

Baliña 1991: Equivalent to hydroquinone 4% cream in melasma severity scores over 24 weeks, with better tolerability. Suitable for pregnancy (Category B) and longer-term use than hydroquinone.

Topical kojic acid 1–2% + glycolic acid

The Garcia & Fulton (1996) combination — additive mechanisms (copper chelation + exfoliation). An HQ-free option for patients who want OTC management.

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The laser controversy

Why many lasers worsen melasma

Q-switched lasers, fractional lasers, and IPL can worsen melasma through:
Thermal stimulation of melanocytes — heat activates c-Kit receptor signaling → melanogenesis
Post-procedure inflammation → PIH superimposed on melasma → worse net outcome
Paradoxical darkening from incomplete treatment or treating dermal melanophages that then release melanin

Lasers that are used for melasma:
Low-fluence Q-switched Nd:YAG (1064 nm, "toning"): Used in experienced hands for recalcitrant melasma — the low energy prevents thermal activation. Multiple sessions required; results variable.
Picosecond lasers: Shorter pulse duration → less thermal effect → potentially safer for melanocytes. Growing evidence base.

Critical caveat: All laser treatment for melasma requires meticulous pre- and post-procedure UV protection and is performed by experienced operators. Laser should not be the first-line treatment; it is reserved for melasma unresponsive to 3–6 months of topical therapy.

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Why melasma always comes back

Melasma is a chronic condition, not a curable one:

Melanocytes in melasma-affected areas are permanently hyperresponsive to UV and hormonal stimulation
Treatment clears the visible pigmentation but does not normalize the underlying melanocyte biology
Any significant UV exposure after treatment reignites melanin production in the same locations
Maintenance therapy (daily SPF + depot depigmenting agent) is required indefinitely, not just until the spots clear

The practical message for patients: "We are managing your melasma, not curing it. Your skin is now requiring active management like any chronic condition — maintenance treatment and disciplined sun protection will keep it controlled."

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Maintenance protocol

Daily (indefinitely):
Tinted SPF 50+ with iron oxides (visible light + UV protection)
Reapply SPF every 2 hours during outdoor exposure
Niacinamide 5% AM
Tranexamic acid 2–3% AM or PM

PM maintenance:
Tretinoin 0.025–0.05% (3–5× per week)
Azelaic acid 15% on non-tretinoin nights

Trigger management:
Evaluate OCP containing drospirenone (less androgenic progestin; may have less melasma-worsening effect than levonorgestrel-containing pills)
Avoid facial heat treatments (steam, saunas, hot yoga) — heat independently stimulates melanogenesis

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