WOMEN’S HEALTH
MELASMA IN CLINIC
Dr Ginni Mansberg outlines the assessment, triggers and evidence-based management for treating melasma in the clinic.
DR GINNI MANSBERG
Dr Ginni Mansberg is a GP, TV presenter, podcaster, author and columnist. She is a physician specialising in women’s health, menopause and all things skin. She is also the co-founder and medical director of science-based cosmeceutical skincare brand, ESK.
Melasma remains one of the most common, and most frequently mismanaged presentations in aesthetic practice. Patients often arrive having already relapsed on a succession of pigmentation products, frustrated that improvement never seems to hold. For practitioners, the real challenge is more about framing melasma as a chronic, relapsing condition and building a protocol around long-term control rather than a single course of treatment.
RECOGNISING AND CLASSIFYING
Melasma is an acquired disorder of facial hyperpigmentation, presenting as symmetrical, ill-defined brown to grey-brown patches typically distributed across the cheeks, forehead, upper lip and chin. It largely affects women of reproductive age with Fitzpatrick skin types III–V, though an estimated 10% of cases occur in men. Prevalence varies substantially by population, from around 9% in Latino women in the southern United States to as high as 40% in some Southeast Asian cohorts, reflecting the combined influence of genetics, baseline pigmentation and cumulative UV exposure.
Clinically, melasma should be distinguished from solar lentigines and other forms of hyperpigmentation. Wood’s lamp examination remains a useful adjunct for estimating pigment depth: epidermal melasma shows enhanced contrast, while mixed and dermal patterns show little accentuation and generally respond more slowly to topical therapy, often needing adjunctive procedural intervention. This distinction matters for setting realistic timelines before treatment begins.
UNDERSTANDING THE TRIGGER PROFILE
Oestrogen upregulates tyrosinase activity directly via melanocyte hormone receptors.
UV exposure is the principal activating trigger, stimulating melanocytes both directly and via inflammatory signalling from surrounding keratinocytes. Daily broad-spectrum photoprotection is consequently non-negotiable; zinc oxide formulations provide superior UVA coverage, and tinted, iron-oxide-containing sunscreens add meaningful protection against visible light.
Heat activates melanogenesis via pathways separate from UV. This has direct procedural relevance: any heat-generating device, carries a theoretical risk of worsening melasma even where the intended effect is pigment reduction. Patients should also be advised on cumulative heat exposure from dailing activities, which can undermine a regimen.
Genetic susceptibility is significant and permanent: in a global survey of 324 women with melasma, 48% reported a family history, and 97% of those had an affected relative.
BUILDING AN EVIDENCE-BASED PROTOCOL
Effective management operates across three mechanisms: inhibiting new melanin synthesis, reducing melanosome transfer, and supporting turnover of pigmented cells.
For tyrosinase inhibition, 4-n-butylresorcinol has outperformed hydroquinone, arbutin and kojic acid in direct biochemical comparisons of tyrosinase inhibition, with a favourable tolerability profile. Azelaic acid (15–20%) offers comparable efficacy with useful anti-inflammatory action.
Vitamin C contributes both tyrosinase inhibition and antioxidant protection against UV-generated free radicals.
Tranexamic acid, topical or oral, interrupts keratinocyte–melanocyte signalling and has strong emerging trial evidence; oral dosing of 500–1500 mg daily has produced meaningful reductions in melasma, though long-term compliance in practice is often poor.
Niacinamide reduces melanosome transfer by 35–68% in co-culture models and produces clinically visible improvement from four weeks, with the benefit of barrier support.
For skin cell turnover, retinal is generally better tolerated than higher-strength retinoids in this population, while AHAs warrant caution given melasma’s inflammatory component. PHAs are the gentler alternative.
Procedurally, superficial peels are preferred over medium-depth or deep peels. Low-fluence Q-switched Nd:YAG and picosecond devices, conservatively settled, are the better-evidenced energy-based options. All laser and light modalities carry some risk of rebound pigmentation and should be reserved for patients who have demonstrated tolerance to, and partial response with, topical therapy.
EXPECTATIONS AND MAINTENANCE
Patients should be counselled from the outset that melasma cannot currently be cured, only controlled. Without a maintenance plan, approximately 72% of patients relapse within two months of stopping active treatment; even with a structured maintenance regimen, roughly half experience some pigment return within six months. A realistic timeline is useful at the first consultation: initial change from around weeks four to eight, more meaningful improvement by weeks eight to 16, and a genuine assessment point at three to six months, with dermal-component melasma requiring longer and often combination approaches.
The most valuable thing a practitioner can offer a melasma patient is not a stronger active, but an honest framework: consistent photoprotection, a sustainable long-term topical routine, cautious use of heat-generating procedures, and a maintenance plan built in from day one rather than added after relapse.
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