Melasma · Pigment Lasers · A Physician's Perspective
Before I treat the brown, I look at the red.
The short answer
I do not approach melasma as a problem of melanin alone. When pigmentation sits on top of significant erythema, irritation or vascular activity, I pay attention to the red before I target the brown.
When the skin is stable enough for laser, I usually begin with Hollywood Spectra 1064 nm Spectra mode at 0.3 ms, using a 6–8 mm spot, before moving to QS or PTP delivery for the pigment.
I call that first step noise cancellation. Melanin is the signal I eventually want to treat. Redness, inflammation and vascular activity are background noise. Clinically, I find that calming some of that background first makes the pigment-directed part of the treatment more controlled.
This is not a claim that 0.3-ms Nd:YAG is a substitute for a dedicated vascular laser, and my exact Spectra-first sequence has not been tested against other sequences in a controlled trial.
If somebody arrives with severely inflamed or unstable skin, I may not laser them at all that day. A good laser treatment cannot compensate for an environment that keeps recreating the problem.
Melasma is not just a pigment problem
The classic laser model is clean: identify the chromophore, choose the wavelength, choose the pulse duration, adjust for skin type, then treat the target. For melasma, I think that model is incomplete.
The melanocyte lives inside an epidermal and dermal environment influenced by keratinocytes, fibroblasts, endothelial cells, inflammatory signalling, ultraviolet exposure, visible light and hormonal factors. The brown we see is an output of that system, not the whole system.
I have written separately about melasma and pigmentation in Asian skin, which covers the diagnosis and the non-laser side of management in more detail. This article is about one narrower question: what I look at before I fire anything.
One of the most interesting parts of that environment is the vasculature.
In 2007, Kim and colleagues compared melasma lesions with nearby normal facial skin in 50 Korean women. Melasma skin had significantly greater erythema, increased numbers and sizes of dermal blood vessels, increased VEGF expression, and an association between vessel number and pigmentation.
The vessels may not be innocent bystanders.
The 2026 study that got my attention
Li and colleagues published a retrospective cohort in 2026 that separated 75 melasma patients into predominantly pigmentary melasma (42 patients) and mixed pigmentary–vascular melasma (33 patients).
One detail in the methods matters before the numbers. Treatment was adapted to severity rather than held identical across the cohort. Mild cases received oral tranexamic acid alone. Moderate cases received oral tranexamic acid plus low-fluence Q-switched 1064 nm Nd:YAG at 6 mm, 2.6–3.0 J/cm², 10 Hz, every four weeks for six sessions. Severe cases received that plus topical 3% tranexamic acid. Everyone used high-factor photoprotection.
So this is not a clean comparison of one protocol applied to two phenotypes. It is a comparison of two phenotypes under a severity-adapted plan, and the mild group was not lasered at all.
The response was still very different.
The pattern inside that average is the part I keep thinking about. In mild disease the two phenotypes landed in roughly the same place. The gap opened in moderate disease and widened in severe disease, where 92.3% of mixed pigmentary–vascular patients failed to reach even a 30% reduction in mMASI, against 25.0% of the pigmentary group.
The phenotype also held up as an independent negative predictor after adjustment for severity and disease duration.
It is worth being careful about what that does and does not show. The study was retrospective, the groups were not randomised, and treatment intensity tracked severity. It establishes that mixed pigmentary–vascular melasma responded worse. It does not establish that the vascularity itself caused the poorer response. Vascular involvement may simply mark a more entrenched disease rather than act as a lever you can pull.
The authors suggested that severe mixed pigmentary–vascular cases may warrant adjunctive anti-vascular or anti-inflammatory strategies before intensifying pigment-directed therapy.
I do not read that as “vascular laser for every melasma patient.” I read it as something more useful:
Same brown. Different biology.
Blood vessels are part of the conversation
The vascular idea did not begin with the 2026 paper. A systematic review published in Dermatologic Surgery identified 34 original studies examining vascularity or antivascular approaches in melasma: laboratory work, diagnostic studies and therapeutic studies. The authors found promising evidence for a vascular component while also calling for better clinical trials.
That is the level of certainty I am comfortable with. Vascularity matters. Exactly how much it matters in each patient, and how best to treat it, is still being worked out.
So when I see erythema underneath or around melasma, I do not automatically think, “there is a vessel; destroy it.”
I think:
This pigment is living inside a different tissue environment.
My “noise cancellation” approach
This is where my own treatment sequence comes in.
When the patient's skin is stable enough to treat, I usually start with Hollywood Spectra 1064 nm Spectra mode at 0.3 ms, commonly with a 6–8 mm spot. Only after that do I move toward more pigment-specific QS or PTP delivery.
Hollywood Spectra's 1064 nm platform gives me very different pulse domains to work with. The manufacturer's published specifications list approximately 5–10 ns for QS/PTP delivery and 0.3 ms for Spectra mode. One is much more photoacoustic in character; the other gives me a controlled photothermal interaction.
I do not think of 0.3-ms Spectra mode as a replacement for a dedicated vascular system. It is not PDL, and it is not the same as a conventional millisecond long-pulsed vascular treatment.
What I find clinically is that using it first can make the background skin feel more settled before I concentrate on the pigment.
Melanin is the signal I eventually want to treat.
Redness, inflammation and vascular activity are the noise around it.
My goal is not to erase every bit of redness before touching pigment. It is to avoid treating melanin as though the tissue around it does not matter.
There is precedent for the pulse domain, but not my exact sequence
A small 2004 clinical study treated facial skin with a 300-microsecond 1064 nm Nd:YAG. Among the patients who had pre-existing erythema, photographic assessment showed improvement after treatment. It was a small study, only four evaluable patients had noticeable baseline erythema, and it was not a melasma trial, so I would not stretch it further than that.
There is also a melasma study by Kang, Kim and Goo, published in Laser Therapy in 2011, that deliberately combined two pulse domains on the SPECTRA platform. Thirty Fitzpatrick IV women were treated first with 5 ns Q-switched 1064 nm at 1.2 J/cm² through an 8 mm handpiece, then immediately with 300-microsecond Spectra mode at 7.0 J/cm² through a 5 mm. At the final assessment, 20 of the 30 were rated as having fair-to-excellent improvement.
That paper is relevant, but the order is the opposite of mine.
They used QS first, then 300 µs. I prefer to settle the background first, then target the pigment.
So the study does not validate my sequence. What it shows is that combining nanosecond pigment-directed delivery with microsecond photothermal 1064 nm delivery in melasma is not a biologically strange idea.
Red does not automatically mean vascular laser
This distinction matters because it is easy to turn a useful observation into another protocol sheet.
Redness can mean many things: vascular participation in the melasma phenotype, active irritation, barrier disruption, rosacea, recent treatment, excess heat exposure, aggressive skincare, or another inflammatory process.
The finding changes my thinking. It does not automatically choose the machine.
Sometimes I want to influence the vascular component. Sometimes I want to reduce inflammation. Sometimes I modify how I laser. And sometimes I do nothing with a laser that day.
When I don't laser on the first visit
If a first-time patient arrives with severe erythema, irritation or obviously unstable skin, I generally do not see a reason to rush into treatment.
Before adding another controlled injury, I want to understand why the skin is already inflamed.
What are they applying every morning and night? Are they over-exfoliating? Layering acids and retinoids? Constantly changing products? Getting excessive UV, visible light or heat exposure? Is there dermatitis or rosacea that needs to be dealt with first?
If the patient goes home and keeps recreating the environment that triggered the problem, the laser has a ceiling.
You cannot out-laser an uncontrolled trigger.
Education, skincare simplification, photoprotection and behaviour change can therefore be part of the laser plan even when no laser is fired that day.
PIH teaches the same lesson from another direction
I would not describe post-inflammatory hyperpigmentation as primarily a vascular disease. The connection there is inflammation.
When visible pigmentation follows inflammatory injury, the brown is an aftermath of biological activity that started earlier. If significant erythema is still present, I have to ask whether that process is actually finished before I add another source of thermal or photoacoustic stress.
This is one of the easiest mistakes in pigment practice: seeing brown and immediately wanting to remove it.
Sometimes the pigment is the footprint. The active problem is what made the footprint.
This is where DALASS came from
Traditional laser teaching leans heavily on Fitzpatrick skin type. Fitzpatrick is useful, but it does not tell me what condition the skin is in today.
That is one reason I built DALASS — Dr. Andy's Laser Aggressiveness Scoring System around more than skin type. The framework also asks me to look at skin health and erythema, along with tissue thickness, before deciding how aggressive I am willing to be.
DALASS does not diagnose vascular melasma. It does not tell me what Hollywood Spectra fluence to choose, and it does not replace wavelength, pulse duration, spot size, cooling, clinical endpoint or device-specific knowledge.
What it does is force one question before I look at the parameter screen:
What condition is this skin in today?
Two patients can both be Fitzpatrick IV. One has calm, healthy, stable skin. The other has diffuse erythema, irritation and reactive melasma.
They have the same Fitzpatrick number.
They do not have the same skin.
The distinction I care about
Fitzpatrick tells me something about pigment and photoreactivity. Erythema tells me something about the environment that pigment is living in.
Neither one, by itself, is a treatment plan.
What is still open
The evidence supports several pieces of this way of thinking: melasma lesions can show increased vascularity and VEGF; a systematic review found meaningful evidence for a vascular component; and the 2026 cohort found poorer treatment response in mixed pigmentary–vascular melasma than in predominantly pigmentary melasma.
There is also limited clinical evidence that 300-microsecond 1064 nm treatment can influence facial erythema, and older work has combined microsecond and nanosecond 1064 nm delivery in melasma.
What the evidence does not establish is my exact protocol.
No controlled trial has shown that starting every appropriate melasma session with 0.3-ms Spectra mode before QS or PTP is superior to the reverse sequence or to pigment-directed treatment alone. Visible erythema settling after treatment is not proof that the biological drivers of melasma have been switched off. DALASS itself is a clinical framework, not a validated melasma outcome score.
That is the part I would most like to see studied properly.
The bottom line
I do not think melasma should be approached as a pile of excess pigment waiting to be destroyed.
The melanocyte is sitting inside a much more complicated biological environment, and vascularity and inflammation appear to be part of that environment in at least a meaningful subset of patients.
My own sequence reflects that:
Understand the skin.
Identify the triggers.
Stabilize the background.
Reduce the noise.
Then target the signal.
For me, Hollywood Spectra's 0.3-ms Spectra mode is one tool for that first laser step before I move into QS or PTP pigment treatment.
But the philosophy is bigger than one machine.
Before I treat the brown, I look at the red.
Sources
Retrospective cohort of 75 patients, 42 predominantly pigmentary and 33 mixed pigmentary–vascular, treated on a severity-adapted protocol. Source for the mMASI reductions overall and by severity stratum, the treatment-resistance rates, the multivariable analysis and the authors' discussion of adjunctive anti-vascular or anti-inflammatory strategies.
Fifty Korean women. Source for higher erythema, increased dermal vessel number and size, increased VEGF expression and the association between vessel number and pigmentation in melasma lesions.
Systematic review of 34 original studies: four laboratory, 15 diagnostic and 15 therapeutic studies. Source for the broader evidence base around vascularity in melasma and the need for more rigorous trials.
Thirty Fitzpatrick IV women treated with 5 ns Q-switched 1064 nm at 1.2 J/cm² through an 8 mm handpiece, followed immediately by 300 µs Spectra mode at 7.0 J/cm² through a 5 mm. Twenty of thirty were rated fair-to-excellent. Relevant as precedent for combining nanosecond and microsecond 1064 nm delivery, but it used the reverse order from the technique described in this article.
Small clinical study of 300 µs 1064 nm treatment. Four patients with noticeable baseline erythema showed photographic improvement, which is supportive background rather than direct validation of a melasma protocol.
Manufacturer source for the Hollywood Spectra platform's 1064/532 nm wavelengths, nanosecond pigment-directed modes and 0.3 ms Spectra photothermal mode.
The author's clinical framework using skin type, skin health/erythema and skin thickness to structure decisions about treatment aggressiveness.
Accurate as of October 2026. Melasma research is evolving, and the clinical sequence described here should be read as a physician's current approach rather than a validated universal protocol.