Lichen Planus Pigmentosus (LPP): The Complete Guide to Diagnosis, Treatment, Skincare & Living With It

If you have recently been told you may have lichen planus pigmentosus, you have probably already noticed that most of what you can find online is either a dense dermatology paper or a page trying to sell you a brightening serum. This guide is neither. It sets out what the published evidence actually establishes, what it does not, and where the honest answer is that nobody knows yet. Every substantive claim below links to the source it came from.

The short answer

Lichen planus pigmentosus is an uncommon inflammatory skin condition that leaves grey-brown pigment sitting deep in the skin, where ordinary brightening products cannot reach it. There is no treatment guideline and no cure. Realistic goals are to stop new pigment forming, protect the skin from sun and visible light, and avoid making it worse.

Five things worth understanding first

1. It is not ordinary dark spots, and it is not melasma. The pigment is created by a different process and sits at a different depth.
2. There is usually an inflammatory phase and a later phase where mainly leftover pigment remains. These need different approaches, and telling them apart is a job for a dermatologist.
3. The first objective is normally to stop new pigmentation forming — not to bleach what is already there.
4. Skincare has a supporting role, not a leading one. No cosmetic ingredient has been shown to clear this kind of pigment.
5. There is no guideline, no Cochrane review, and no treatment that reliably works for everyone. That is not a gap in what follows — it is the state of the field.

Contents — 16 sections

1. How to read the evidence labels
2. What lichen planus pigmentosus actually is
3. How it differs from melasma and post-inflammatory marks
4. Active or settled — and why you cannot answer that alone
5. What might have set it off
6. Getting the diagnosis right
7. How treatment actually works
8. What skincare can and cannot do
9. Skincare by situation
10. Ingredients: supportive, uncertain, and worth care
11. Sun protection
12. Is it coming from inside?
13. Peels, lasers, microneedling and PRP
14. Living with it
15. Common questions
16. What science still does not know

How to read the evidence labels in this guide

The research on this condition is small, and a great deal of what circulates about it is borrowed from other pigmentation conditions and quietly presented as if it were about this one. So every substantive claim below carries a tag showing where its evidence actually comes from.

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1. What lichen planus pigmentosus actually is

Direct LPPLichen planus pigmentosus is a variant of lichen planus that produces pigmentation rather than the raised, itchy purple bumps most people associate with that condition. DermNet describes it as being "characterised by ill-defined oval, greyish brown marks on the face and neck or trunk and limbs without an inflammatory phase."² The British Association of Dermatologists puts it in almost the same words for patients, adding that "this type of lichen planus is more common in people with darker skin tone."³

That absence of a visible rash beforehand is one of the most useful facts in this guide. It is why so many people describe the pigment as having simply appeared, and why it is so often mistaken for something else at first.

Why the pigment ends up where brightening products cannot reach it

Direct LPPThe underlying process is an immune reaction. Merck Manual describes lichen planus as "a T cell–mediated autoimmune reaction against basal epithelial keratinocytes in people with genetic predisposition."⁵ In plain terms: immune cells attack the cells at the very bottom of the epidermis — the layer that normally holds pigment in place.

When that bottom layer is damaged, the pigment it was holding falls through into the dermis below. There it is swallowed up by scavenger cells called melanophages, which are long-lived. The AAD's own commentary on this condition quotes the histology directly: the dermis "exhibits incontinence of pigment with scattered melanophages."⁴ DermNet adds that "pigmentation in acquired dermal macular hyperpigmentation is often due to persistent melanophages in the dermis."¹

ExtrapolatedDepth matters enormously, and it is well documented. StatPearls states plainly that "dermal postinflammatory hyperpigmentation is generally more resistant to treatment compared to epidermal postinflammatory hyperpigmentation due to the depth of the pigment," and that dermal hyperpigmentation "is blue-gray and can be permanent."⁶ That chapter is about post-inflammatory hyperpigmentation generally rather than this condition specifically, but the physics of depth is the same.

Who tends to get it, and where

Direct LPPDermNet reports that it "affects middle-aged people of South Asian and African/Middle Eastern descent."¹ The published cohorts are consistent on the broad picture: in a study of 100 patients, the face was affected in 54% and the neck in 48%, followed by the upper back at 36% and the upper limbs and chest at 32% each; the average age was 31 and there were slightly more women than men.⁹ Reported skin phototypes cluster at Fitzpatrick IV to VI.^{10, 14}

One caveat about that evidence, which matters if you are reading these numbers about yourself: nearly all of the published cohorts come from single centres in India and Nepal. That is a narrow evidence base geographically, and it shapes what is known.

Direct LPPSymptoms vary. DermNet describes the condition as "generally asymptomatic," though it can be "pruritic in its early phases."¹ In the 100-patient cohort, 41% reported itching and 30% reported nothing at all, while 68% came in because of the appearance.⁹ A separate 50-patient study found that none of its patients recalled itching or redness before the pigmentation appeared.¹⁰

Direct LPPThere is also a flexural variant — lichen planus pigmentosus inversus — which appears in the armpits, groin and skin folds rather than sun-exposed sites, and which has a noticeably different profile: older patients, more often women, and in the published series more often people with lighter skin.^{4, 15}

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2. How it differs from melasma and post-inflammatory marks

This distinction is worth spending time on, because a long detour through melasma treatment is one of the most common experiences people describe before the right name is put to it.

Direct LPPDermoscopy can help separate them. One pattern is neatly opposite: in melasma the pigment tends to spare the area immediately around hair follicles, whereas in lichen planus pigmentosus it is often accentuated around them.¹⁶

An honest complication

Expert consensusLichen planus pigmentosus sits inside a group of conditions now usually called acquired dermal macular hyperpigmentation, alongside erythema dyschromicum perstans (ashy dermatosis) and Riehl's melanosis or pigmented contact dermatitis. A 2023 Delphi consensus of sixteen experts reached agreement that this umbrella term should cover all of them, and that there are "minimal differences" between the entities — histopathology and dermoscopy can confirm dermal pigmentation but "cannot differentiate the entities."¹¹

DermNet says the same thing more bluntly: these conditions "overlap significantly," "subtypes may manifest in the same patient, and they lack clear-cut clinical and histological differences."¹

So if two dermatologists give you two different names, that is not necessarily either of them being wrong. Some of the disagreement in this area is a naming problem rather than a diagnostic one, and a global consensus meeting was convened in 2019 precisely because "different regions in the world describe similar conditions under different names."¹²

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3. Active or settled — and why you cannot answer that alone

The distinction between disease that is still actively inflaming and disease that has burnt out, leaving pigment behind, shapes almost every decision that follows: what a dermatologist reaches for first, whether treatment appears to be working, and whether a procedure should even be discussed.

Expert consensusIt is worth being precise about the status of this idea. It is expert consensus rather than trial evidence. The 2026 global consensus states directly that "lasers or IPL should be avoided during the active inflammatory stage of LPP to prevent exacerbation," and that "pre-treatment with topical or oral agents is recommended before initiating procedural treatments."⁹³ Two named reviews say the same thing about lasering specifically — "lichen planus pigmentosus should be treated only when the condition has stabilized and there is no spread of the disease"²⁵ and "ensuring disease stabilization prior to initiating laser therapy is important to avoid disease exacerbation, especially for lichen planus pigmentosus."²⁶

Expert consensusAnd the one expert body that formally voted on the underlying premise did not endorse it. The 2023 Delphi panel considered whether inflammatory changes on biopsy could be used to assess disease activity and justify starting systemic treatment. It reached 64% agreement — below its own 80% threshold for consensus.¹¹ The same panel agreed that an objective severity scoring system is still needed.

What a clinician can bring to the question that you cannot: examination of the whole affected area, dermoscopy, and where appropriate a biopsy. A validated severity score for this group of conditions does exist — the Dermal Pigmentation Area and Severity Index, tested across 55 patients by three independent raters with an inter-rater reliability of 0.997 — so serial measurement is possible in principle.³³

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4. What might have set it off

UnknownThe most honest place to start is DermNet's own sentence: "the exact cause of acquired dermal macular hyperpigmentation is unknown."¹ The mechanisms it lists as proposed are genetic susceptibility, UV exposure, contact reactions to chemicals, medications and viral infection.

Within that, some things are better documented than others.

Reasonably well documented

Direct LPPSun exposure. DermNet states the condition "can be provoked by sun exposure, but it can also arise in sun-protected sites such as the armpits."² That sentence carries its own caveat, which is why we like it — sun is implicated, and sun is not the whole story.

Direct LPPHair dye and contact allergens. This is the best-evidenced contact trigger, because it rests on patch testing rather than recall. DermNet reports that "up to 36% of patients were reported to have a positive patch test reaction to hair dye" across this group of conditions.¹ In a study that patch-tested fifty patients with facial disease, there were 26 relevant positive reactions in 17 people (34%) — para-phenylenediamine and hair dyes in five, nickel in three, and, notably, the patient's own cosmetics in nine. The authors' own conclusion was carefully worded: the results "suggest a probable role of allergens/cosmetics in causing LPP on face."¹⁰

Direct LPPFriction, in the flexural variant. For lichen planus pigmentosus inversus specifically, friction is described as a triggering stimulus.¹⁵ This does not appear to be established for the facial form.

Medications that cause look-alike eruptions. Merck lists beta-blockers, NSAIDs, ACE inhibitors, sulfonylureas, gold, antimalarials, penicillamine and thiazides as causes of lichenoid drug eruptions.⁵ These cause a mimic rather than this condition itself — which is exactly why your medication list belongs in the conversation.

Reported, but much weaker than it looks

Direct LPPMustard oil. You will see this named everywhere. The 100-patient cohort recorded mustard oil use in 62% of patients, hair dye in 48%, aftershave in 36% and perfumes in 24%.⁹ But that study had no control group, in a population where mustard oil use is close to universal. A 62% exposure rate in patients tells you very little about risk without knowing the rate in people who do not have the condition. Treat it as something frequently reported, not as something shown to cause it.

What we could not verify at all

No LPP evidenceAmla oil appears in a great deal of secondary web content as a trigger for this condition. We could not confirm it in any source we were able to read — not DermNet, not the AAD, not the published cohorts. We have therefore left it out rather than repeat it, and we would rather tell you that than pass along a claim we could not check.

Diet is in the same category, and section 11 covers it.

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5. Getting the diagnosis right

Expert consensusThe 2023 Delphi consensus endorsed three investigations: biopsy, dermoscopy, and patch testing for hair dyes and cosmetics.¹¹ DermNet's page on the condition lists history, patch testing, dermoscopy and biopsy — and notably lists no blood tests at all.¹

Direct LPPDermoscopy findings are supportive rather than definitive. In the 50-patient study, dots or globules were the commonest finding at 86%, and their presence correlated with the degree of pigment incontinence on biopsy.¹⁰ Biopsy remains the way to confirm the interface pattern; in one series, the characteristic Civatte bodies were present in 78% of cases.¹⁷

Questions worth taking to your appointment

• Does this look like lichen planus pigmentosus, and what else is on the list?
• Do you think it is still active, or has it settled?
• Could this be pigmented contact dermatitis instead — and would patch testing help tell them apart?
• Are there any signs at my hairline, eyebrows or scalp that we should be watching?
• Should any of my current medications be considered?
• What is the first objective — stopping it spreading, or working on the colour?
• How will we know whether treatment is working, and by when should we review?
• Are there specific products or exposures you want me to stop?

Signs that deserve attention rather than watchful waiting

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6. How treatment actually works

Before anything else, the size of the evidence base, because it changes how you should read every claim you encounter about this condition.

Two different jobs

Treatment is generally approached as two separate problems, and confusing them is a reliable source of frustration.

What dermatologists have reported using

What follows is a description of the published literature, not a recommendation and not a list to request. Doses are omitted deliberately.

Direct LPPTopical calcineurin inhibitors are the best-evidenced topical option, which is a low bar. In the most-cited study, 13 patients within a 33-patient cohort were treated with tacrolimus 0.03% twice daily, and 7 of 13 (53.8%) showed lightening at 12 weeks.^{18, 19} Tacrolimus 0.1% also served as the comparator arm in the only randomised trial in this group of conditions.²²

No LPP evidenceTopical corticosteroids are widely used but have no trial in this condition — not one controlled or prospective study of a topical steroid on its own. In the related ashy dermatosis, one report found that 49% of patients showed no significant improvement after more than a year of follow-up.¹⁹ Facial steroid use carries its own risks, including skin thinning.⁹¹

Direct LPPLow-dose oral isotretinoin has the strongest prospective evidence for the inflammatory phase. In an open-label pilot study, 27 of 32 enrolled patients completed six months of treatment: 15 had moderate improvement, 7 had good improvement and 2 had mild improvement. Itching settled at 9 to 14 days and disease stabilised at 4 to 6 weeks in those who responded.²⁰ The AAD's commentary flags it as "possibly a promising treatment modality," while noting "minimal improvement" with most other options.⁴

Direct LPPOral tranexamic acid has three small uncontrolled datasets, one of which is heavily confounded because nearly all patients also received a potent steroid and hydroquinone.⁹² The one registered trial closed having enrolled a single participant. It carries real contraindications that require screening before it is prescribed — including a history of venous or arterial thromboembolism, active thromboembolic disease, current anticoagulant therapy, severe renal impairment, and pregnancy or breastfeeding.⁹²

Direct LPPColchicine is listed by DermNet² but the published evidence in this condition is case reports.

Direct LPPHydroxychloroquine deserves a specific note, because it appears in both halves of this topic. As a treatment there is one case report, and it cannot be attributed to the drug because three agents were given together. As a cause of pigmentation it is well documented: in 316 patients taking it for more than six months, 26.3% developed hyperpigmentation, with the face affected in 60% of those, and only 17% showed any regression after stopping.²⁹ It also requires ophthalmic monitoring for retinal toxicity on long-term use, which is a prescriber matter rather than a detail to weigh yourself.

Direct LPPJAK inhibitors are the genuinely new development. A retrospective series of 15 patients treated with oral tofacitinib reported improvement in physician assessment, pigmentation severity and patient satisfaction, and there are published case reports of topical ruxolitinib and oral tofacitinib.^{88, 89} This is early, uncontrolled evidence — promising rather than established. Oral JAK inhibitors also carry a substantial systemic safety profile: DermNet notes they "increase susceptibility to serious bacterial, fungal, mycobacterial, and viral infections," that some "may be associated with an increased risk of arterial and venous thromboembolism, particularly tofacitinib and baricitinib," that a possible association with malignancy is under investigation, and that tuberculosis and hepatitis screening are required before starting.⁹⁵

No LPP evidenceHydroquinone has no efficacy trial in this condition, and there is a documented reason for particular caution. A case report exists specifically because exogenous ochronosis — a paradoxical darkening caused by hydroquinone itself — and this condition can be confused on the same face; that paper notes ochronosis is "most common in Black populations" and can follow courses "as short as 3 months" at concentrations above 4%.³⁰

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7. What skincare can and cannot do

This is the section we would most want you to read, and it is the one where we have the least to sell you.

ExtrapolatedAn important distinction sits inside that. Several of these ingredients work by reducing how much new pigment the skin makes — niacinamide, for instance, by limiting pigment transfer between cells. That mechanism is not useless here, because reducing new pigment is a real goal. What none of them has been shown to do is remove pigment already sitting inside melanophages. Melasma is also often mixed rather than purely epidermal, so the two are not cleanly separate conditions. The honest position is narrower than "nothing works" and much narrower than the marketing: no cosmetic ingredient has demonstrated reliable clearance of dermal pigment in this condition.

That is not for want of looking. It is what the literature contains. A 2026 review of hyperpigmentation mechanisms and clinically proven actives notes that "epidermal PIH may resolve better and faster than dermal PIH where melanin accumulates in long-lived melanophages" — and contains no statement that topical actives address those melanophages.⁶⁶ DermNet says that peels, lasers and light therapies "may be helpful for epidermal pigmentation" but "are not effective in dermal hypermelanosis," and can aggravate it by injuring the epidermis.³⁸

Two ingredients deserve naming individually because they appear so often in advice about this condition:

• Topical tranexamic acid has no published evidence in this condition at all — no case report, no series, no trial. And in melasma, where it has been studied, pooled topical monotherapy did not reach statistical significance.⁴⁹
• Azelaic acid's trial evidence sits at 15% and 20% prescription strength.⁵⁰ Cosmetic products at 10% have no pigmentation efficacy trials. The FDA label for prescription azelaic acid also warns that it "has not been well studied in patients with dark complexions" and that such patients "should be monitored for early signs of hypopigmentation."⁵¹

So what is skincare genuinely for here?

What it can reasonably do: keep the skin barrier comfortable and intact; reduce avoidable irritation; carry sun and visible-light protection, which is the part with the strongest rationale; and remove exposures that may be contributing.

What it cannot do: diagnose anything; replace medical control of active disease; remove pigment sitting inside melanophages; or guarantee an outcome.

There is one more thing skincare can do, and it works in the wrong direction if you get it wrong. Irritation itself drives pigmentation in richly pigmented skin. DermNet describes how "epidermal inflammation stimulates melanocytes to produce more pigment, while basal layer injury releases melanin that becomes trapped in the dermis," and notes this is more common and more persistent in darker skin.³⁸ The AAD's advice on fading dark spots in darker skin tones is a single sentence worth memorising: "If a product burns or stings when you apply it, stop using it."³⁶

An aggressive brightening routine, in other words, is capable of creating exactly the problem it is meant to solve.

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8. Skincare by situation

There is no single routine for this condition, because the right approach depends far more on what the skin is currently doing than on whether you have oily or dry skin. Four situations cover most people. They overlap, and you may move between them.

One new product at a time

This matters more here than in almost any other skincare context, for a specific reason: contact allergens are a documented contributor to this group of conditions, and cosmetics the patient already owned accounted for nine of the relevant positive patch tests in that 50-patient study.¹⁰ If you introduce four products at once and the skin reacts, you have no way of knowing which one did it — and neither does your dermatologist.

Introduce one new leave-on product, give it several weeks, and only then consider another.

Do you need toner, essence, ampoule, serum and the rest?

No. As a K-beauty and J-beauty retailer we are aware of how that sounds coming from us, but the honest answer for this condition is that three steps carry almost all of the value: cleanse, moisturise, protect. Everything else has to earn its place.

Toners, essences and ampoules are vehicles — different textures for delivering hydration or an active. They are not obligatory steps, and in a condition where cumulative product exposure is a plausible contributor, a shorter routine is a defensible choice rather than a compromise.

What we stock, and what we do not

This condition rarely stays on the face. In the published cohorts the neck was affected in almost half of patients, the upper back in around a third, and the arms and chest in roughly a third each.⁹ So the products below are split by where you need them. For anything larger than a few patches, a body-formulated product is the sensible choice — a 50ml facial cream will not cover a back, and using it that way gets expensive fast.

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9. Ingredients: supportive, uncertain, and worth care

Supportive foundation — the ones with the firmest ground under them

• Colloidal oatmeal. The strongest regulatory footing of any ingredient here. It is an FDA-recognised over-the-counter skin protectant, permitted to claim it "temporarily protects and helps relieve minor skin irritation and itching."⁶²
• Glycerin. Also an FDA-recognised skin protectant, at 20–45%.⁶² At the lower levels used in most cosmetics it is a humectant — useful, but not a monograph protectant.
• Ceramides. Real clinical trial data as barrier ingredients, including studies where ceramide-dominant creams performed comparably to topical prescription treatments in atopic dermatitis.⁶³
• Panthenol. Genuine randomised evidence, if small: 2.5% dexpanthenol twice daily for a week significantly improved hydration and reduced water loss versus vehicle in 60 volunteers.⁶⁴

May have a role once things have settled — with their real indication attached

Use with care, or leave to a specialist

• Hydroquinone. No efficacy evidence in this condition, and a documented risk of exogenous ochronosis — a paradoxical darkening — particularly in richly pigmented skin at concentrations above 4%.³⁰
• Strong acids, scrubs and peel systems at home. Physical treatments can aggravate dermal pigmentation by injuring the epidermis.³⁸
• Retinoids. Useful for post-inflammatory pigmentation⁵⁹ but only case-report level in this condition. If you are pregnant or trying to conceive: the FDA label for prescription tretinoin states it "should not be used during pregnancy,"⁶¹ and UKTIS advises that use during pregnancy "is therefore not generally recommended."⁶⁰ Discuss it with your doctor rather than deciding from a product page.
• Fragrance and essential oils. "Natural" does not mean non-irritating, and fragrance mixes appeared among the relevant positive patch tests in facial disease.¹⁰ This is one of the few areas where a blanket precaution is justified for this condition specifically.

And one myth worth retiring: the strongest whitening ingredient is not the best strategy here. Given that irritation drives pigmentation in richly pigmented skin,³⁸ and that none of these ingredients has been shown to reach the pigment in question, the aggressive route carries most of the risk and none of the demonstrated benefit.

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10. Sun protection

This is the part of a skincare routine with the strongest rationale in this condition, and it deserves its own chapter for that reason.

The basics, from the guidelines

ExtrapolatedThe AAD recommends an SPF of 30 or higher, broad spectrum, and water resistant.³⁴ For pigmentation specifically, DermNet recommends "broad-spectrum very high protection factor (SPF50+) sunscreen containing iron oxides" and year-round use.³⁷ On quantity, the AAD is specific: about a teaspoon for the face, roughly the amount that covers the length of your index and middle fingers, applied 15 minutes before going out and reapplied every two hours and after swimming or sweating.³⁵ The BAD gives a slightly wider reapplication window of every two to three hours.³⁹

How much you apply matters as much as the number on the bottle. The European reference dose used in SPF testing is 2 mg per square centimetre — roughly six teaspoons for a whole adult body.⁵⁵ Most people apply considerably less than that, which means the protection achieved in real life is lower than the label figure.

Visible light, and why tint is not decoration

ExtrapolatedUltraviolet is not the only part of daylight that produces pigment. Controlled studies show that visible light induces pigmentation in melanin-rich skin — darker and more sustained than that produced by long-wave UVA, and with no equivalent effect in lighter skin.⁴¹ A separate study found that a single exposure produced little pigmentation but repeated exposures produced darker, sustained pigmentation lasting ten days.⁴⁰

ExtrapolatedMost untinted UV sunscreens do not provide reliable, clinically meaningful protection against visible light. Iron oxides do. And there is one experimental finding that should change how anyone in a sunny climate shops: in a study in Fitzpatrick IV skin, iron-oxide-containing formulations significantly protected against visible-light-induced pigmentation compared with untreated skin or with a mineral SPF 50+ sunscreen.⁴² The untinted SPF 50+ did not do the job.

Tone-up is not the same as tinted

This distinction costs people real money. A great many Korean sunscreens are marketed as "tone-up" — they contain white or pink pigments that lighten the appearance of the skin cosmetically. That is not the same as an iron-oxide tint formulated to match skin and absorb visible light. A tone-up sunscreen may contain no iron oxides at all.

In our range, the product that contains iron oxides — CI 77491, CI 77492 and CI 77499 — is the Beauty of Joseon Daily Tinted Fluid Sunscreen, which the manufacturer lists at SPF 40 across twelve sheer shades. There is also an SPF 50 version of the same product in some regions, so check the bottle you are actually buying. Three honest caveats come with it:

• It is SPF 40, not the SPF 50+ DermNet recommends for pigmentation. That is a genuine trade-off, and the right answer may be to use it and be scrupulous about reapplication, or to apply one reliable broad-spectrum sunscreen correctly, let it set, and add a compatible iron-oxide complexion product over the top if you want the extra visible-light cover.
• It contains a fairly high level of denatured alcohol, which is a common complaint about this product and may not suit skin that is currently irritated. If it stings, that is your answer.
• A tint you cannot see is unlikely to be doing much. Reviews of visible-light protection note that effective protection requires tinted formulations that are perceptible on the skin.⁴⁵ Shade matching therefore matters — an unwearable tint is not protective, because you will not wear it.

One further complication worth knowing: an analysis of 37 tinted sunscreens found that 97.3% did not list iron oxide as an active ingredient, so consumers largely cannot tell how much is present.⁴⁶ There is no published threshold percentage, and anyone quoting you one is going beyond the evidence. The presence of iron oxides on an ingredient list is not by itself proof of any particular level of visible-light protection.

Wearing it in Mauritius

Direct LPPThe Mauritius Meteorological Services describes the climate as "a warm humid summer extending from November to April and a relatively cool dry winter from June to September," with mean summer temperature of 24.7 °C and daily bright sunshine ranging from 6.5 to over 8 hours.⁸¹

ExtrapolatedThe Meteorological Services does not publish a UV index. The closest defensible figure comes from Réunion — the same latitude, around 230 km away — where measurements put the UV index at around 8 in winter and up to 16 in summer.⁸² A monitoring network across the western Indian Ocean, which includes a station on Rodrigues, reports that UV indices in these regions "can exceed 10 almost all year round."⁸³ On the WHO scale, anything above 11 is classed as extreme.⁸⁴ We are labelling the Réunion figure as a proxy rather than presenting it as a Mauritius measurement.

What that means practically: sun protection here is a year-round matter rather than a summer one, reapplication after sweating is not optional, and the texture you choose determines whether you actually reapply. A lightweight fluid you will reapply at lunchtime protects you better than a rich cream you avoid because it feels heavy in humidity. Shade and a wide-brimmed hat do work that no bottle does.

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11. Is it coming from inside?

This is a natural question to ask, and it is where the largest amount of money tends to get spent on the smallest amount of evidence. The short answer: this is an immune-mediated skin process, and there is no proven internal cause that every person needs to hunt down.

What no guideline recommends

Expert consensusStart here, because it is the clearest finding in this whole section. No guideline, consensus statement or authoritative source recommends any blood test for this condition. The 2023 Delphi consensus endorses biopsy, dermoscopy and patch testing — and nothing else.¹¹ DermNet's page lists no blood tests at all.¹ The major treatment reviews contain no laboratory work-up.^{19, 21}

That does not mean your dermatologist is wrong to order a test. It means the decision belongs to them, based on you, rather than to a list you found online.

Thyroid — the most directly studied association

Direct LPPA case-control study of 54 patients and 54 matched controls found biochemical hypothyroidism in 31.7% of patients versus 2 people in the control group, with significantly higher thyroid peroxidase antibody levels. The authors recommended routine thyroid function testing and added that "further research is warranted."¹³ A separate 100-patient cohort found a significant association between hypothyroidism and the diffuse pattern.⁹

Two honest qualifications. First, that recommendation appears in the discussion sections of those two studies — it is not in any guideline or consensus document. Second, an association is not a cause: nothing in either paper shows that thyroid dysfunction produces the pigmentation, or that treating the thyroid clears it. Frontal fibrosing alopecia, covered in section 5, is arguably the more consistently reported association of the two.

What we could not find evidence for at all

• Vitamin D, iron, ferritin and vitamin B12 in this condition. We found no direct clinical evidence in lichen planus pigmentosus at all — not weak evidence, none. Searching returns studies in oral lichen planus, a different condition in different tissue. DermNet states directly that vitamin D's "association with other types of LP remains unexplored."²
• Diabetes and metabolic syndrome. We found no controlled study.
• Smoking and alcohol. We found nothing specific to this condition. The published smoking data are in oral lichen planus.

If you have symptoms of a deficiency, that is a reason to be tested for its own sake. It is not a reason to expect the pigmentation to change.

Diet

No LPP evidenceThere is no established diet for lichen planus of any form, and no randomised trial of any diet. The Cochrane protocol for cutaneous lichen planus was withdrawn in 2018 with no trials analysed.⁶⁷

ExtrapolatedOn gluten specifically: the lichen planus–coeliac literature is association-only. A systematic review concluded that "both immunological processes correlate but there is no causation," and identified no evidence that a gluten-free diet improves lichen planus.⁷⁹ Dairy elimination, sugar elimination and autoimmune protocol diets have no studies in this condition at all. On "detoxing," the US National Center for Complementary and Integrative Health states there is "no compelling research to support the use of 'detox' diets."⁷⁸

Eating well is worth doing. It is not a treatment for this, and nobody should be made to feel that their pigmentation is a consequence of what they ate.

Supplements

We sell products containing several of the ingredients below. That is precisely why we would rather you read this before buying any of them.

We stock glutathione, kojic acid and turmeric products. None of them is a strategy for this condition, and we would rather say so plainly than let you assume otherwise. That money is better spent on a sunscreen you will wear every day.

Stress

ExtrapolatedDermNet lists "physical and emotional stress" among the contributors to lichen planus.² The AAD's own causes page does not.⁸ The quantitative evidence is cross-sectional — a meta-analysis found depression in 27% and anxiety in 28% of people with lichen planus, but 75% of the included studies had fewer than 50 patients, almost all used self-report questionnaires, and the direction of the relationship cannot be established.⁸⁰ Living with a visible skin condition is stressful; that much is not in doubt. Whether stress drives the condition is not established.

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12. Peels, lasers, microneedling and PRP

The common advice is that laser is the next step once topical treatment disappoints. The evidence does not support that as a general rule — but it also does not support a blanket refusal. It is more interesting than either.

Direct LPPThe overall picture, from a 2026 review of 16 studies of procedures in this condition: "evidence was limited by small sample sizes, lack of randomized controlled trials, and reliance on case reports and series. Most studies included fewer than 20 participants."⁸⁷

Should procedures wait until things have settled?

Expert consensusYes — and this is the clearest recommendation in the whole field. The 2026 global consensus states it as a formal consensus statement: "lasers or IPL should be avoided during the active inflammatory stage of LPP to prevent exacerbation," alongside "pre-treatment with topical or oral agents is recommended before initiating procedural treatments for LPP."⁹³ Two named reviews say the same — "should be treated only when the condition has stabilized and there is no spread of the disease"²⁵ and "ensuring disease stabilization prior to initiating laser therapy is important to avoid disease exacerbation."²⁶ The PRP study operationalised it, requiring six months of stability to enter.²⁸ There is also a published case of the flexural variant being triggered by the Koebner phenomenon after laser hair removal.⁸⁵

ExtrapolatedFor completeness: a 2026 systematic review of light-based therapy across inflammatory skin conditions — 57 studies, over 900 patients — concluded these treatments are "safe and do not consistently precipitate disease exacerbation."⁸⁶ That review is not specific to this condition, and it does not override a consensus statement written about it directly. Wait until it has settled.

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13. Living with it

How long does it take?

We are going to decline to give you a number, and we want to explain why rather than just leave a gap.

No LPP evidenceThere are several tempting figures in circulation and none of them are about this condition. The NHS says lichen planus on the skin "usually gets better on its own in about 9 to 18 months" — that is classic lichen planus, and the NHS does not mention the pigmented form at all. The AAD's "months to years for dark spots to fade" refers to pigmentation after classic lichen planus. StatPearls' 6-to-12-month figure is for epidermal post-inflammatory pigmentation.⁶ Transferring any of them here would be a real accuracy error, and it is the mistake most secondary content about this condition makes.

Direct LPPThe one authoritative long-horizon statement specific to this condition is DermNet's, and it is sobering: while a related condition "tends to resolve spontaneously within months to years," by contrast "the pigmentation of lichen planus pigmentosus can persist for decades."¹

UnknownNo relapse rate has been published. Published disease durations at the point patients present — 2 to 60 months in one cohort, 5 months to 15 years in another^{9, 10} — describe how long people had it before seeking help, not how long it lasts.

Judging whether things are improving

Because the colour changes so slowly, judging progress by colour alone is demoralising and often misleading. A more useful order of things to notice:

1. Itching or burning settles, if you had it.
2. No new areas appear.
3. Existing areas stop expanding at the edges.
4. The colour gradually becomes less intense — and only then.

Steps two and three can represent treatment succeeding while the mirror shows nothing. That is worth holding onto.

Expert consensusPhotographs help, but only if they are comparable. Standardised photography for this kind of assessment means the same position, the same lighting, the same distance and the same camera.¹⁹ Monthly is plenty — daily photographs mostly capture lighting, and checking obsessively tends to make people feel worse rather than better informed. Take them without makeup, and bring them to appointments.

Makeup and camouflage

Wanting to cover visible pigmentation is not vanity, and nobody should have to justify it. A few practical points:

• Choose low-irritant, fragrance-free formulations where you can — the same reasoning as the rest of this guide.
• Remove gently. Do not scrub. Aggressive removal is a source of the very irritation you are trying to avoid.
• Colour-correction principles genuinely help with grey and slate tones, which behave differently from ordinary brown spots. A peach or orange-toned corrector counteracts blue-grey, and usually means less opaque foundation is needed on top.
• A tinted sunscreen can do double duty here, providing visible-light protection and some evening of tone in one step.
• If you suspect a cosmetic is causing a reaction, that is worth raising with a dermatologist rather than working through it alone — patch testing exists for exactly this question.¹⁰

The part that is not about skin

This is measurable, and it measures higher than most people expect.

Direct LPPA cross-sectional study compared quality-of-life scores across three conditions: 125 people with lichen planus pigmentosus, 113 with vitiligo and 121 with melasma. Mean Dermatology Life Quality Index scores were 10.9 for lichen planus pigmentosus, 9.73 for vitiligo and 8.39 for melasma. The difference from melasma was significant (p<0.001); the difference from vitiligo was not.³¹ A 2024 systematic review across 7 studies and 259 patients reached the same conclusion — the burden of this group of conditions is greater than melasma's and similar to vitiligo's.³²

If this is affecting your confidence, your social life or your mood, that is a documented feature of the condition rather than an overreaction, and it deserves attention alongside the skin. It is a reasonable thing to raise with your doctor.

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14. Common questions

Is it contagious?

No. It is an immune-mediated process, not an infection.⁵

Is it cancer, or could it become cancer?

No. It is a benign pigmentary condition. Any lesion that is changing rapidly or behaving differently from the others should still be examined, as with any skin change.

Is lichen planus pigmentosus the same as lichen planopilaris?

No — and this is a well-documented source of confusion, because both are abbreviated "LPP." Lichen planopilaris is a scarring hair-loss condition of the scalp. Frontal fibrosing alopecia is a variant of lichen planopilaris, not of the pigmentation condition.⁷ They are reported together often enough to be worth watching for, but they are separate diagnoses.¹⁴

Will skincare cure it?

No. No cosmetic ingredient has published evidence for clearing pigment held in dermal melanophages. Skincare supports the barrier, reduces irritation and carries sun protection — all worthwhile, none curative.⁶⁶

Should I exfoliate it away?

No. The pigment is below the layer exfoliation reaches, and physical treatments can aggravate dermal pigmentation by injuring the epidermis.³⁸

Do I need a tinted sunscreen?

It is a reasonable choice, with a caveat you should know. Iron oxides protect against visible light where standard filters do not, and in one study an untinted mineral SPF 50+ failed to prevent visible-light-induced pigmentation while iron-oxide formulations did.⁴² But that evidence is from melasma and experimental studies — there is no tinted-sunscreen study in this condition.⁴³ Note also that "tone-up" sunscreens are not the same thing and may contain no iron oxides at all.

Should I stop dyeing my hair?

Worth discussing with your dermatologist rather than deciding either way alone. Hair dye is the best-evidenced contact trigger in this group of conditions, with up to 36% of patients showing positive patch tests to it.¹ Patch testing can establish whether it is relevant for you specifically, which beats guessing.

Should I change my diet, or take glutathione?

There is no established diet for lichen planus of any form and no randomised trial of any diet.^{67, 79} Oral glutathione's best trial found no statistically significant effect,⁷¹ and injectable glutathione for skin lightening is not approved and carries documented safety warnings.⁷²

Do I need blood tests?

No guideline or consensus recommends any blood test for this condition.^{11, 1} Thyroid testing is suggested by the authors of two small studies that found an association,¹³ but that decision belongs to your dermatologist.

Can I treat acne at the same time?

Usually yes, but gently. The AAD's guidance for acne in darker skin tones is that "what really works to clear acne is gentle skin care," and that scrubbing and harsh products make it worse.⁹⁰ Since irritation drives pigmentation, an aggressive acne routine works against you on both counts.

Can it stop spreading, and can the pigment fade?

Yes to the first for many people — arresting the active process is the more achievable of the two goals. The second is slower and much less certain: DermNet states the pigmentation "can persist for decades."¹ Some people improve substantially, some stabilise with pigment remaining, and some have persistent disease. No treatment has been shown to reliably clear it for everyone.

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What science still does not know

Any honest account of this condition has to include the questions nobody can answer yet. These are the ones that matter most to someone living with it.

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Where Adilsons Beauty fits

Adilsons Beauty is a top K-beauty and J-beauty retailer in Mauritius. Our role in a condition like this one is supportive skincare education — not diagnosis and not medical treatment.

What we can genuinely help with: gentle cleansing, barrier support, choosing a sunscreen you will actually wear in this climate, reading cosmetic ingredient lists, and avoiding routines that create more irritation than they resolve. Diagnosis, prescription treatment, patch testing, blood investigations and procedures all belong with an appropriate healthcare professional.

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Sources

Every numbered claim above links here. Some references are paywalled at the publisher — where that is the case the link resolves to the PubMed abstract or the DOI record. Every numbered claim above links to the source it came from — original studies, systematic reviews, expert consensus statements and clinical reference works. Some are behind journal paywalls, in which case the link opens the abstract or the DOI record. Where a claim could not be traced to a reliable source, it was left out rather than repeated.

Condition overview, classification and consensus

• 1. DermNet. Acquired dermal macular hyperpigmentation.
• 2. DermNet. Lichen planus.
• 3. British Association of Dermatologists. Lichen planus — patient information.
• 4. American Academy of Dermatology. The darkness of lichen planus pigmentosus. Dermatology World Insights and Inquiries.
• 5. Merck Manual Professional Edition. Lichen planus.
• 7. StatPearls. Lichen planopilaris. NCBI Bookshelf.
• 8. American Academy of Dermatology. Lichen planus: signs and symptoms.
• 11. Sarkar R, Vinay K, Bishnoi A, et al. A Delphi consensus on the nomenclature and diagnosis of lichen planus pigmentosus and related entities. Indian J Dermatol Venereol Leprol 2023;89(1):41–46. DOI 10.25259/IJDVL_804_2021.
• 12. Kumarasinghe SPW, et al. A global consensus statement on ashy dermatosis, erythema dyschromicum perstans, lichen planus pigmentosus, idiopathic eruptive macular pigmentation, and Riehl’s melanosis. Int J Dermatol 2019;58(3):263–272. PMID 30176055.
• 16. Diffuse facial melanosis: an overview of etiology and dermoscopic findings. J Skin Sex Transm Dis.
• 93. Passeron T, Desai SR, Abdallah M, Al-Niaimi F, Dlova N, Grimes PE, Ocampo-Candiani J, Sarkar R, Xiang LF, Miot HA. Global consensus on the management of melanin hyperpigmentation disorders. J Eur Acad Dermatol Venereol 2026;40(5):760–772. DOI 10.1111/jdv.70185. PMID 41362125.

Epidemiology, clinical features and diagnosis

• 6. StatPearls. Postinflammatory hyperpigmentation. NCBI Bookshelf.
• 9. Mendiratta V, et al. Clinico-epidemiological study of lichen planus pigmentosus (n=100). 2019. PMID 31149573.
• 10. Sharma VK, et al. Dermoscopy and patch testing in patients with lichen planus pigmentosus on face: a cross-sectional observational study in fifty Indian patients. Indian J Dermatol Venereol Leprol 2017.
• 15. Lichen planus pigmentosus inversus. Indian J Dermatol Venereol Leprol case series.
• 17. Lichen planus pigmentosus: a clinicopathological study from northeast India (n=42). Cureus 2024.
• 33. Kumaran MS, Dabas G, Vinay K, Parsad D. Reliability assessment and validation of the dermal pigmentation area and severity index. J Eur Acad Dermatol Venereol 2019;33(7):1386–1392. PMID 30801771.

Medical treatment

• 18. Al-Mutairi N, El-Khalawany M. Clinicopathological characteristics of lichen planus pigmentosus and its response to tacrolimus ointment. J Eur Acad Dermatol Venereol 2010;24(5):535–540. PMID 19840200.
• 19. Syder NC, Lo Sicco K, Gutierrez D. Updates in therapeutics for lichen planus pigmentosus. J Drugs Dermatol 2022.
• 20. Muthu SK, Narang T, Saikia UN, Kanwar AJ, Parsad D, Dogra S. Low-dose oral isotretinoin therapy in lichen planus pigmentosus: an open-label non-randomized prospective pilot study. Int J Dermatol 2016;55(9):1048–1054. PMID 27062273.
• 21. Literature review of treatment in lichen planus pigmentosus (102 patients across 14 studies). Br J Dermatol 2022;187(S1):85.
• 29. Yin C, et al. Hydroxychloroquine-induced hyperpigmentation: a cross-sectional study of 316 patients. Rheumatology 2025;64(3):985–993.
• 30. Narayanan D, Tyring SK. Hyperpigmented macules and patches on the face: exogenous ochronosis or lichen planus pigmentosus? J Drugs Dermatol 2024;23(7):567–568.
• 88. Singh, Sharma, et al. Tofacitinib in lichen planus pigmentosus: a retrospective hospital-based study (n=15). J Gen Proced Dermatol Venereol Indones 2026.
• 89. Recalcitrant lichen planus pigmentosus treated with topical ruxolitinib. JAAD Case Reports 2023.
• 91. DermNet. Topical steroid.
• 92. Tranexamic acid for the treatment of hyperpigmentation: a review of routes, dosing and safety. Clin Cosmet Investig Dermatol, Dove Press.
• 94. DermNet. Isotretinoin.
• 95. DermNet. Janus kinase inhibitors.

Procedures, lasers and peels

• 22. Sarkar R, et al. Efficacy of glycolic acid peels in combination with topical therapy in common facial melanosis in skin of colour: a randomized clinico-dermoscopic study. J Cutan Aesthet Surg 2026.
• 23. Rutnin S, Smitthisakda S, Wittayabusarakam N, et al. Efficacy of 1064-nm picosecond laser in the treatment of lichen planus pigmentosus: a split-face randomized controlled trial. J Cosmet Dermatol 2026. DOI 10.1111/jocd.70846.
• 24. Tarafdar N, Joseph M, Liu C. Laser therapy for lichen planus pigmentosus and erythema dyschromicum perstans: a systematic review. Dermatol Surg 2025. DOI 10.1097/DSS.0000000000004872.
• 25. Aurangabadkar SJ. Optimizing Q-switched lasers for melasma and acquired dermal melanoses. Indian J Dermatol Venereol Leprol 2019;85(1):10–17.
• 26. Garg S, Vashisht KR, Garg D, Oberoi B, Sharma G. Advancements in laser therapies for dermal hyperpigmentation. J Clin Med 2024;13(7):2116. DOI 10.3390/jcm13072116.
• 27. Kroon MW, et al. Non-ablative 1550 nm fractional laser therapy for erythema dyschromicum perstans and postinflammatory hyperpigmentation: a randomized pilot study. J Dermatolog Treat 2012. PMID 21756152.
• 28. Kiatsurayanon C, et al. Platelet-rich plasma for lichen planus pigmentosus: a prospective pilot study. Health Sci Rep 2025;8(4):e70455. DOI 10.1002/hsr2.70455.
• 85. Alghamdi NH, et al. Lichen planus pigmentosus inversus induced by the Koebner phenomenon following laser hair removal. JAAD Case Reports 2026;70. DOI 10.1016/j.jdcr.2026.01.029.
• 86. Tucci M, et al. Light-based therapies in inflammatory dermatoses: a systematic review (57 studies, >900 patients). Lasers Surg Med 2026. DOI 10.1002/lsm.70198.
• 87. Ezekwe U, et al. Cosmetic procedures for treating lichen planus pigmentosus: a review. J Drugs Dermatol 2026. PMID 41642153.

Hair loss and frontal fibrosing alopecia

• 14. Abdel Azim S, Whiting C, Friedman A. Highlighting the link between lichen planus pigmentosus and frontal fibrosing alopecia. J Drugs Dermatol 2024;23(3).

Photoprotection and visible light

• 34. American Academy of Dermatology. How to select a sunscreen.
• 35. American Academy of Dermatology. How to apply sunscreen.
• 36. American Academy of Dermatology. How to fade dark spots in darker skin tones.
• 37. DermNet. Melasma.
• 38. DermNet. Postinflammatory hyperpigmentation.
• 39. British Association of Dermatologists. Sun protection fact sheet, 2024.
• 40. Randhawa M, Seo I, Liebel F, Southall MD, Kollias N, Ruvolo E. Visible light induces melanogenesis in human skin through a photoadaptive response. PLOS ONE 2015.
• 41. Mahmoud BH, Ruvolo E, Hexsel CL, et al. Impact of long-wavelength UVA and visible light on melanocompetent skin. J Invest Dermatol 2010;130:2092–2097. PMID 20410914.
• 42. Dumbuya H, Grimes PE, Lynch S, et al. Impact of iron-oxide containing formulations against visible light-induced skin pigmentation in skin of color individuals. J Drugs Dermatol 2020.
• 43. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, Fuentes-Ahumada C, Torres-Álvarez B. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed 2014;30:35–42. PMID 24313385.
• 44. Boukari F, Jourdan E, Fontas E, et al. Prevention of melasma relapses with sunscreen combining protection against UV and short wavelengths of visible light. J Am Acad Dermatol 2015;72(1):189–190.e1.
• 45. Visible light protection strategies for diverse populations. Dermatol Ther (Heidelb) 2025. DOI 10.1007/s13555-025-01642-5.
• 46. Iron oxides in tinted sunscreen for hyperpigmentation: product analysis and literature review. J Drugs Dermatol 2026.

Cosmetic ingredients, formulation and regulation

• 47. Hakozaki T, et al. The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer. Br J Dermatol 2002;147(1):20–31.
• 48. Navarrete-Solís J, Castanedo-Cázares JP, Torres-Álvarez B, et al. A double-blind, randomized clinical trial of niacinamide 4% versus hydroquinone 4% in the treatment of melasma. Dermatol Res Pract 2011.
• 49. Kim HJ, Moon SH, Cho SH, Lee JD, Kim HS. Efficacy and safety of tranexamic acid in melasma: a meta-analysis and systematic review. Acta Derm Venereol 2017;97(7).
• 50. Al Shami A. Azelaic acid versus hydroquinone for managing patients with melasma: systematic review and meta-analysis of RCTs. Cureus 2023;15:e41796.
• 51. US Food and Drug Administration. Azelex (azelaic acid) cream 20% prescribing information, 2024.
• 52. de Dormael R, Bastien P, Sextius P, et al. Vitamin C prevents ultraviolet-induced pigmentation in healthy volunteers: Bayesian meta-analysis of 31 randomized controlled studies. J Clin Aesthet Dermatol 2019.
• 53. Al-Niaimi F, Chiang NYZ. Topical vitamin C and the skin: mechanisms of action and clinical applications. J Clin Aesthet Dermatol 2017.
• 54. Hollinger JC, Angra K, Halder RM. Are natural ingredients effective in the management of hyperpigmentation? A systematic review. J Clin Aesthet Dermatol 2018;11(2):28–37.
• 55. European Commission. Commission Regulation (EU) 2024/996 amending Regulation (EC) No 1223/2009 as regards the use of vitamin A, alpha-arbutin, arbutin and certain substances. EUR-Lex.
• 56. Mansouri P, et al. Evaluation of the efficacy of cysteamine 5% cream in the treatment of epidermal melasma: a randomized double-blind placebo-controlled trial. Br J Dermatol 2015;173(1):209.
• 57. DermNet. Cysteamine cream.
• 58. Efficacy and tolerability of 0.2% Thiamidol cream for facial hyperpigmentation: a randomized controlled trial in Fitzpatrick III–V skin (n=200). Dermatol Ther (Heidelb) 2025.
• 59. DermNet. Topical retinoids.
• 60. UK Teratology Information Service. Use of tretinoin in pregnancy.
• 61. US Food and Drug Administration. Renova (tretinoin cream) 0.02% prescribing information.
• 62. US Code of Federal Regulations, Title 21 Part 347 — Skin protectant drug products for over-the-counter human use. eCFR.
• 63. Review of barrier-repair ingredients including ceramides and colloidal oatmeal. Cosmetics 2022;9(4):75.
• 64. Review of dexpanthenol in dermatology, including Proksch et al. randomized controlled trial (n=60). J Clin Med 2022;11:3943.
• 65. Sun B, et al. Therapeutic potential of Centella asiatica and its triterpenes: a review. Front Pharmacol 2020;11:568032.
• 66. Passeron T, et al. Decoding hyperpigmentation: from biological mechanisms to actives with clinically proven topical efficacy. Dermatol Ther (Heidelb) 2026.
• 90. American Academy of Dermatology. Acne in skin of color: skin care that can help.

Internal health, diet and supplements

• 13. Karn D, KC S, Timalsina M. Thyroid profile in patients with lichen planus pigmentosus: a case-control study. Kathmandu Univ Med J 2016;14(53):36–40. PMID 27892439.
• 67. Gorouhi F, et al. Interventions for cutaneous lichen planus (protocol). Cochrane Database of Systematic Reviews CD008038 — withdrawn 2018.
• 68. Moayeri A, et al. The effect of curcumin on oral lichen planus: a systematic review and meta-analysis (10 studies, 355 patients). BMC Oral Health 2024.
• 69. National Institutes of Health. LiverTox: Turmeric. NCBI Bookshelf, updated 2025.
• 70. Medsafe New Zealand. Turmeric and warfarin interaction. Early warning system alert, 2018.
• 71. Sitohang IBS, et al. Oral glutathione with ascorbic acid for skin lightening: a double-blind randomized controlled trial (n=83). J Clin Aesthet Dermatol 2021;14(7):E53–58.
• 72. Philippine Food and Drug Administration. FDA Advisory No. 2019-182: unsafe use of glutathione as a skin-lightening agent.
• 73. Khanna R, et al. Efficacy and safety of topical glutathione: a systematic review. J Clin Aesthet Dermatol 2025;18(9):51–54.
• 74. Lack of efficacy of oral N-acetylcysteine in facial melasma: a randomized trial. An Bras Dermatol 2024.
• 75. Egido-Moreno S, et al. Vitamin D and oral lichen planus: a systematic review and meta-analysis. Med Oral Patol Oral Cir Bucal 2024.
• 76. National Institutes of Health, Office of Dietary Supplements. Vitamin D — fact sheet for health professionals.
• 77. National Institutes of Health, Office of Dietary Supplements. Zinc — fact sheet for health professionals.
• 78. National Center for Complementary and Integrative Health. Detoxes and cleanses: what you need to know.
• 79. Hamid M, et al. Systematic review on lichen planus as a precursor for celiac disease in the adult population. Cureus 2020.

Quality of life and psychological burden

• 31. Gupta V, Yadav D, Satapathy S, et al. Psychosocial burden of lichen planus pigmentosus is similar to vitiligo, but greater than melasma: a cross-sectional study. Indian J Dermatol Venereol Leprol 2021;87(3):341–347.
• 32. Jiang M, Wang E, Rodrigues M. Quality of life in patients with acquired dermal macular hyperpigmentation: a systematic review. Clin Exp Dermatol 2024;49(12):1504–1509. PMID 38994566.
• 80. Jalenques I, et al. Prevalence and odds of anxiety and depressive disorders in patients with lichen planus: a systematic review and meta-analysis. Acta Derm Venereol 2020;100:adv00330.

Mauritius climate and ultraviolet exposure

• 81. Mauritius Meteorological Services. Climate of Mauritius.
• 82. Cadet JM, et al. Solar UV radiation in the tropics: human exposure at Reunion Island during summer outdoor activities. Int J Environ Res Public Health 2020;17:8105.
• 83. Lamy K, et al. Ultraviolet radiation modelling and measurement in the southwest Indian Ocean: the UV-Indien network. Earth Syst Sci Data 2021;13:4275–4301.
• 84. DermNet. Global solar ultraviolet index.