Dermatological Considerations in Skin of Colour

Skin of colour (SOC) refers to the deep or rich end of the skin-pigmentation spectrum (Fitzpatrick types IV-VI, though Fitzpatrick typing was developed for UV sensitivity and correlates imperfectly with constitutive colour). The clinical relevance is not cosmetic — melanin density changes how disease looks, how fast it's recognized, and how it heals. Erythema, the visual cue most treatment-severity decisions and scoring tools (SCORAD, EASI, PASI) are built around, is frequently attenuated or absent in darkly pigmented skin and instead appears violaceous, grey, or hyperpigmented — which means relying on redness alone systematically under-recognizes active inflammation and delays escalation. The single most consequential downstream effect of that delay, and of skin inflammation in this population generally, is post-inflammatory hyperpigmentation (PIH): a disproportionate, often prolonged, and distressing dyspigmentation that follows essentially any cutaneous inflammation or injury and disproportionately affects patients with darker skin.^[1] This chapter covers the pharmacotherapy consequences of these differences — not a general dermatology review, but the specific prescribing, dosing, and counselling adjustments skin of colour requires.

Why the same disease looks different

Melanocyte density does not differ meaningfully by skin colour — pigmentation differences come from the ratio of eumelanin (brown-black) to pheomelanin (yellow-red), total melanin output, and melanosome size/distribution/degradation rate. Because melanin absorbs light broadly, it visually competes with the red of erythema, muting or masking it. The practical result: inflammation in darkly pigmented skin commonly reads as violaceous, grey, or simply as new hyperpigmentation rather than as classic redness. This is true across essentially every inflammatory dermatosis — eczema/atopic dermatitis and psoriasis both follow this pattern (see those chapters for full disease-specific management; the presentation difference described here is what should prompt more careful, non-erythema-reliant severity assessment before applying their treatment algorithms in a patient with skin of colour), and it is equally true of the drug reactions and infections pharmacists are positioned to catch.

Baseline assessment principles

Establish the patient's own baseline skin colour early (an objective tool is preferable to a subjective description) so later changes can be judged against it rather than against an assumed norm. Compare the affected area to adjacent healthy skin for colour, texture, shininess, and tightness (subtle swelling can present only as smoother or more widely spaced pores), and to touch for temperature, firmness, and texture. Ask directly about pain, itch, and altered sensation rather than assuming these track visible severity. Examine interdigital areas, the sides of fingers/toes, and palms/soles specifically — skin cancers, including melanoma, occur at these non-sun-exposed sites disproportionately in skin of colour (see Red Flags & Refer).

Nail findings

Longitudinal melanonychia (a brown/black band or streak running the length of the nail plate) is a common benign finding in darkly pigmented skin, generally involving multiple digits on more than one hand. This must be distinguished from subungual melanoma, which typically involves a single digit (most often a thumb in an adult) and carries specific warning features.

• Fitzpatrick skin type IV-VI (or simply darker constitutive pigmentation — Fitzpatrick typing was designed for UV/burn sensitivity and correlates imperfectly with true pigmentation).
• For post-inflammatory hyperpigmentation specifically: any active inflammatory dermatosis (acne, eczema, psoriasis, insect bites), mechanical or chemical skin irritation (including from topical acne/retinoid therapy itself), and delayed treatment of the underlying inflammation.
• For melasma: female sex, sun/UV and visible-light exposure, hormonal exposure (pregnancy, combined oral contraceptives, hormone replacement therapy), and family history.
• For keloid/hypertrophic scarring: family history, high-tension anatomic sites (chest, shoulders, upper back, earlobes), and any dermal injury including piercing, surgery, vaccination, and acne itself.
• For traction alopecia: tightly applied head coverings (turbans, hijabs, wig caps), and tight hairstyles maintained for a prolonged period — braids, ponytails, buns, weaves, and hair extensions.
• For central centrifugal cicatricial alopecia (CCCA): occurs almost exclusively in women of African descent; traumatic hair practices (heat styling, chemical relaxers, tight styling) are proposed contributing factors, though the exact cause is unknown and likely multifactorial.
• For pseudofolliculitis barbae: shaving of tightly curled/coiled facial or neck hair, which re-enters the skin as it grows and triggers a foreign-body-type inflammatory reaction.
• For acral lentiginous melanoma specifically: increasing age; this is the most common melanoma subtype in patients with darkly pigmented skin, occurring on palms, soles, and the nail apparatus — sites not primarily explained by cumulative UV exposure, so sun-exposure counselling alone does not reduce this risk.

History

• Document Fitzpatrick type or another structured pigmentation descriptor at baseline, not just at the time of a pigmentary complaint — this is what later change gets compared against.
• For any inflammatory dermatosis: ask specifically about pain, itch, burning, and warmth in addition to inspecting for colour change, since erythema may be attenuated or absent.
• Ask about current and recent hair-care practices (relaxers, heat styling, weaves/braids/extensions, tension level, head coverings) when hair loss, scalp irritation, or scarring is a concern — this history frequently identifies a modifiable cause.
• Ask specifically about use of skin-lightening products, including unregulated or imported preparations, which may contain high-dose hydroquinone, corticosteroids, or heavy metals (mercury) — patients may be reluctant to disclose this due to stigma, and undisclosed concurrent use changes both the differential and the safe treatment plan.
• For suspected melasma: ask about hormonal exposures (pregnancy, hormonal contraception, hormone replacement therapy) and sun/visible-light exposure pattern.

Examination

Perform a full skin, hair, scalp, nail, and mucous-membrane examination using the non-erythema-reliant cues above. Examine palms, soles, and the nail apparatus specifically in any patient with darkly pigmented skin presenting with a new or changing pigmented lesion, given the disproportionate contribution of acral lentiginous melanoma at these sites in this population.^[2] Where weaves, braids, or wig caps limit direct scalp inspection, or where personal, cultural, or religious beliefs make a physical scalp exam infeasible, a detailed verbal history of the hair-loss pattern and timeline is still obtainable and should be taken.

When biopsy is, and is not, indicated

Biopsy any atypical pigmented lesion per the Red Flags criteria above rather than presuming a benign process (dermatosis papulosa nigra, benign melanonychia, seborrheic keratosis) without examination — these benign entities are common in skin of colour, but their presumptive diagnosis should not substitute for biopsy when a lesion has any atypical feature. Biopsy is not routinely needed to diagnose PIH itself, which is a clinical diagnosis based on a documented preceding inflammatory event or injury at the same site plus the characteristic macular, non-palpable colour change.

• Recognize and treat the underlying inflammatory dermatosis promptly enough — and, when needed, more assertively than erythema-based severity assessment alone would suggest — to limit the duration and intensity of inflammation that drives post-inflammatory hyperpigmentation.
• Resolve or substantially fade established PIH and melasma using an evidence-based topical regimen, without causing new irritation-driven pigmentation or exogenous ochronosis in the process.
• Sustain photoprotection (UV and visible light) as the foundation of any pigmentary treatment plan, since ongoing sun/light exposure undermines every other therapy.
• Minimize keloid/hypertrophic scar risk when a procedural or injectable option is being chosen, and treat an established keloid with an approach matched to its risk of recurrence.
• Halt progression of scarring alopecia (CCCA) and traction alopecia before permanent follicle loss occurs — regrowth is not possible once true scarring has developed, so early intervention is the entire objective.
• Preserve adherence to irritating but necessary topical regimens (retinoids, benzoyl peroxide, hydroquinone) through deliberate titration and vehicle selection, since irritation itself can trigger the same PIH the regimen is meant to prevent.

Photoprotection — the essential adjunct to every pigmentary treatment

"Skin of colour doesn't need sunscreen" is a persistent and incorrect belief — melanin provides only partial, incomplete photoprotection, and UV/visible light is a major driver of both melasma and PIH severity in this population; broad-spectrum sunscreen SPF 30 or higher, reapplied through the day, is foundational to every pigmentary treatment plan here, not optional.^[1]

• Recommend a tinted sunscreen containing iron oxide (in addition to zinc oxide/titanium dioxide) rather than an untinted mineral or chemical sunscreen for any patient being treated for melasma or PIH — untinted mineral sunscreens block UV but not visible light, and visible light (including from sun and from screens/indoor lighting) is a specific, underrecognized driver of hyperpigmentation in darker skin. Iron oxide blocks a large proportion of visible light and measurably improves outcomes on top of UV protection alone.^[6]
• Address the practical adherence barrier directly: many mineral/physical sunscreens leave a visible white or ashy cast on darker skin, which is the actual reason many patients stop using them, not a lack of understanding that sunscreen matters. Recommending a tinted formulation solves both problems at once — it improves visible-light protection and blends into the skin tone, which is why tinted sunscreen counselling measurably improves real-world adherence in this population rather than being a cosmetic afterthought.^[6]
• Reapplication every 2 hours with sun exposure, and after swimming/sweating, applies the same as for any patient — photoprotection benefit is dose- and consistency-dependent, and inconsistent reapplication is the most common reason topical pigmentary treatment fails to work despite correct drug selection.

Hair-care and hairstyling counselling (traction alopecia, CCCA, pseudofolliculitis barbae)

• Wear head coverings loosely where the head covering itself is the traction source, and loosen or remove braids/extensions immediately if pain or scalp irritation develops rather than continuing the style.
• Limit any single braided/woven style to a defined period (generally no more than 2 months) before removing and giving the scalp a rest interval.
• Prefer looser, shoulder-length styles over longer or tighter ones, and prefer sewn-in weaves over bonding glue, to reduce chronic tension.
• For pseudofolliculitis barbae: stop shaving for a defined period (commonly at least 8 weeks) to allow inflamed follicles to settle; when shaving resumes, use an electric razor rather than a blade where possible, shave in the direction of hair growth with gentle strokes, apply warm compresses before and a pre-shave oil/cream, and replace blades frequently.

Adjunctive scar-prevention measures

• Silicone gel or silicone sheeting applied to a healing wound once re-epithelialized, continued for an extended course, is the lowest-risk, best-evidence measure for reducing hypertrophic scar/keloid formation in a high-risk patient.
• Compression garments or dressings are used adjunctively at some anatomic sites at high risk for hypertrophic scarring.

Pregnancy

Melasma frequently develops or worsens in pregnancy ("mask of pregnancy," chloasma) and often fades spontaneously postpartum. During pregnancy, manage with photoprotection alone as the primary strategy. Hydroquinone, tretinoin, and tazarotene have meaningful systemic absorption/teratogenicity concerns and are not used in pregnancy — defer active topical pigment-lightening therapy until postpartum (and, if breastfeeding, until breastfeeding has finished, for the same agents) rather than treating through pregnancy. Azelaic acid has a more favourable pregnancy safety profile among the depigmenting agents and may be considered when treatment cannot reasonably wait, but confirm current product-specific guidance before use. Oral tranexamic acid is not used for melasma in pregnancy given pregnancy's own prothrombotic state.

Breastfeeding

As above, defer hydroquinone, tretinoin, and tazarotene until breastfeeding has finished unless the specific product's monograph states otherwise; azelaic acid is generally the more favourable option if treatment during lactation cannot reasonably wait.

Pediatrics

Pseudofolliculitis barbae and acne-associated PIH can both begin in adolescence. Hydroquinone and the retinoids used here are not established for routine use in young children; use in adolescents follows the same irritation-titration and duration-limit principles as in adults, started at the lower end of concentration/frequency. Traction alopecia can begin in early childhood from tight hairstyling and is fully preventable with the hairstyling counselling in Non-Pharmacologic Treatment — this is a genuine opportunity for early pharmacist counselling of caregivers before any permanent change occurs.

Patients using undisclosed skin-lightening products

Ask directly and non-judgmentally about use of imported or unregulated lightening products, since stigma can make patients reluctant to volunteer this. These products may contain high-concentration hydroquinone, potent topical corticosteroids, or mercury, each with its own toxicity profile (corticosteroid-induced acne, skin atrophy, or secondary infection; mercury causing systemic toxicity). Identifying this use changes both the differential for a presenting complaint and the safety of any new regimen prescribed on top of it.

• Hydroquinone: reassess at 2 months; discontinue if no improvement, and do not continue past the product's labelled maximum duration even if response is ongoing — use a treatment-free interval before any further course. At every visit, examine the treated area specifically for early paradoxical darkening or a blue-grey tone, which signals exogenous ochronosis and requires immediate discontinuation and referral rather than a dose increase.^[7]
• Melasma/PIH generally: reassess adherence to photoprotection at every visit — inadequate photoprotection is the most common reason a correctly chosen topical regimen appears to fail — and reassess pigment response at 6-8 weeks; maintain the regimen if a meaningful improvement is present, or step up to combination therapy/procedural referral if not.
• Retinoid/benzoyl peroxide-treated patients: ask specifically about irritation at follow-up, since irritation is the dominant reason for silent nonadherence in this population, and adjust frequency/vehicle before assuming the drug itself has failed.
• Keloid/hypertrophic scar under intralesional therapy: reassess lesion size, symptoms, and injection-site skin changes (atrophy, hypopigmentation) at each scheduled visit; a lesion enlarging or becoming newly symptomatic despite treatment needs specialist reassessment.
• Scarring alopecia (CCCA)/traction alopecia: monitor for continued progression with standardized photographs over time; any new area of smooth, scarred-appearing scalp without follicular openings signals irreversible loss in that area and should prompt an urgent rather than routine follow-up interval.

1. Confirm photoprotection adherence first, for any pigmentary complaint (PIH or melasma) — inadequate or inconsistent sunscreen use is the single most common cause of apparent topical-treatment failure, and no depigmenting agent works reliably against ongoing UV/visible-light exposure.
2. Confirm the underlying inflammatory dermatosis (if PIH-driving) is actually controlled — persistent low-grade inflammation (e.g., undertreated acne or eczema) will continue generating new PIH faster than existing PIH can fade.
3. Confirm correct application technique, frequency, and duration of the topical agent, and screen specifically for irritation causing silent nonadherence — irritation is more often the real cause of "no response" than true drug failure.
4. If genuinely no response after an adequate trial (generally 8-12 weeks) of an appropriately applied first-line agent, move to combination topical therapy (e.g., add a retinoid to hydroquinone or azelaic acid) rather than simply extending the same single agent, particularly for hydroquinone where extending past its duration limit raises ochronosis risk rather than improving outcomes.
5. For melasma or PIH still inadequate after combination topical therapy, refer for a procedural option (chemical peel, laser) under specialist direction — these carry their own PIH/dyspigmentation risk in darker skin and should not be self-referred to an unfamiliar provider.
6. For an established keloid not responding to intralesional corticosteroid monotherapy, add intralesional fluorouracil before considering surgical excision, which carries a high recurrence risk on its own and is generally reserved for refractory cases combined with adjunctive therapy.
7. For progressive scarring alopecia (CCCA) not stabilizing on initial therapy, refer to dermatology for escalation (systemic agents, closer monitoring) — the treatment goal is halting progression, and continued progression on a stable regimen is itself the trigger to escalate, not a reason to wait longer.

• Judging the severity of an inflammatory dermatosis by redness alone in a patient with darkly pigmented skin, and under-treating or delaying escalation as a result — ask about and examine for pain, warmth, swelling, and duration instead.
• Telling a patient with skin of colour that sunscreen is unnecessary or less important for them — melanin provides only partial protection, and inadequate photoprotection is the leading cause of pigmentary-treatment failure in this population.^[1]
• Recommending only untinted mineral sunscreen without addressing the visible white/ashy cast that is the actual reason many patients stop using it — offer a tinted, iron-oxide-containing formulation instead of simply repeating the same recommendation.
• Using hydroquinone continuously beyond its labelled duration, at high concentration, or without a treatment-free interval — this is the dominant preventable cause of exogenous ochronosis, which is itself very difficult to treat once established.
• Escalating a retinoid or benzoyl peroxide regimen too quickly, causing irritation that itself triggers new PIH — the very outcome the regimen was meant to prevent — rather than titrating frequency and using a buffering technique.
• Assuming a nail pigment band is benign melanonychia without checking for the specific atypical features (single digit, broad width, blurry border, variegated colour, nail-fold extension) that should trigger biopsy referral instead.
• Missing or delaying diagnosis of acral lentiginous melanoma by not examining palms, soles, and the nail apparatus as part of routine skin assessment in this population.
• Continuing to counsel tight braiding, weaves, or head coverings without modification once a patient reports scalp pain, irritation, or early hair thinning — this is the point at which the traction itself needs to change, not just be monitored.
• Treating an established keloid with excision alone as a first step, without adjunctive intralesional therapy or a discussion of recurrence risk.

How to use this table: Doses are adult doses and require patient-specific confirmation. Select any drug name to open its complete Pharmasist Drug Database page. Retinoid and benzoyl peroxide dosing for acne specifically is covered in full in the Acne Vulgaris chapter and is not repeated here beyond the irritation-titration notes relevant to PIH prevention.

Melasma — bilateral, blotchy grey-brown facial pigmentation, classically involving the cheeks, forehead, and upper lip. (Elord, Wikidocs, CC BY-SA 3.0, Wikimedia Commons)

Auricular keloid — a firm, rubbery nodule extending beyond the boundary of the original injury (here, an earlobe piercing) and not regressing spontaneously; the earlobe is a classic high-tension keloid site. (Htirgan, CC BY-SA 3.0, Wikimedia Commons)

Pseudofolliculitis barbae — hyperpigmented, firm papules and pustules concentrated in the shaved beard area, from curled hairs re-entering the skin. (Madigan Army Medical Center Dermatology / US Army Medical Department, public domain, Wikimedia Commons)

Hydroquinone (established PIH and melasma)

The most effective single topical depigmenting agent, but the only one with a genuine dose- and duration-dependent risk of exogenous ochronosis (a paradoxical, difficult-to-treat blue-grey darkening) — this is why duration limits are not a formality.

Non-hydroquinone depigmenting/adjunct agents

Preferred where a longer-term or lower-irritation option is needed, or where hydroquinone is contraindicated or not tolerated.

Keloid and hypertrophic scar therapy

Intralesional corticosteroid remains the pharmacologic backbone for an established lesion; 5-fluorouracil is added, not substituted, for lesions responding inadequately to corticosteroid alone. Excision alone carries a high recurrence risk and is reserved for refractory lesions combined with adjunctive therapy.<cite data-reference-id="cd2e0491-e1a4-468f-a075-82a97f106d8e"></cite>

Traction alopecia and central centrifugal cicatricial alopecia (CCCA) adjuncts

Hair-practice modification (see Non-Pharmacologic Treatment) is the primary intervention for traction alopecia. For CCCA, evidence for any single agent is limited and response is often modest — the overriding goal is halting progression, since established scarring is permanent.<cite data-reference-id="3ece3a9e-37cc-4914-a8be-57e8099d7195"></cite>

Pseudofolliculitis barbae adjuncts

Shaving modification (see Non-Pharmacologic Treatment) is the primary intervention; topical therapy is adjunctive for inflammatory lesions and secondary infection prevention.<cite data-reference-id="9c42fe03-e120-4f9a-872e-7e2b426850e1"></cite>