The acne consultation I run for a patient with Fitzpatrick type V skin is structurally different from the one I run for a patient with Fitzpatrick type I. Not because the underlying disease changes, but because the consequences of my clinical decisions are meaningfully different. If you are applying an identical protocol across all skin tones, you are missing a consistent source of treatment failure.
The Pathophysiology Does Not Change. The Consequences Do.
Acne vulgaris is driven by the same four mechanisms in all skin types: excess sebum production, follicular hyperkeratosis, Cutibacterium acnes proliferation, and the subsequent inflammatory cascade. NICE NG198 applies across the board. The morphology classification, the grading criteria, and the first-line treatment rationale do not change based on skin tone.
What changes is the inflammatory response's downstream effects in skin with higher baseline melanin levels.
Post-inflammatory hyperpigmentation (PIH) is more prevalent, more marked, and more persistent in patients with Fitzpatrick IV to VI skin. For many of these patients, PIH causes as much distress as the active acne itself. Sometimes more. A treatment plan that clears the papules while triggering or worsening PIH has not succeeded. It has exchanged one problem for another.
The second difference is treatment tolerance. Some agents that are well-evidenced for acne management can provoke irritant responses in sensitised skin, and in darker skin types that irritation can itself trigger pigmentary change. Introducing these agents without adequate preparation, or at inappropriately high concentrations, creates a predictable outcome.
A Two-Layer Assessment
I use a two-layer assessment for every patient with Fitzpatrick IV to VI skin.
The first layer is the standard acne assessment: morphology, distribution, grading per NICE NG198 criteria, hormonal pattern if relevant, previous treatments and duration of use.
The second layer is a PIH assessment. How much PIH is already present, and where? What is the distribution relative to the active lesions? Is it resolving, stable, or worsening? Has any previous treatment worsened it?
The PIH assessment changes my opening recommendation. A patient with persistent, widespread PIH overlying mild papulopustular acne may need the PIH addressed first. Clearing the PIH and stabilising the barrier creates a better environment for acne treatment to work without generating further pigmentary disruption.
Treatment Selection
Retinoids. Topical retinoids are appropriate first-line treatment for comedonal and mild papulopustular acne across all skin types. In patients with darker skin, I start at the lowest effective concentration and build gradually. Adapalene 0.1% gel, introduced three nights per week and increased over four to six weeks, minimises the purge response and reduces early irritation-driven PIH risk. Patients need to know that initial redness or flaking is expected, and what the management plan is if it occurs.
Benzoyl peroxide. Effective and appropriate. Lower concentrations, 2.5% to 5%, match the efficacy of higher concentrations against C. acnes with less irritancy. In skin with higher PIH risk, starting low and building slowly is good practice. I mention fabric bleaching at the consultation stage, because this is a practical concern that affects adherence.
Azelaic acid. This is worth prioritising in patients with darker skin because it carries a dual action: it addresses C. acnes activity and suppresses melanin synthesis, providing a direct benefit against PIH. At 20% prescription strength, the evidence for PIH reduction is well-established. When active acne and PIH coexist, azelaic acid is often the most efficient single agent.
Niacinamide. A useful supporting agent. It reduces transepidermal water loss, has anti-inflammatory properties, and inhibits melanosome transfer, which directly targets PIH formation. It does not clear active acne as a standalone, but it is well-tolerated and additive in a regimen.
What to approach cautiously. High-strength glycolic acid peels, aggressive exfoliation, and abrasive in-clinic treatments carry a meaningful PIH risk in darker skin types. If in-clinic procedures are part of the plan, I explain this risk explicitly, document the conversation, start at low concentrations, and leave a longer interval before the next session.
SPF Is Not Optional
UV exposure exacerbates melanin production at sites of inflammation. It is the most consistent factor that worsens PIH, and it is the one that patients most often deprioritise.
A patient who uses all prescribed topicals diligently and skips SPF is working against the treatment plan. A broad-spectrum SPF 50, cosmetically acceptable enough for daily use across all skin tones, is part of every treatment recommendation for this population. This includes winter months, and it includes indoor skin with significant window exposure.
The Referral Decision
Severe nodular acne, significant hormonal drivers that need systemic management, or PIH that has not responded to six months of optimised topical treatment are each referral triggers. Collaboration with a consultant dermatologist with experience in skin of colour is appropriate and in the patient's interest. Knowing the referral threshold is part of the consultation, not an admission of limitation.
If you want to build a more structured clinical approach to acne assessment and treatment planning, Acne Decoded at Aesthetics Unlocked covers morphology classification, treatment selection, consultation frameworks, and the evidence behind each clinical decision. You can find it at aestheticsunlocked.co.uk/courses/acne-decoded.