The most common email I get goes something like this: “I’ve been using a brightening serum for four months and nothing’s changing — what am I doing wrong?”
The answer is almost never that the serum is bad. The answer is that the diagnosis was made by guesswork, and the wrong tool was applied to the wrong condition.
OTC skincare marketing exists in a world with one category: dark spots. Clinical dermatology has at minimum three distinct conditions — melasma, post-inflammatory hyperpigmentation, and dermal melanocytosis (most commonly Hori’s nevus) — that share the visible characteristic of skin appearing darker in patches. The mechanisms differ. The treatment responses differ. The prognoses differ. A protocol designed for one will frequently make another worse.
I’ll walk through the differential in five clinical signals, the diagnostic test that resolves most ambiguity at home, and the treatment paths that pair with each.
Why getting this right matters
Most pigmentation treatment failures I see clinically aren’t molecule failures. They’re classification failures.
A patient with Hori’s nevus using a 4% niacinamide serum will see no change because the pigment is dermal — niacinamide blocks epidermal melanosome transfer and can’t reach it. A patient with melasma using hydroquinone monotherapy will see improvement that disappears with the first hormonal trigger because the underlying driver wasn’t addressed. A patient with PIH applying a fade protocol while their underlying acne flares continues will chase a target that keeps moving.
The 30 seconds spent on the differential before reaching for an ingredient is the highest-leverage clinical move available to anyone working on their own pigmentation.
The Wood’s lamp test
The single most useful diagnostic tool for at-home use is a Wood’s lamp — a UVA-emitting handheld light that’s been used since the 1940s. They run $20-40 on Amazon.
Under Wood’s lamp, epidermal pigment (above the dermal-epidermal junction) enhances — the pigmented area looks darker against the surrounding skin. Dermal pigment (in the dermal layer, below the junction) shows little or no enhancement, or appears slightly bluish-gray.
This single test resolves the Hori’s-versus-the-others differential. Hori’s nevus shows minimal enhancement under Wood’s lamp because the pigment is dermal. Melasma and PIH typically enhance, with melasma showing slightly more dramatic enhancement than PIH in most cases.
Sanchez and colleagues formalized this classification in 1981 (J Am Acad Dermatol) and the Wood’s lamp pattern hasn’t changed. It’s the foundation of the differential.
Melasma — the five signals
Symmetric distribution. Melasma appears bilaterally, almost always in the same pattern on both sides of the face. The classic patterns are centrofacial (forehead, cheeks, upper lip, nose), malar (cheekbones), and mandibular (jawline). Asymmetric pigmentation is almost never melasma.
Hormonal triggers. Melasma is driven by estrogen and progesterone signaling on melanocytes. Onset or worsening during pregnancy, postpartum, on oral contraceptives, or with hormone replacement therapy is the classic history.
Sun-sensitivity. Melasma worsens with even moderate UV and visible light exposure. Patients who report “my dark spots are way worse in summer” are almost always describing melasma.
Slow onset. Melasma develops over months or years, not days. There’s rarely an identifiable inciting event.
Recurrence after treatment. Melasma fades with treatment and returns with triggers. This is diagnostic — PIH treated correctly stays gone unless the underlying inflammation recurs. Melasma comes back.
PIH — the five signals
History of inflammation. PIH follows a specific inflammatory event. Acne lesion, eczema flare, contact dermatitis, picking, ingrown hair, laser treatment, chemical peel, abrasive scrub. There’s usually a specific lesion or zone the patient can identify.
Irregular distribution. PIH appears wherever the underlying inflammation occurred. No symmetric pattern, no consistent location across patients.
Predictable fade timeline. PIH fades on a predictable timeline if the underlying inflammation stops. Fitzpatrick I-III: 6-12 weeks for epidermal PIH. Fitzpatrick IV-VI: 6-12 months. The timeline is the most useful prognostic marker we have. Davis and Callender (J Clin Aesthet Dermatol 2010) is the standard reference.
Inflammation-correlated worsening. New PIH appears when new inflammation occurs. Active acne with persistent PIH means the acne control is failing — that’s the leverage point, not the pigment.
Wood’s lamp enhancement. PIH enhances under Wood’s lamp, sometimes dramatically.
Hori’s nevus — the five signals
Bilateral malar distribution. Hori’s nevus appears almost exclusively over the cheekbones, bilaterally, in a speckled or confluent pattern. Centrofacial and mandibular involvement is rare.
Adult onset, typically 30s-50s. Hori’s nevus emerges in adulthood, distinct from congenital dermal melanocytic lesions. The classic age window is 30-50, with onset usually in the mid-30s.
Predominantly East and Southeast Asian women. The epidemiology skews heavily Asian — particularly Korean, Japanese, Chinese, Vietnamese, Thai, and Filipino populations. Park and colleagues (Br J Dermatol 2008) documented the demographic concentration that’s been replicated in multiple cohorts since.
Slate-gray to brown-gray coloration. Hori’s nevus often has a subtly bluish or gray tone that melasma lacks. Photography under daylight is more useful than mirror inspection for catching this.
Wood’s lamp non-enhancement. The diagnostic separator. Hori’s nevus pigment is dermal, so it doesn’t enhance under UVA.
The treatment divergence
Melasma: triple combination cream (hydroquinone 4% + tretinoin 0.05% + fluocinolone 0.01%) remains the most-evidenced first-line. Tranexamic acid (topical and oral) has accumulated strong evidence over the past decade — Cestari and colleagues’ 2014 review (J Drugs Dermatol) is the standard reference. Aggressive photoprotection including visible-light protection is non-negotiable. Lasers are risky in melasma and should be deferred to specialists.
PIH: treat the underlying inflammation first. For acne PIH, controlling the acne is 60% of the work. Topical azelaic acid, kojic acid, alpha arbutin, and niacinamide all have evidence for epidermal PIH. Tretinoin accelerates fade timeline. Patience is required — the histology takes months.
Hori’s nevus: topical ingredients are largely ineffective. Q-switched Nd:YAG laser (1064 nm) is the established treatment, typically requiring 5-10 sessions. This is where the at-home protocol ends and a clinical referral begins.
The decision table
| Signal | Melasma | PIH | Hori’s nevus |
|---|---|---|---|
| Distribution | Symmetric, bilateral | Irregular, post-inflammatory | Bilateral malar |
| Triggers | Hormones, UV, heat | Inflammation events | Adult onset, no clear trigger |
| Wood’s lamp | Enhances | Enhances | Minimal enhancement |
| Color | Brown to gray-brown | Brown | Slate-gray to brown-gray |
| Treatment | Triple cream + tranexamic | Anti-inflammatory + brighteners | Q-switched laser |
| Prognosis | Recurrent | Resolves with cause control | Permanent without laser |
When to stop self-treating
The clinical heuristic: if you’ve been applying a coherent fade protocol for 12 weeks with no measurable change — and measurable means photographs, not mirror perception — the diagnosis is probably wrong. If Wood’s lamp testing suggests dermal pigment, you need a dermatology referral. If you’re treating “melasma” and it never responds to sun protection improvements, you may have been treating PIH all along.
The 30 seconds spent reading the differential is worth more than the four months spent applying the wrong protocol.
FAQ
*How do I tell if my dark spots are melasma or PIH?*
The biggest clinical separators are symmetry and trigger history. Melasma is bilateral and triggered by hormones and UV exposure. PIH is asymmetric and follows specific inflammatory events. Wood’s lamp testing at home confirms most cases — both enhance, with melasma typically showing slightly stronger enhancement.
*What is Hori’s nevus and why is it mistaken for melasma?*
Hori’s nevus (acquired bilateral nevus of Ota-like macules) is a dermal melanocytic condition affecting predominantly East and Southeast Asian women in their 30s-50s. The bilateral malar distribution mimics melasma, but the pigment is dermal — topical treatments don’t reach it. Wood’s lamp non-enhancement is diagnostic.
*Why does my hyperpigmentation come back even after fading?*
Recurrence after treatment is one of the strongest clinical signals for melasma. PIH treated with the underlying inflammation controlled doesn’t recur. Hori’s nevus doesn’t recur because it doesn’t fade in the first place. Persistent recurrence usually means the diagnosis was melasma all along.
*Can a Wood’s lamp tell me which type I have?*
Wood’s lamp distinguishes epidermal pigment (which enhances) from dermal pigment (which doesn’t). That separates Hori’s nevus from melasma and PIH cleanly. It can’t reliably distinguish melasma from PIH — that requires the clinical history.
References
- Sanchez NP, Pathak MA, Sato S, et al.. Melasma: a clinical, light microscopic, ultrastructural, and immunofluorescence study. J Am Acad Dermatol. 1981. PubMed.
- Park JM, Tsao H, Tsao S. Acquired bilateral nevus of Ota-like macules (Hori nevus): etiologic and therapeutic considerations. Br J Dermatol. 2008. PubMed.
- Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010. PubMed.
- Cestari TF, Dantas LP, Boza JC. Acquired hyperpigmentations: Tranexamic acid in the treatment of melasma. J Drugs Dermatol. 2014. PubMed.
Khabir Uddin is the founder of Elelaf Journal. This article is editorial, not medical advice. For pigmentation that hasn’t responded to OTC protocols within 12 weeks, see a board-certified dermatologist for diagnostic confirmation.