Pigmentation Disorders: A Comprehensive Classification
Skin colour is determined by the amount of melanin produced by specialised cells called melanocytes. Melanin synthesis occurs via the tyrosinase enzyme through the chain: tyrosine → DOPA → dopaquinone → melanin. A disruption at any stage of this mechanism leads to a pigmentation abnormality:
- Hyperpigmentation: Excess melanin production or accumulation — the primary mechanism behind dark spots, melasma, and post-inflammatory hyperpigmentation (PIH)
- Hypopigmentation: Below-normal melanin — melanocytes are present but dysfunctional or of reduced activity; examples include nevus depigmentosus, tinea versicolor, and the white patches of tuberous sclerosis
- Depigmentation: Complete absence of melanocytes; these areas produce bright white fluorescence under Wood's lamp — vitiligo is the most significant example in this category
This classification is clinically vital: a patch merely appearing "pale" is not sufficient to diagnose vitiligo. Diagnostic criteria differ, and treatment approaches and prognoses are entirely separate.
Vitiligo: Types, Active-Stable Distinction, and Pathogenesis
Vitiligo is an autoimmune disease in which T lymphocytes mount a misdirected immune attack against melanocytes. The disease can begin or flare when genetic predisposition combines with triggering factors such as stress, trauma, or sunburn.
Types of Vitiligo
- Non-segmental vitiligo (generalised type): The most common form (85–90%). Bilateral, symmetrical involvement; the backs of the hands, face (periorbital, perioral), genital area, knees, and elbows are frequently affected. Associated autoimmune conditions (thyroid disease, Type 1 diabetes, rheumatoid arthritis) are more frequently observed.
- Segmental vitiligo: Unilateral, dermatomal distribution; stabilises more rapidly and responds better to treatment. More common in childhood.
- Localised vitiligo: Single focus; focal or mucosal involvement
- Acrofacial vitiligo: Involvement concentrated around the hands, feet, and face
Active vs Stable Vitiligo
The most critical distinction for treatment selection is whether the disease is active or stable:
- Active vitiligo: New lesion development or expansion of existing lesions within the past 6–12 months; poor response to treatment; aggressive procedures increase the risk of Koebner phenomenon
- Stable vitiligo: No new lesions for at least 12 months; the most suitable period for repigmentation therapies (NB-UVB, surgery)
Vitiligo vs Melasma: Diagnosis with Wood's Lamp
The most frequently encountered clinical confusion is distinguishing vitiligo from other hypopigmented conditions in which melanin is reduced but not absent (nevus depigmentosus, post-inflammatory hypopigmentation), or from areas of melasma that appear pale.
Wood's lamp test (365 nm UV-A):
- Vitiligo: Bright milky-white fluorescence — very well-defined border indicating the absence of melanocytes
- Nevus depigmentosus: Pale white, less contrast than vitiligo; melanocytes are present
- Epidermal melasma: Becomes more apparent (appears darker)
- Dermal melasma: Does not become more apparent
- Tinea versicolor: Yellow-green fluorescence — due to metabolites produced by Malassezia furfur
Vitiligo Treatment Options Comparison Table
| Treatment | Mechanism | Best Suited For | Efficacy | Notes |
|---|---|---|---|---|
| NB-UVB Phototherapy | Melanocyte stimulation, immunomodulation | Generalised, stable vitiligo | High (50–70% repigmentation) | 2–3 sessions per week; long-term protocol |
| Topical Corticosteroids | Immune suppression, melanocyte protection | Localised, active vitiligo | Moderate (30–40%) | Risk of atrophy with long-term use |
| Calcineurin Inhibitors (tacrolimus, pimecrolimus) | T-cell activation suppression; corticosteroid alternative | Face, neck, genital area (thin skin) | Moderate (40–50%) | No atrophy; ideal for facial and flexural areas |
| JAK Inhibitors (topical ruxolitinib — FDA-approved 2022) | JAK1/JAK2 inhibition; blocks the interferon-γ pathway | Non-segmental vitiligo with facial involvement | High (50%+ repigmentation on the face at 24 weeks) | Currently the most promising topical therapy |
| Melanocyte Transfer (Surgery) | Transplantation of melanocytes from normal skin | Stable vitiligo (≥12 months) | Very high (80–90% in segmental type) | Only in stable patients; contraindicated during active phase |
| Excimer Laser (308 nm) | Targeted NB-UVB; follicular melanocyte stimulation | Small, localised stable patches | High (within limited area) | 2–3 sessions per week; alternative to NB-UVB |
Distinguishing Nevus Depigmentosus from Vitiligo
Nevus depigmentosus (hypopigmented naevus) is a stable area of hypopigmentation present from birth or early childhood. It differs from vitiligo in the following ways:
- Present from birth: Vitiligo develops later in life; nevus depigmentosus is congenital or appears in early childhood
- Stable: It does not grow or spread; vitiligo may be progressive
- Wood's lamp: Nevus depigmentosus shows less contrast; vitiligo displays bright white fluorescence
- Melanocyte status: In nevus depigmentosus, melanocytes are present but dysfunctional; in vitiligo, melanocytes have been destroyed
- Treatment response: Treatments for vitiligo (NB-UVB, JAK inhibitors) are ineffective in nevus depigmentosus
Managing Vitiligo Patients in Aesthetic Procedures: Koebner Phenomenon
Planning aesthetic procedures in patients with vitiligo requires particular caution due to the Koebner phenomenon — the re-emergence of vitiligo patches at sites of skin trauma or irritation.
Procedures carrying Koebner risk:
- Chemical peeling (especially TCA and glycolic acid)
- Microneedling (dermapen)
- Laser treatments (fractional, ablative)
- IPL (especially during active vitiligo phases)
- Botox / filler injections (minimal risk at needle entry points)
Safe approach:
- All ablative and invasive procedures should be postponed during active vitiligo phases
- Procedures are safer during stable phases (at least 12 months of stabilisation)
- Patient information and written informed consent are mandatory
- Planning procedures in areas away from vitiligo patches minimises risk
Can Hyperpigmentation Treatments Be Used in Vitiligo?
This question arises frequently in clinical practice. The majority of hyperpigmentation (dark spot) treatments are ineffective in vitiligo; moreover, some can be harmful:
- Hydroxyurea and hydroquinone: Can worsen the existing condition by causing melanocyte toxicity
- Retinoids: Should be used with caution in active vitiligo; irritation can trigger Koebner phenomenon
- Topical acids: Contraindicated during the active phase; can be used in the stable phase and in areas without vitiligo
- Sun protection: Essential in both dark spot and vitiligo treatment; the white patches in vitiligo lack the protection of melanin and are extremely vulnerable to UV damage
Psychosocial Dimension and Multidisciplinary Approach
Vitiligo is not merely a skin disease; anxiety and depression are seen in 30–40% of patients, and social isolation is common. Effects are particularly profound in individuals with darker skin tones and those with facial involvement. For this reason, psychological support and patient education should be included in the treatment plan.
The Vitiligo European Task Force (VETF) and American Academy of Dermatology guidelines recommend a multidisciplinary approach (dermatology + psychology/psychiatry + nutrition + aesthetic consultation) in vitiligo treatment.
This article is for informational purposes only. Please consult a qualified physician for treatment decisions.