Clinical diagnosis is usually sufficient; bedside confirmation relies on sharply demarcated depigmentation and accentuation under Wood’s lamp.
Dermoscopy typically shows absent pigment network, perifollicular repigmentation, and sharp borders in active/stable lesions.
Biopsy is reserved for atypical cases; histology shows loss of melanocytes and reduced/absent melanin (Fontana-Masson), with interface changes in subsets.
Rule out mimickers using a structured differential table; consider limited labs (e.g., thyroid) per guideline and symptom profile.
Severity/activity tracking with VASI/F-VASI/T-VASI, photography, and activity signs (confetti, Koebner) guides therapy.
Abstract
This article outlines a practical, evidence-informed approach to diagnosing vitiligo, including bedside tools (Wood’s lamp, dermoscopy), indications for biopsy, targeted labs, and structured differential diagnosis. It also summarizes severity and activity scoring systems to support longitudinal care and clinical trials.
Bedside Diagnostic Workflow
History: onset/progression, Koebner triggers, autoimmune history, family history.
Examination: distribution (acrofacial, generalized, segmental), hair depigmentation, mucosae.
Wood’s lamp in dark room to accentuate depigmentation and delineate margins.
Dermoscopy for pattern recognition (border, follicular signs, residual pigment).
Biopsy only if atypical, inflammatory, or suspicious for other conditions.
Wood’s Lamp Findings
Table 1. Typical Wood’s lamp patterns.
Feature
Vitiligo
Notes
Lesion contrast
Bright chalk-white accentuation
Sharp edges; reveals subclinical spread
Border
Sharp, often pseudo-satellites in active disease
Helps map treatment field
Hair
Leukotrichia accentuated
Predicts slower response
Dermoscopy
Table 2. Dermoscopic clues in vitiligo vs mimickers.
Parameter
Vitiligo
Mimickers
Pigment network
Absent/attenuated
Often preserved or mottled (PIH, pityriasis alba)
Border
Sharp cutoff
Ill-defined in PIH/alba; scaly edge in tinea versicolor
Perifollicular pattern
Islands of repigmentation
Less typical
Scale
Usually absent
Fine scale in tinea versicolor/alba
Biopsy & Histology
Indications: diagnostic uncertainty, atypical inflammation, suspected hypopigmented MF, chemical leukoderma.
Correlation with clinic/dermoscopy essential due to sampling limitations.
Laboratory Screening
No universal lab panel is required for diagnosis. Consider targeted testing (e.g., TSH ± thyroid antibodies) when symptoms, family history, or local guidelines suggest autoimmune thyroid disease or other comorbidities.
Differential Diagnosis
Table 3. Common mimickers and distinguishing features.
Condition
Clues
Helpful tests
Tinea versicolor
Hypo-/hyperchromic macules, fine scale
KOH prep; scale under dermoscopy
Pityriasis alba
Poorly defined hypopigmented patches in children
Clinical; mild scale; improves with emollients
Post-inflammatory hypopigmentation
History of prior dermatitis/trauma
Wood’s lamp less accentuated; pigment network present
Idiopathic guttate hypomelanosis
Small guttate macules on shins/forearms in older adults
Clinical; stable speckles
Nevus depigmentosus
Congenital/early onset, stable
Wood’s lamp less bright; serrated borders
Piebaldism / albinism variants
Stable leukoderma; family history
Genetic context; no inflammatory signs
Hypopigmented mycosis fungoides
Persistent patches, sometimes pruritic
Biopsy (atypical lymphocytes), T-cell clonality
Chemical leukoderma
Exposure pattern to phenols/catechols
Occupational history; patch testing context
Lichen sclerosus/planus (hypopigmented)
Atrophic plaques or polygonal papules
Clinical/biopsy if uncertain
Severity & Activity Scoring
VASI (T-VASI, F-VASI) for extent and response tracking.