Vitiligo
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Direct answer
Vitiligo is an acquired depigmenting disorder in which melanocytes are destroyed, producing chalk-white, well-demarcated macules that glow bright white under Wood's lamp. It divides into non-segmental vitiligo — the commoner, bilateral, progressively fluctuating type with Koebnerisation and autoimmune associations — and segmental vitiligo, a unilateral dermatomal type that stabilises early. Treatment combines topical corticosteroids or calcineurin inhibitors, narrow-band UVB phototherapy for widespread disease, and surgical grafting for stable refractory lesions, with honest counselling that response is slow and depigmentation, not cure, is the aim of extensive disease.
What you must remember
- Depigmentation, not hypopigmentation: vitiligo macules are chalk-white with complete melanocyte loss — the critical distinction from the hypopigmented (off-white, less-white) patches of leprosy, pityriasis alba and pityriasis versicolor.
- Sensation is intact in vitiligo — a hypoaesthetic white patch is leprosy until proved otherwise, the single most important Indian examination point.
- Non-segmental vitiligo: acrofacial (fingers, toes, lips — the hardest to repigment), generalised, universal and mucosal subtypes; associated with Koebner phenomenon, leucotrichia (white hair in lesions), trichrome and confetti macules, halo naevi, and autoimmune thyroid disease, diabetes and alopecia areata.
- Segmental vitiligo: unilateral, dermatomal or quasi-dermatomal, onset young, stabilises within a year or two, leucotrichia early, responds better to autologous grafting because it does not keep reactivating.
- Wood's lamp: chalk-white autofluorescence with sharp margins confirms the diagnosis; skin biopsy (only if needed) shows complete absence of melanocytes with no infiltrate of significance.
- Treatment ladder: localised — topical corticosteroid or tacrolimus/pimecrolimus (preferred on face and neck, flexures and around eyes); generalised — narrow-band UVB two to three times weekly for months; rapidly progressing disease — mini-pulse oral steroids to stabilise; stable (usually about a year of inactivity) — surgical methods such as mini-punch grafting, suction blister grafting or cultured melanocyte transplantation; extensive (>50 percent or cosmetically intolerable) — depigmentation with monobenzylether of hydroquinone.
- Counselling is treatment: vitiligo is non-contagious, not caused by any food, and carries heavy social and matrimonial stigma in India; camouflage cosmetics and support matter as much as prescriptions, and associated thyroid screening is reasonable.
Common confusion
The white-patch differential is the exam's favourite. Leprosy: hypopigmented, hypoaesthetic patch with thickened nerves; post-kala-azar dermal leishmaniasis: nodular or macular hypopigmentation over the face in (or after) kala-azar, endemic in Bihar and Jharkhand; pityriasis alba: dry, faintly scaly, off-white patches of the face in children with atopy; pityriasis versicolor: fawn or hypopigmented scaly macules of the trunk with fine scale that KOH shows full of yeast and hyphae, often called "the fever of summer"; nevus anaemicus: a vasoconstricted patch that abolishes with pressure of a glass slide while vitiligo does not change; and ash-leaf macules of tuberous sclerosis — present at birth, on the trunk, alongside shagreen patch and adenoma sebaceum. Sensation testing and diascopy separate most of these at the bedside.
Exam-focused takeaway
NEET-PG shows a photograph of chalk-white macules — hands and face are favourites — and asks the diagnosis, the type (segmental versus non-segmental) or the differentiating feature from leprosy (intact sensation, bright Wood's lamp). Stems test the Koebner phenomenon, leucotrichia and the autoimmune associations, and management options revolve around NBUVB, tacrolimus for facial lesions, and grafting only for stable disease. Expect at least one assertion-reason stem built on "vitiligo is contagious" — it is not, and saying so plainly is part of both the exam answer and ethical practice.
Frequently asked questions
How is vitiligo different from a hypopigmented patch?
Vitiligo is depigmented — complete melanocyte loss gives chalk-white, Wood's-lamp-bright macules — whereas hypopigmented patches of leprosy or pityriasis alba merely have reduced pigment and look off-white.
What distinguishes vitiligo from leprosy at the bedside?
Sensation: vitiligo macules feel normally, leprosy patches are hypoaesthetic with thickened nerves; Wood's lamp and, if needed, a skin biopsy settle doubtful cases.
What is segmental vitiligo?
Unilateral dermatomal-type vitiligo of early onset that stabilises within a couple of years; because it stops activating, it is the best candidate for surgical grafting.
What is the treatment of choice for generalised vitiligo?
Narrow-band UVB phototherapy two to three times weekly, continued for months; topical tacrolimus or corticosteroids serve localised and facial disease, and surgery suits stable refractory patches.
When is depigmentation therapy used?
In extensive vitiligo involving more than half the body, or disease the patient finds cosmetically intolerable, monobenzylether of hydroquinone removes remaining pigment to achieve uniform tone — irreversible, hence a considered decision.
Is vitiligo hereditary or contagious?
Not contagious; there is a genetic predisposition with autoimmune mechanisms, and an association with thyroid disease and other autoimmune conditions in the patient or family.