Dermatology, Venereology and Leprosy
Vitiligo
Vitiligo for MBBS and NEET-PG: autoimmune melanocyte loss, milky-white macules, distinction from leprosy and pityriasis, Wood's lamp, topical therapy and phototherapy, mapped to NMC codes DR2.
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Vitiligo
Vitiligo for MBBS and NEET-PG: autoimmune melanocyte loss, milky-white macules, distinction from leprosy and pityriasis, Wood's lamp, topical therapy and phototherapy, mapped to NMC codes DR2.
Vitiligo is a common cause of depigmentation and a favourite differential for the hypopigmented patch. This chapter covers its autoimmune basis and associations, the clinical recognition of milky-white macules with retained sensation, the distinction from leprosy and other hypopigmented disorders, and a treatment ladder from topical agents to phototherapy.
High-yield: Vitiligo
- Vitiligo is an acquired disorder of depigmentation caused by autoimmune destruction of melanocytes, giving sharply defined milky-white macules.
- The lesions are typically symmetrical and favour the face, hands, elbows, knees and body openings such as the mouth and eyes.
- Depigmented patches show accentuation under Wood's lamp, appearing bright bluish-white, which helps confirm the diagnosis in fair skin.
- Vitiligo is associated with other autoimmune conditions, especially thyroid disease, pernicious anaemia, type 1 diabetes and Addison's disease.
- The Koebner phenomenon means new lesions appear at sites of trauma such as scratches and pressure.
- Segmental vitiligo follows a dermatomal pattern, is usually unilateral, stabilises early and is less linked to autoimmunity.
- Leucotrichia, whitening of hairs within a patch, indicates loss of the follicular melanocyte reservoir and predicts poorer repigmentation.
- Vitiligo is differentiated from pityriasis versicolor, pityriasis alba, leprosy and post-inflammatory hypopigmentation, which are hypopigmented rather than fully depigmented.
- Unlike the hypopigmented anaesthetic patch of leprosy, vitiligo retains normal sensation over the lesions.
- Topical corticosteroids and calcineurin inhibitors such as tacrolimus are first-line for limited disease.
- Narrowband ultraviolet B phototherapy is the treatment of choice for extensive or progressive vitiligo.
- Surgical options such as melanocyte transfer are considered for stable segmental disease that has not responded to medical treatment.
- Depigmentation therapy is an option only for very extensive vitiligo where restoring colour is not feasible.
- Photoprotection is important because depigmented skin lacks melanin protection and burns easily.
Vitiligo versus other pale patches
- **Vitiligo:** Complete depigmentation, normal sensation, Wood's lamp accentuation, autoimmune links.
- **Leprosy:** Hypopigmented patch with sensory loss, thickened nerves.
- **Pityriasis versicolor:** Fine scaly hypopigmented patches, positive KOH, spaghetti and meatballs.
- **Pityriasis alba:** Ill-defined pale scaly patches in atopic children on the face.
NMC competencies in this chapter
- **DR2.1:** Differentiating vitiligo from other causes of hypopigmented lesions
- **DR2.2:** Treatment of vitiligo
Frequently Asked Questions
How is vitiligo distinguished from a leprosy patch?
Vitiligo produces a completely depigmented milky-white macule with normal sensation, whereas the hypopigmented patch of leprosy has reduced or absent sensation and may be associated with thickened peripheral nerves.
What autoimmune diseases are linked to vitiligo?
Thyroid disease is the commonest association, along with pernicious anaemia, type 1 diabetes and Addison's disease, so screening for thyroid dysfunction is reasonable.
What is the first-line treatment for limited vitiligo?
Topical corticosteroids or calcineurin inhibitors such as tacrolimus for small areas, with narrowband ultraviolet B phototherapy for extensive or spreading disease.
Why does hair within a patch matter?
Whitening of hairs, called leucotrichia, means the follicular melanocyte reservoir is lost, so that patch is less likely to repigment with treatment.
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