Vitiligo
Exam Tips
- In OSCEs, describe lesions as "well-demarcated, non-scaly depigmented macules/patches" and state whether distribution suggests segmental or non-segmental disease.
- Explicitly mention Koebner phenomenon and leukotrichia as markers of active/follicular involvement.
- Always ask and screen for autoimmune thyroid disease in vitiligo history-taking.
- If scale, induration, scarring, or marked inflammation is present, broaden differential away from classic vitiligo.
- Counselling marks are high-yield: chronic relapsing course, variable repigmentation, sun protection, and psychological impact.
Definition
Vitiligo is an acquired chronic pigmentary disorder in which functional melanocytes are lost, producing well-demarcated depigmented macules and patches of skin, and sometimes white hair or mucosal depigmentation. It is classified into non-segmental disease (usually bilateral/symmetrical and most common) and segmental disease (typically unilateral, earlier onset, and often rapidly stabilising), with mixed forms also recognised.
Pathophysiology
Vitiligo is multifactorial, with converging mechanisms causing melanocyte loss. In non-segmental vitiligo, the strongest evidence supports autoimmune cytotoxic T-cell-mediated destruction of melanocytes, with melanocyte-specific lymphocytes seen in blood and lesional margins; oxidative stress, inflammatory cytokines, and melanocyte-detachment mechanisms likely amplify injury. Segmental vitiligo was historically considered neurogenic, but current evidence suggests overlapping immune-inflammatory pathways with non-segmental disease. Genetic susceptibility is polygenic and interacts with triggers such as trauma/friction (Koebner phenomenon), sunburn, psychosocial stress, and exposure to phenolic/catecholic chemicals.
Risk Factors
- Family history of vitiligo (first-degree relative risk increased several-fold)
- Personal or family history of autoimmune disease, especially autoimmune thyroid disease (for example Hashimoto thyroiditis)
- Other autoimmune comorbidity risk: type 1 diabetes, pernicious anaemia, Addison disease, alopecia areata, rheumatoid arthritis, psoriasis, inflammatory bowel disease, SLE
- Mechanical trauma/friction or prior sunburn (Koebnerisation)
- Possible chemical exposure (phenolic/catecholic compounds in some occupational/cosmetic products)
- Childhood/adolescent onset is common (many cases present before age 20)
Clinical Features
Symptoms
- Usually asymptomatic colour loss of skin; occasional pruritus may precede new lesions
- Cosmetic concern and psychological distress (embarrassment, social withdrawal, low mood/anxiety)
- History of progressive spread or episodic activity/inactivity
- Possible triggering history: stress, skin injury, friction, chemical exposure
Signs
- Well-demarcated, flat, non-scaly depigmented macules/patches (often chalk-white)
- May begin as hypopigmented lesions; trichrome pattern can occur
- Non-segmental pattern often bilateral and symmetrical; segmental pattern usually unilateral/dermatomal or along Blaschko lines
- Common sites: fingers/hands, wrists, face (periorificial), axillae, groin/genital skin; mucosal involvement may be prominent
- Leukotrichia (white hair/eyelashes) from follicular involvement
- Activity markers: Koebner phenomenon, confetti-like depigmentation, inflamed advancing edge
- Absence of scale, induration, scarring, or marked inflammation supports vitiligo over alternatives
- Image correlation: compare with clinical photos in DermNet vitiligo atlas (as suggested by NICE CKS)
Investigations
Management
Lifestyle Modifications
- Acknowledge psychosocial burden; screen for anxiety/depression and offer support resources
- Sun protection to reduce burn risk/contrast (broad-spectrum SPF 30-50, protective clothing, shade)
- Camouflage cosmetics/self-tanning products to improve quality of life
- Reduce friction/trauma to limit Koebnerisation; avoid known chemical triggers where possible
- Use baseline and follow-up photographs to track treatment benefit
Pharmacological Treatment
Topical corticosteroids (localized non-facial vitiligo)
- Mometasone furoate 0.1% cream/ointment, apply thinly once daily for up to 8 weeks then review
- Betamethasone valerate 0.1% (potent) once daily, limited-duration courses with monitoring
Use the weakest effective potency and limited body surface area; avoid prolonged continuous use on face/flexures/genitals due to atrophy/striae/telangiectasia. Caution near eyes (glaucoma/cataract risk with chronic periocular steroid exposure). Review regularly for efficacy and adverse effects.
Topical calcineurin inhibitors (especially face/flexures; off-label for vitiligo in UK practice)
- Tacrolimus 0.1% ointment twice daily in adults/adolescents
- Tacrolimus 0.03% ointment twice daily in children (age-appropriate specialist advice)
- Pimecrolimus 1% cream twice daily
Useful where steroid adverse effects are a concern. Common early burning/stinging. Advise photoprotection; avoid application to infected skin. Contraindications/cautions include hypersensitivity and immunocompromised states; discuss off-label status and document consent where relevant.
Phototherapy (specialist-led for extensive or active disease)
- Narrowband UVB phototherapy 2-3 times weekly (hospital protocol, usually several months)
Preferred light therapy for widespread vitiligo. Counsel on erythema/burn risk and long-term cumulative UV exposure; avoid in photosensitivity disorders and use caution with photosensitizing drugs. Face/trunk tend to respond better than acral/lip lesions.
Systemic immunomodulation for rapidly progressive disease (specialist use)
- Oral prednisolone short course, for example 0.3-0.5 mg/kg once daily then taper (dermatology protocol)
Not routine in primary care; reserved for active spread. Check contraindications (uncontrolled infection, poorly controlled diabetes, severe osteoporosis risk, peptic ulcer risk, psychiatric adverse effects) and provide steroid safety counselling.
Surgical / Interventional
- For stable, treatment-refractory focal/segmental vitiligo: suction blister epidermal grafting, split-thickness grafting, or melanocyte-keratinocyte transplantation in specialist centres
- Best outcomes in stable disease without recent progression or Koebner activity
Complications
- Psychological morbidity: anxiety, depressive symptoms, low self-esteem, social/relationship difficulties, stigma
- Sun sensitivity/sunburn in depigmented skin
- Association with autoimmune disease, particularly thyroid autoimmunity
- Treatment-related adverse effects (topical steroid atrophy; phototherapy erythema/burn; systemic steroid complications when used)
Prognosis
Vitiligo is typically chronic with alternating active and stable phases. Non-segmental disease has an unpredictable course and higher relapse risk after repigmentation (around 44% within 1 year after stopping treatment), while segmental vitiligo often spreads early then stabilises and tends to relapse less often once repigmented. Response is generally better on face/neck/trunk than lips and distal acral sites; spontaneous repigmentation can occur but is uncommon.
Sources & References
🏥BMJ Best Practice(1)
✅NICE Guidelines(1)
- Vitiligo[overview]
📖Textbook References(2)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1682)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 146)[context]