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BASICS

  • Acquired depigmentation due to loss of melanocytes.
  • Major variants:
  • Nonsegmental (generalized, acrofacial, mixed, mucosal, rare variants like trichrome, quadrichrome).
  • Segmental (dermatomal distribution, often unilateral).
  • Universal vitiligo affects >80% BSA and often has familial association.
  • Can present from infancy to late adulthood.

EPIDEMIOLOGY

  • 50% cases begin before age 20.
  • Equal sex distribution, but females more likely to seek treatment.
  • Prevalence ~1% in US and Europe; up to 8.8% in Gujarat, India.

ETIOLOGY AND PATHOPHYSIOLOGY

  • Multifactorial; convergence theory.
  • Autoimmune: humoral autoantibodies, skin-homing T cells targeting melanocytes.
  • Neural dysregulation.
  • Viral triggers: CMV, EBV, hepatitis C found in lesions.
  • Oxidative stress with increased H2O2, NO; decreased catalase and glutathione.
  • Genetic predisposition: polygenic/multifactorial inheritance; ~20% familial history.
  • Associated HLA and SNPs identified.

RISK FACTORS

  • Family history of vitiligo or autoimmune disease.
  • Personal history of autoimmune thyroid disease, pernicious anemia, rheumatoid arthritis, etc.
  • Exposure to skin trauma (Koebner phenomenon), emotional stress, or infections.

ASSOCIATED CONDITIONS

  • Endocrine: thyroid disorders (hypo/hyperthyroidism), Addison disease, insulin-dependent diabetes.
  • Dermatologic: psoriasis, alopecia areata, atopic dermatitis, halo nevi.
  • Pernicious anemia, ocular abnormalities (up to 40%), elevated ANA and thyroid antibodies.
  • Syndromic associations: MELAS, Alezzandrini, Schmidt, APECED.

DIAGNOSIS

History

  • Ask about onset, progression, recent sunburns, trauma, pregnancy, stress.
  • Family and personal autoimmune history.
  • Assess psychological impact and quality of life (e.g., DLQI).

Physical Exam

  • Well-demarcated, depigmented macules/patches.
  • Use Wood lamp to highlight lesions and distinguish depigmentation from hypopigmentation.
  • Check for repigmentation, especially perifollicular.

Differential Diagnosis

  • Infectious: tinea versicolor, leprosy, leishmaniasis.
  • Inflammatory: postinflammatory hypopigmentation, scleroderma.
  • Genetic: piebaldism, Waardenburg syndrome, hypomelanosis of Ito.
  • Chemical and occupational causes.
  • Melasma, halo nevi, lichen sclerosus.

Tests

  • Labs: TSH, CBC, ANA, thyroid antibodies, vitamin B12.
  • Skin biopsy rarely needed; compare lesional and perilesional skin.
  • Ophthalmologic and audiologic exams if indicated.

TREATMENT

  • Untreated disease often progresses, especially with mucosal involvement and family history.
  • Best response on face, recent onset, darker skin, younger patients.

General Measures

  • Sunscreen to prevent sunburn and contrast accentuation.
  • Cosmetic camouflage.

Medications

  • Topical corticosteroids: midpotency, with intermittent holidays to reduce side effects.
  • Topical calcineurin inhibitors: tacrolimus, pimecrolimus (preferred for sensitive areas).
  • Topical vitamin D analogues (calcipotriene).
  • Phototherapy: Narrowband UVB preferred; PUVA less used due to carcinogenic risk.
  • Laser therapy: Excimer 308 nm preferred.
  • Systemic corticosteroids: pulse therapy in select cases.
  • Oral vitamin D and antioxidants may aid repigmentation.

Surgery

  • For stable lesions refractory to medical therapy.
  • Techniques: melanocyte transplantation, grafting.
  • Risks: Koebner phenomenon, keloid formation, scarring.

ONGOING CARE

  • Regular monitoring for disease progression.
  • Monitor for steroid side effects.
  • Psychological support for psychiatric comorbidities (depression, anxiety).

PATIENT EDUCATION

  • Explain chronic, unpredictable course.
  • Avoid trauma/friction (Koebner phenomenon).
  • Encourage adherence and realistic expectations.

PROGNOSIS

  • Spontaneous repigmentation uncommon.
  • Generalized vitiligo often progressive before stabilization.

COMPLICATIONS

  • Treatment side effects (atrophy, telangiectasia).
  • Psychological morbidity: depression, low self-esteem, sexual dysfunction.
  • Social stigma varies culturally.

REFERENCES

  1. Ezzedine K, Eleftheriadou V, Whitton M, et al. Vitiligo. Lancet. 2015;386(9988):74-84.
  2. Bacigalupi RM, Postolova A, Davis RS. Evidence-based, non-surgical treatments for vitiligo: a review. Am J Clin Dermatol. 2012;13(4):217-237.
  3. Whitton ME, Pinart M, Batchelor J, et al. Interventions for vitiligo. Cochrane Database Syst Rev. 2015;(2):CD003263.
  4. Ju HJ, Bae JM, Lee RW, et al. Surgical interventions for patients with vitiligo: a systematic review and meta-analysis. JAMA Dermatol. 2021;157(3):307-316.

ICD10

  • L80 Vitiligo

Clinical Pearls

  • Vitiligo can cause significant psychological distress.
  • Screen for associated autoimmune diseases, especially with late onset.
  • Individualize treatment based on disease extent, skin type, and patient preference.
  • Refer to dermatology for extensive or facial involvement or advanced therapy.