Vitiligo

ETIOLOGY:

• The exact etiology is not known and may vary from one pattern of disease to another

Genetic

• A genetic factor is definitely important. since about 20-30% of patients give a positive family history.
• Inheritance may be polygenic.
• Autoimmune hypothesis
  • Evidence points to autoimmune etiology because
  • Vitiligo is frequently associated with autoimmne disorders like alopecia areata and thyroid disorder. 
  • Antibodies to melanocytes have also been demonstrated.
  • Histopathology of early lesions demonstrate presence of lymphocytes in the lesions.
• Neurogenic hypothesis
  • Dermatomal distribution of some types of vitiligo (e.g. segmental vitiligo) suggests that a toxin, which destroys melanocyte is released at the nerve endings.

ASSOCIATED SYNDROMES:

Vitiligo is associated with the following autoimmune diseases :-

• Alopecia areata
• Diabetes mellitus
• Hyperthyroidism
• Hypothyroidism
• Pernicious anemia
• Addison disease
• Multiple endocrinopathy syndrome
• Vogt-Koyanagi syndrome(Uveitis associated with vitiligo & auditory defects)

CLINICAL FEATURES:

Morphology

• Depigmented macules are the hallmark of vitiligo.
• Typical macule of vitiligo has a chalky or milky white colour, but the pigment loss may be partial in some lesions.
• Sometimes three shades arichrome) occur in the same lesion i.e. the depigmented centre is surrounded by hypopigmented rim which in turn has normally pigmented skin around it.
• The macules have a scalloped outline and on fusion with neighbouring lesions form geographical patterns.
• The hairs in the lesion may remain normally pigmented though in older lesions the hair pigment may be lost (leucotrichia).
• Koebner’s phenomenon can occur in active phase.

Sites

• The lesion can occur in any part of the body.
• Areas subjected to repeated trauma and friction are frequently affected e.g. the backs of hands and feet, elbows and knees.

Clinical variants

• Trichrome vitiligo: An intermediate zone of hypochromia is located between the achromic center and the peripheral unaffected skin, resulting in 3 shades of color—brown, tan, and white—in the same patient
• Marginal inflammatory vitiligo: Lesions have a red, raised border, which is present from the onset of vitiligo (in rare cases) or may appear several months or years after the initial onset; mild pruritus may be present
• Quadrichrome vitiligo: Reflects the presence of a fourth color (ie, dark brown) at sites of perifollicular repigmentation 
• Blue vitiligo: Results in blue coloration of vitiligo macules
• Koebner phenomenon: Development of vitiligo in sites of specific trauma, such as a cut, burn, or abrasion.

Vitiligo can be classified as follows:

Localized

• Focal: Characterized by 1 or more macules in 1 area, most commonly in the distribution of the trigeminal nerve
• Segmental: Manifests as 1 or more macules in a dermatomal or quasidermatomal pattern; occurs most commonly in children; more than half the patients with segmental vitiligo have patches of white hair or poliosis
• Mucosal: Mucous membranes alone are affected

Generalized

• Acrofacial: Depigmentation occurs on the distal fingers and periorificial areas
• Vulgaris: Characterized by scattered patches that are widely distributed
• Mixed: 

Universal:

• Universal vitiligo results in complete or nearly complete depigmentation. It is often associated with multiple endocrinopathy syndrome.

DIAGNOSIS

The diagnosis of vitiligo is based upon.

• Age of onset (usually not present at birth).
• Depigmented macules (milky white) with scalloped borders.
• Leucotrichia
• Koebner’s phenomenon
• Predilection for sites of trauma.
• Woods lamp test is used in diagnosis of  P. versicolor, Vitiligo & Porphyria

Microscopic examination of involved skin :

• It shows a complete absence of melanocytes in association with a total loss of epidermal pigmentation. 
• Superficial perivascular and perifollicular lymphocytic infiltrates may be observed at the margin of vitiliginous lesions, consistent with a cell-mediated process destroying melanocytes.

MANAGEMENT:

Nonsurgical treatments

• Systemic phototherapy: Induces cosmetically satisfactory repigmentation.
• Laser therapy:NBUVB – Narrow Band Ultraviolet -B Phototherapy(Psoralen – A )
• Steroid therapy
• Vitiligo vulvaris, best treatment is PUVA
• Steroids & Coaltar are also used
• Depigmentation therapy: If vitiligo is widespread and attempts at repigmentation have not produced satisfactory results, depigmentation may be attempted in selected patients
• Micropigmentation: Tattooing can be used to repigment depigmented skin in dark-skinned individuals

SurgeryThe basic types of repigmentation surgery are as follow :

• Noncultured epidermal suspensions
• Thin dermoepidermal grafts
• Cultured epidermis with melanocytes or cultured melanocyte suspensions.

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