it is an acquired common skin condition in which a patchy complete loss of epidermal melanocytes results in circumscribed depigmentation of the skin.
From the Latin word vitellus that means “Veal” (pale)
Prevalence 0.5–2% of the general population worldwide.
Peak incidence at 10–30 years but can occur in any age group.
Affect males and females equally.
Found in all races.
Family history in 30% of patients. in the generalized type.
Etiology
Unknown / Multifactorial :
Genetic predisposition (its inheritance is polygenic).
Autoimmune destruction of melanocytes: melanocytes are the target of a cell-mediated autoimmune attack or self-destruction as a result of an inability to remove toxic melanin precursors in the generalized type .
Oxidative stress (free radicals).
Intrinsic defects of melanocytes.
Triggering factors :
stress /sunburn
skin injury or trauma
Kӧbner phenomenon “isomorphic response’’: (the appearance of new skin lesions on previously unaffected skin secondary to trauma.)
Dermatomal distribution/ unilateral/ doesn’t cross the Medline
No clear segmental distribution/ no progression/ limited to one or few areas
In distal extremities and face
MC/Scattered patches that are widely distributed
Whole body (rare; more than 80% of skin is depigmented)
Localized
Generalized
is less likely to be associated with autoimmune diseases.
Clinical course
1- Generalized/non-segmental
Sharply defined, usually symmetrical white patches on the back of the hands, wrists, fronts of knees, neck and around body orifices. The hair of the scalp and beard may depigment too=Leukotrichia
Unpredictable course ,Lesions may remain static or spread.
Occasionally, repigment spontaneously from the hair follicles.
2- Segmental
Restricted to one part of the body, but not necessarily to a dermatome.
Responds poorly to most treatments
Spontaneous repigmentation occurs more often in this type.
Trichrome vitiligo
A variant of the generalized pattern.
Trichrome vitiligo consists of an intermediate zone of hypopigmentation(2) located between the depigmentation center(1) and the normal unaffected skin(3).
Differential diagnosis
Contact with depigmentaion chemicals: hydroquinones, substituted phenols in rubber industry.
Pityriasis(tinea) versicolor: fine scaling, patches tend to be paler than surrounding skin.
Idiopathic guttate hypomelanosis (a common acquired form of leukoderma that presents as small pale or white spots)
Nevus depigmentosus (a congenital nonprogressive hypopigmented macule or patch that is stable in its relative size and distribution throughout life).
Post inflammatory depigmentation: improves spontaneously, loss of pigment is partial.
Leprosy: must be excluded by sensory testing and general examination.
Wood lamp examination: The vitiligo lesions appear as well-defined blue-white areas + can help differentiate between hypopigmentation and depigmentation.
Dermoscopy: vitiligo lesions have a characteristic perilesional hyperpigmentation and telangiectasia
Skin biopsy and histology: Melanocytes are absent, perilesional lymphocytes may be observed.
Serological markers of autoimmune disease (e.g., thyroid function tests and antithyroid antibodies) once vitiligo is confirmed.
Wood lamp examination
Treatment
General measures :
Sunscreen (with a high sun protection factor helps in preventing the vitiliginous areas from burns)
Concealing makeup for cosmetic reason (camouflage)
Localized irradiation of the skin can also be performed with laser
Surgery (grafts)
Finally, depigmentation should be considered in patients with greater than 50% cutaneous involvement who fail to respond or are unwilling to undergo treatment.
