Fig. 13.1
Central nervous system and local skin stress response

Stress response coupled with genetic susceptibility and environmental factors cause different diseases in susceptible individuals, hence reported association of stress with some skin disorders such as Vitiligo, Psoriasis, Atopic Dermatitis, etc.

Psychological stress could be a potential trigger in Vitiligo patients, so patients should be screened for stressors [8].

Trapp et al. study showed a higher vegetative arousal in Vitiligo patients comparing to age and gender matched healthy control group [9].

Clinical Features

Age of onset varies and peaks in second and third decades, there is no age, sex, or racial preference in Vitiligo [3, 4].

Vitiligo has different clinical subtypes including:

  • Generalized Vitiligo (Vitiligo vulgaris) is the most common form. It has widespread depigmented macules and patches usually symmetrically placed in acral areas/extensor surfaces and around body orifices.

  • Acrofacial Vitiligo is when the lesions are limited to acral and periorificial areas of the body.

  • The Koebner phenomenon is the occurrence of lesions on areas of injury. This happens in Vitiligo as well as some other skin diseases such as psoriasis.

  • Segmental Vitiligo is usually unilateral patches occurring on dermatomal distribution. This subtype has an earlier age of onset and is usually rapidly progressive.

  • Mixed Vitiligo is the coexistence of segmental and generalized Vitiligo. It usually starts as segmental form and spreads later. Halo nevi and Leukotrichia could be predictors of mixed forms [10].

  • Focal Vitiligo is when macules are present only in an isolated area.

  • Mucosal Vitiligo causes lesions on mucosal membranes only.

  • Universal Vitiligo causes complete or almost complete loss of pigment.

Clinical presentations within the subtypes include: Vitiligo punctué with confetti-like depigmented macules, inflammatory Vitiligo with erythematous rim around lesions. In trichrome and quadrichrome Vitiligo different hues from depigmented to pigmented skin are seen.

Figures 13.2 and 13.3 present the difference in contrast with normal skin comparing to diseased skin in darker and lighter skinned individuals.


Fig. 13.2
Vitiligo on Fitzpatrick skin type VI


Fig. 13.3
Vitiligo on Fitzpatrick skin type II

Differential Diagnosis

Hypopigmented and depigmented skin lesions could be seen in:

  • Nevus depigmentosus (achromic nevus); usually solitary, appears at birth or shortly after and is stable.

  • Idiopathic guttate hypomelanosis; multiple small depigmented macules on extremities.

  • Postinflammatory hypopigmentation; after injuries and inflammation of skin.

  • Chemical depigmentation with phenol or other depigmenting chemicals in hair dyes. Imiquimod could induce Vitiligo as well.

  • Tinea versicolor in darkly pigmented individuals could cause hypopigmented macules with fine superficial scaling.

  • Pityriasis alba; small patches of hypopigmentation usually on face but sometimes on extremities of children due to mild eczematous dermatitis. There is usually history of atopic dermatitis.

  • Piebaldism; an inherited disorder of pigmentation characterized by depigmented patches with hyperpigmented borders on midline body and forehead.

  • Hypomelanosis of ito (incontinential pigmenti achromians); typically appears at birth or shortly after with hypopigmented patches following lines of Blaschko. It is associated with other neurologic, ocular, and skeletal abnormalities.

  • Morphea; skin texture on hypopigmented areas is sclerotic and firm.

  • Lichen sclerosus; skin texture on lesions is atrophic and thinned or inflamed.

  • Leprosy; hypopigmented anesthetic patches on skin. In the past, patients with Vitiligo would be chased out of town for fear of leprosy.

  • Vogt-Koyanagi-Harada syndrome; associated with neurologic, ophthalmologic and skin manifestations including Meningismus, Uveitis, as well as Polisosis, Vitiligo, and Alopecia.

  • Sometimes Vitiligo-like patches may precede melanoma and it is important to have a full skin check in patients to rule out melanoma.


Diagnosis is usually clinical. Wood’s lamp examination helps to distinguish hypopigmented from depigmented macules. Biopsy is usually not necessary unless other differentials such as morphea or lichen sclerosus are suspected.

Work up includes screening for other autoimmune diseases:

  • Recommendation includes evaluating thyroid function (TSH, anti-thyroid antibodies), fasting blood glucose, complete blood count with differential, B12 level (R/O pernicious anemia) and other autoantibodies based on clinical suspicious and family history.

  • Ophthalmology exam due to occasional association with ocular abnormalities in case of symptoms is important.


Vitiligo could be very distressing. It is one of the highest stigmatizing skin disorders. It can affect patients’ social functioning as well as intimate relationships.

Support groups play an important role in helping patients cope with the disease.

Some examples include:

The American Vitiligo research foundation:

  • There has been some research breakthrough in the discovery of Vitiligo susceptibility genes that may play an important role in future treatment.

In regards to treatment strategies, protection of Vitiligo affected skin is important to avoid sunburn and increased risk of skin cancer.

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Sep 16, 2017 | Posted by in Dermatology | Comments Off on Vitiligo
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