Vitiligo

Published on 02/04/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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160 Vitiligo

Instruction

Look at this patient.

Salient features

History

• Age of onset (about half the patients present before the age of 20)

• Whether or not it runs in the family (familial in 36% of cases)

• About other autoimmune disorders (hypothyroidism, hyperthyroidism, thyroiditis, Addison’s disease, diabetes mellitus, pernicious anaemia).

Examination

• Hypopigmented patches (Fig. 160.1) that are distributed symmetrically; sometimes the border may be hyperpigmented. The distribution often includes wrists, axillae, perioral, periorbital and anogenital skin

• White hairs in the vitiliginous area

• Some spontaneous re-pigmentation in the sun exposed regions (in a third of cases).

Fig. 160.1 Vitiligo.

Proceed as follows:

• Look at the scalp for alopecia and white hair.

Note: Scratching when the disease is active may induce lesions along the scratch marks; this is termed isomorphic response or Koebner’s phenomenon. It is also seen in response to the friction or pressure resulting from such common activities as brushing hair, drying skin with a towel and wearing a belt or watch.

Diagnosis

This patient has vitiligo (lesion), which is of autoimmune origin (aetiology) and can be cosmetically distressing to the patient (functional status).

Advanced-level questions

Mention some associated conditions

Organ-specific autoimmune conditions:

• Thyroid disease: Graves’ disease, myxoedema, Hashimato’s disease

• Pernicious anaemia

• Diabetes mellitus

• Alopecia areata

• Addison’s disease.

What are the types of vitiligo?

Non-segmental vitiligo. White patches that are often symmetric and that usually increase in size over time, corresponding to a substantial loss of functioning epidermal melanocytes and sometimes hair-follicle melanocytes. The key precipitating factors include immunologic factors, oxidative stress or a sympathetic neurogenic disturbance. Accounts for 85–90% all cases of vitiligo.

Segmental vitiligo. Unilateral distribution that may completely or partially match a dermatome. In most patients there is one unique segment of depigmentation. Rarely, two or more segments with ipsilateral or contralateral distribution may occur. A neurogenic sympathetic disturbance is considered a key precipitating factor. Seen in autoimmune diseases.

Which fungal condition can be mistaken for vitiligo?

Pityriasis versicolor (caused by the fungus Malassezia furfur).

How would you confirm the diagnosis?

Examination with a Wood’s lamp in a completely dark room after the examiner’s eyes have adapted to the darkness (it is less useful in patients with darker skin types). It is a hand-held ultraviolet A (UVA) irradiation device that emits at approximately 365 nm. Wood’s lamp provides bright reflection of white patches and enhanced details on intermediate pigment tones. Lamps that incorporate a magnifying lens are useful in evaluating terminal and vellus pigmentation of hair. A complete examination should include inspection of the genitalia and areas of skin folds as these areas can be easily overlooked.

How would you manage such patients?

• Cosmetics are useful for concealing disfiguring patches.

• When <20% of the skin is involved: topical methoxsalen with long-wavelength UVA is used, followed by thorough washing and application of an SPF 15 sunscreen.

• When >20% of the skin is affected: oral methoxsalen with UVA.

• Non-segmental vitiligo: phototherapy, preferably narrow-band UVB. Acral lesions and lesions with depigmented hairs will hardly or not react.

• When extensive: good cosmetic results may be obtained when normal skin is ‘de-pigmented’ with a bleaching agent such as hydroquinone.

• New lesions of vitiligo: may benefit from topical steroids.

• Segmental vitiligo or stable non-segmental vitiligo in a limited area (<200 cm²): epidermal autografts and cultured epidermis combined with PUVA (split-thickness skin grafting, punch-grafting, suction blister epidermal grafting, non-cultured epidermal cell suspension grafting).

Note: On the whole, treatment of vitiligo remains unsatisfactory.

What is the histology of vitiligo?

Characteristically there is partial or complete loss of pigment-producing melanocytes in the epidermis. In contrast, some forms of albinism have melanocytes but no melanin pigment is produced because of lack of, or a defect in, the tyrosinase enzyme.

Why are melanocytes progressively lost in this condition?

The various theories of pathogenesis include:

• autoimmune destruction from circulating antibodies against the melanocytes and impaired cell-mediated immunity

• self-destruction by toxic intermediates of melanin production

• neurohumoral factors.

Further reading

Gawkrodger DJ, Ormerod AD, Shaw L, et al. Guideline for the diagnosis and management of vitiligo. Br J Dermatol. 2008;159:1051-1076.

Parsad D, Gupta S. Standard guidelines of care for vitiligo surgery. Ind J Dermatol Venereol Leprol. 2008;74(Suppl):S37-S45.

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