🩺 MedAtlax

Vitiligo

4 min read

Vitiligo

Dr Sami Aldaham

Introduction

  • Vitiligo is a common acquired disorder.

  • Characterized by well-marginated white spots resulting from loss of melanocytes.

  • Vitiligo is associated with some autoimmune disorders.

  • Is associated with social stigma.

  • Confusion with leprosy is partly responsible for this.

Aetiology & Pathogenesis

  • Susceptibility to the disease may be inherited.

  • 1/4 to 1/3 of patients have family members affected with the disease.

  • A multifactorial pattern of inheritance is revealed in most studies.

  • There are three possible mechanisms that may cause destruction of melanocytes.

  • However, multiple mechanisms may be responsible for the causation of vitiligo in an individual.

The three possible mechanisms of vitiligo

  1. The autoimmune hypothesis

    • Originated from the observation that vitiligo is associated with some autoimmune diseases.
    • Suggets that there is an autoimmune damage to melanocytes.

  2. The autocytotoxic or self-destruct hypothesis

    • Suggests that some toxic molecules produced during the biosynthesis of melanin are responsible for melanocyte damage in susceptible individuals.

  3. The neural hypothesis

    • Postulates that neurochemicals liberated from nerve endings are toxic to melanocytes.

Clinical Features

  • Vitiligo affects all races with an average frequency of 1% to 2% of the population.

  • Both sexes are affected equally.

  • The disease may develop at any age, the peak age of onset is between 10 and 30 years.

  • Stressful life events or physical trauma can often precipitate the onset of disease.

  • Typically, macule of vitiligo is well-circumscribed depigmented of varying sizes.

  • The hairs on the patch may turn grey.

  • There may be a single or numerous depigmented macules distributed all over the body.

  • With time, the macules may enlarge and coalesce to produce extensive pigment loss.

  • The lesions are asymptomatic.

Clinical types

  • According to:
    • The extent of involvement
    • Pattern of distribution

Is clinically categorized into the following types:

  1. Focal vitiligo
  • Is an isolated macule or a few macules in a localized non-dermatomal distribution.
  1. Segmental vitiligo
  • Is characterized by macules in a unilateral dermatomal distribution.

  1. Generalized vitiligo - patches generally
  • Is the most common type showing macules in a generalized widespread distribution.
  • There is often symmetry of affection.
  • Sites: Face (particularly around the orifices), neck, bony prominences of hands, legs, axillae and mucosal surfaces are particularly affected.

  1. Acro-facial vitiligo
  • Affects distal end of fingers and facial orifices.

  1. Universal Vitiligo - 80% body surfaces
  • Implies loss of pigment over the entire body surface area with only isolated islands of normal pigmentation remaining.

Associated diseases

  • Patients with vitiligo have an increased risk of developing autoimmune diseases like:
    1. Alopecia areata
    2. Thyroid diseases
    3. Addison’s disease
    4. Pernicious anaemia
    5. Insulin-dependent diabetes mellitus.

Psychosocial impact of vitiligo

  • Although vitiligo by itself is asymptomatic and does not cause any physical discomfort or disability.
  • It may be associated with devastating psychological and social consequences.
  • Feeling of stress and embarrassment on social contacts, lowered self-esteem may be detrimental to the patients, particularly when the lesions are on visible area of the body.

Treatment

  • With treatment, re-pigmentation occurs around the hair follicles, which is achieved by stimulation and migration of follicular melanocytes.
  • Spread of pigmentation from the margin of the patch can also occur.
  • Whatever the mode of therapy, patient education and reassurance is very importance.
  • Explanation of the benign nature of the disease and psychological support is needed in all patients.

1- Topical steroids

  • Are effective in the management of disease limited to small area.
  • Lesions on face and neck respond better than other parts or the body. Hydrocortisone is the topical agent of choice.
  • More potent steroids can also be used intermittently.

2- PUVA therapy

  • PUVA therapy (Psoralen + Ultraviolet A) is the mainstay of management of vitiligo.
  • Topical PUVA involves painting the area with psoralen solution and exposing the area to UVA.
  • Patients with limited involvement are best suited for this mode of therapy.
  • Is used in patients with extensive vitiligo.
  • Is avoided in children below the age of 12.
  • It is contraindicated in pregnancy and lactation.

3-Surgical treatment

  • When topical steroids or PUVA therapy fails to repigment, surgical treatment may be undertaken such as skin graft, melanocyte transplant
  • Best suited for segmental and localized vitiligo.

3- Depigmentation

  • In patients with extensive vitiligo.
  • Depigmentation of the remaining islands of normal skin may be more cosmetically acceptable.
  • To achieve this, hydroquinone in a concentration of 20% is applied twice a day on the pigmented skin.
  • It may take months to establish depigmentation, which is usually permanent.

Graph View

Backlinks