5th June 2025

Vitiligo

Vitiligo is an acquired disorder where there is complete depigmentation of affected skin due to loss of melanocytes and a chalky-white appearance of affected skin. It is an autoimmune disease and is associated with other such diseases. Lesions can occur in a focal or generalised distribution and can coalesce into almost complete depigmented areas.  It is often dismissed as a cosmetic issue due to the contrast between depigmented skin and normal skin, especially in dark skinned individuals. However, the disease can be psychologically devastating and those with vitiligo experience stigmatisation, social isolation and low self-esteem.

Cause 

The selective loss of melanocyte functioning in the epidermis causes the depigmented skin seen in Vitiligo. The exact mechanism for the destruction of melanocytes is not known but likely to be a multifactorial polygenic disease, with autoimmune responses (T-cell mediated destruction), oxidative stress, generation of inflammatory mediators, and melanocyte detachment mechanisms playing a role, depending on the disease subtype. 

Possible triggers for vitiligo have been identified and include emotional stress or illness, chemical exposure (phenolic/catecholic derivative in deodorant, oils, hair dye, disinfectants) and hormonal changes such as childbirth. The Koebner phenomenon where depigmentation occurs at a site of skin injury such as cuts, sunburn or abrasion is also a proposed trigger.

Prevalence 

Vitiligo is known to be the most common depigmenting skin condition and onset increases through the first two decades of life. However, it is uncommon in children less than 2 years of age.

Classification 

There are two main types of vitiligo: non segmental vitiligo and segmental vitiligo. Non segmental vitiligo is more common and roughly 90% of people with the condition have this. The different forms of non-segmental vitiligo include focal, mucosal, acrofacial, generalised and universal. Usually, depigmented lesions are symmetrical and bilateral. Segmental vitiligo has a more rapid onset, is less common and affects more children than adults. Typically, it is unilateral and has a dermatomal distribution that follows Blaschko’s lines. It may also involve hair follicle depigmentation. The subtypes include focal, mucosal, uni-, bi- and pluri-segmental.

Prognosis 

Vitiligo has an unpredictable clinical course and is usually a chronic and progressive disease. The prognosis is dependent on the patient’s age, disease subtype, distribution, activity and extent. Spontaneous re-pigmentation is rare. With treatment the majority of patients experience more than 75% re-pigmentation but certain areas are less responsive to treatment including distal extremities and lips and there is a possibility of recurrence of disease despite treatment.

Risk factors:

• Age <30 years old 
• Family history of vitiligo 
• Personal or family history of other autoimmune disease: Thyroid disease, Addison’s disease, pernicious anaemia, diabetes mellitus, systemic lupus erythematosus and discoid lupus, alopecia areata, rheumatoid arthritis, psoriasis, inflammatory bowel disease, Sjogren’s syndrome

Diagnosis 

Vitiligo is a clinical diagnosis presenting as lesions of depigmented skin (or hair). It is asymptomatic however at disease onset itchiness can be a symptom.  

These are the following characteristics of the lesions:

• Colour– macules and patches that are hypopigmented then progress to become chalky white and depigmented. Pink patches are noted in more vascular areas. The term trichrome vitiligo can also be used if there is a white centre with a surrounding pale area. 
• Margins– well-demarcated lesions 
• Palpation– Non-scaly and flat lesions 

Extent and distribution– Lesions can be localised or generalised. They are usually bilateral and symmetrical. Sites most commonly affected are distal extremities, axillae, groin, genitalia, face and periorificial skin. It can also affect hair and the epithelium of retina and choroid. The lesions can also be seen at sites of mechanical trauma (like abrasions or burns) which is known as the Koebner phenomenon.

Image Source: Wikimedia Commons (2015). Vitiligo, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Vitiligo2.JPG (Accessed 20 May 2025).

Image Source: Wikimedia Commons (2006). Eyelid Vitilito, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/w/index.php?search=Eyelid_vitiligo_06.jpg&title=Special:MediaSearch&type=image (Accessed 20 May 2025).

Investigation  

Wood’s lamp can be used as it accentuates the contrast between affected and unaffected skin. It is a distinctive blue fluorescence seen in vitiligo but not in simply hypopigmented skin. 

Laboratory investigations include blood tests for thyroid disease, diabetes, pernicious anaemia and Addison’s disease. Autoimmune disorders are associated with Vitiligo and autoimmune thyroiditis is the most commonly associated.

Management

• General measures 
  • Although vitiligo is not life threatening, those with the condition have a reduced quality of life and low self-esteem. 
  • The treatment goal is to improve the appearance of affected skin. 
  • Sun protection such as high factor sunscreen offers both UV-A and UV-B protection all over the body. 
  • Also as reduced sun exposure is being recommended vitamin D levels should be tested and supplementary vitamin D prescribed if necessary. 
  • Minimise skin trauma to prevent new white patches appearing in these sites
  • Camouflage creams and powders especially for dark skinned individuals where the disease appears more obvious.
  • Alternatively, over the counter tanning products and cosmetic micropigmentation and tattoo are options.  
  • Dermatologist referral for management is appropriate when: condition rapidly progressing, uncertain diagnosis, segmental vitiligo, face affected, child affected, pregnant woman, large areas of body affected, person distressed about condition and initial treatment has been unsuccessful.
• Topical therapy
  • Topical corticosteroid and calcineurin inhibitors are first-line treatments in limited (less than 10% body area) or segmental vitiligo.
  • Topical corticosteroids are anti-inflammatory and work by suppressing the immune response against melanocytes and have the most effective response on darker skin, new lesions and sun exposed sites. 
  • The treatment is however not suitable for the face or pregnant woman.
  • Topical corticosteroids commonly used in vitiligo are mometasone or betamethasone valerate 0.1% for a month. 
  • Extended treatment with topical corticosteroid can cause corticosteroid induced atrophy and hypertrichosis. 
  • Hence patients should be monitored for adverse effects such as skin thinning, purpura and striae distensae and treatment response monitored. 
  • Topical calcineurin inhibitors such as tacrolimus and pimecrolimus cream are preferred in children and when lesions are spreading on thin skin or if they are on the face and neck. In comparison to corticosteroid treatment they have better short-term safety profiles including reduced risk of skin thinning. 
• Oral corticosteroid 
  • Can be useful if vitiligo is progressing fast but side effects outweigh benefit so it is not a preferred treatment
• Phototherapy
  • This is an option in widespread vitiligo (more than 10% body surface area), progressive disease or limited vitiligo that has significant psychological impact. 
  • It is also the second line for those where topical therapy has been unsuccessful. 
  • Narrow-band- UVB is safe and effective in adults and children. 
  • To achieve the most optimum response it should be used 2-3 times weekly for 12 months if possible. 
  • Improved efficacy is also seen when combined with topical therapies. 
  • It is more effective in darker skin types.
• Surgery
  • Surgery is third line treatment and used in stable segmental or stable non-segmental localised vitiligo when medical therapy has not been successful. 
  • The surgical treatment is reserved for cosmetically sensitive sites with no lew lesion, no history of Koebner phenomenon and no change in the lesion in the last 12 months. 
  • It uses surgical grafting where healthy melanocytes are transferred to the depigmented lesion by several techniques. 
  • The several techniques include punch grafting, epidermal blister grafting or ultrathin epidermal sheet grafting. 
  • Successful surgical outcome is more common in younger patients and those with stable segmental vitiligo. 
  • The adverse effects of surgery are scarring or mottled pigmentation on the recipient area. The Koebner phenomenon may also occur at the donor site.
• Depigmentation therapy 
  • Fourth line and used in adults with extensive generalised vitiligo (more than 50% body surface area affected or refractory). 
  • It is a suitable option in dark skinned patients where facial or hand vitiligo is more visible. 
  • Chemicals such as monobenzone 20% or laser therapy are used for depigmentation therapy so that all skin is the same colour. 
  • It can take up to four months to work.