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Author: Dr Delwyn Dyall-Smith FACD, Dermatologist, 2010. Updated February 2014 by Vanessa Ngan, Staff Writer.
Contact leukoderma is the loss of skin colour (whitening of skin) following contact with chemicals known to destroy the skin pigment cells (melanocytes). It is usually due to chemicals found in the workplace, but it can also follow the use of certain cosmetic products. It is also known as chemical leukoderma and may be spelt leucoderma.
Contact leukoderma may develop in the setting of pre-existing idiopathic vitiligo, suggesting a genetic predisposition. This genetic susceptibility may explain why only some people will get leukoderma upon contact with certain chemicals. Liver and thyroid disease have been reported in some patients. However, in the majority of patients, there is neither a personal nor family history of vitiligo nor other autoimmune disease.
The main chemicals that have been known to cause contact leukoderma include aromatic or aliphatic derivatives of phenols and catechols. Monobenzylether of hydroquinone (MBH) was the first identified chemical to cause leukoderma in leather manufacturing workers who wore rubber gloves cured with MBH. Other chemicals that are known to cause occupational leukoderma include the phenolic compounds, para-tertiary butylphenol, para-tertiary octylphenol and para-tertiary butylphenolformaldehyde.
The most common cause of contact leukoderma from cosmetics is para-phenylenediamine (PPD) in hair dyes. The hair dye may have been used by the patient, or they may have applied it to someone else. As PPD can also be found in black socks and footwear, the leukoderma may also affect the feet. Sensitization to PPD may have followed the application of a temporary black henna tattoo, also leaving a white mark. Frequent use of hair dye has also been associated with an increased risk of developing vitiligo.
Contact leukoderma due to the azo dyes has been reported with the use of facial cosmetics in the following products:
Contact leukoderma can also be caused by para-tertiary butyl phenol (PTBP) in deodorants and spray-on perfumes.
A series of cases followed the use of skin lightening cream containing monobenzylether of hydroquinone on the hands. Monobenzylether of hydroquinone has also been deliberately applied to pigmented areas to reduce the unsightliness of extensive vitiligo.
A skin lightening cream containing rhododendrol (another phenolic compound) resulted in localised contact leukoderma and widespread vitiligo in about 18,000 users in Japan in 2013.
Methylphenidate patches (used to treat attention-deficit/hyperactivity disorder) may rarely cause permanent loss of skin colour at the site of application.
Also, it has been reported with cultural practices, particularly in India, related to the use of alta, an azo dye painted on the feet. The specific azo dye identified in alta was solvent yellow 3. Contact leukoderma has also been reported in Asian women with an adhesive bindi, the coloured spot applied to the forehead. The chemical associated with bindi leukoderma is PTBP in the adhesive.
Contact leukoderma presents as a white patch(es) of skin, initially at the site(s) of application but can spread beyond the area of known contact in approximately one-quarter of patients. A single lesion occurs in approximately one-third of patients; multiple patches are more common.
Contact leukoderma is never present at birth.
Contact leukoderma due to cosmetics occurs most frequently on the face. The eyelids are particularly involved. Contact leukoderma due to hair dyes applied to the patient usually affects the hair margin rather than the scalp skin. It can subsequently lead to white patches in distant sites (vitiligo.
Typically there are small confetti-sized flat spots of white skin with a sharply defined margin seen under magnification. The skin is not scaly.
Wood lamp examination shows an accentuation of the pigment loss although this is not always as clear as in vitiligo.
Preceding contact allergic dermatitis does not occur in the majority of cases. However, an itch is reported more commonly with contact leukoderma than with vitiligo.
Contact leukoderma must be distinguished from vitiligo. This can sometimes be difficult as both show the same features on histology of a skin biopsy with loss of melanocytes and melanin.
Listed below is suggested diagnostic criteria for contact leukoderma (Ghosh S, Mukhopadhyay S. 2009). A patient should have three of the four criteria.
Avoidance of the cosmetic product results in the recovery of skin colour in the majority of cases, particularly if there was no history of pre-existing vitiligo. However, further extension of the leukoderma has been reported despite strict avoidance of the chemical and this may indicate a genetic tendency to vitiligo. Topical and systemic corticosteroids have been reported to speed recovery of skin colour. Narrow-band ultraviolet B phototherapy and PUVA photochemotherapy may also be used in some cases.
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