Chemical Leucoderma

Chemical leucoderma is acquired depigmentation caused by repeated skin contact with certain chemicals that are toxic to melanocytes. It looks like vitiligo and can spread beyond the site of contact.

Common causes are phenols and catechols in rubber products, adhesives, bindis, footwear, hair dyes, germicidal soaps, rubber gloves, plastics and cosmetics. Monobenzone (used for depigmentation in extensive vitiligo) and p-tert-butylphenol are the best known.

It occurs in occupational and domestic settings, and is more visible in people with darker skin. It affects people of all ages.

Pathophysiology.

These chemicals resemble tyrosine and are oxidised by tyrosinase into reactive quinones, which damage melanocytes and create neoantigens. In susceptible people, this can trigger an immune response that destroys melanocytes at distant sites, in the same way as vitiligo.

• Depigmented macules at the site of contact (hands, forearms, face, feet, forehead from a bindi), often with a pattern matching the object.
• Confetti like macules with distant spread, and possible mild preceding erythema or itch.
• Sites follow exposure, and lesions may extend to hairy sites and mucosa.

• History of exposure (occupation, cosmetics, adhesives, rubber products), timing of onset and improvement away from the exposure. Pattern at the site of contact.
• Wood's lamp shows chalk white macules. Biopsy is seldom needed (absence of melanocytes).
• Patch testing is of limited help, since the process is a toxic effect rather than allergy.

Differential diagnosis.

• Vitiligo (generalised or segmental) and post-inflammatory hypopigmentation.
• Idiopathic guttate hypomelanosis, pityriasis alba and tinea versicolor.
• Leprosy, lichen sclerosus and chemical burns.

• Identify and remove the cause: stop the product or change gloves, footwear, adhesive or bindi. Workplace changes with occupational health advice.
• Topical corticosteroid (clobetasol 0.05% daily for 2 months, then rest) or tacrolimus 0.1% twice daily, for several months.
• Narrowband ultraviolet B 2 to 3 times each week for 3 to 12 months, or excimer light for localised patches.
• Repigmentation after removing the cause is possible but may be slow or incomplete.
• Camouflage cosmetics and sunscreen. Depigmentation of the remaining skin is an option only for extensive, resistant disease.
• Do not use monobenzone unless depigmentation of the whole skin is intended.

Monitoring. Review every 3 months for repigmentation and relapse.

Referral and escalation. Dermatology; occupational health for workplace exposure.