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Chemical leukoderma
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Chemical leukoderma

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Contributors: Caroline M. West MS, Bethany K. H. Lewis MD, MPH, Martin Agyei MD, Jason E. Hawkes MD, Amanda Truong BS, Douglas L. Powell MD, Jamie L. Woodcock MD
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Chemical leukoderma is an acquired hypo- or depigmenting dermatosis caused by repeated or sometimes a single exposure to specific toxic substances. These substances compete with tyrosine for hydroxylation by tyrosinase, thereby impeding synthesis of melanin in melanocytes. Other names for chemical leukoderma include contact leukoderma and occupational leukoderma.

Chemicals in the phenol and catechol families are the most widely recognized causative agents in chemical leukoderma, including monobenzylether of hydroquinone found in some "acid-cured" rubber gloves, germicides such as para-tertiary butylphenol (PTBP), and pymethroid insecticides. Exposure to these types of agents typically occurs in an industrial setting. Additionally, phenols and catechols can be found in many common household materials, including wallets, decorative coloring agents for skin, footwear, watchstraps, hearing aids, deodorants, hair treatments, cosmetics, eyewear, and detergents. Other implicated toxins include mercurials, arsenics, sulfhydryls, and azelaic acid, as well as medications often used by primary care physicians and dermatologists, including corticosteroids and tretinoin.

Chemical leukoderma is common in developing countries where manufacture of consumer products is often not strictly regulated. In developed countries, exposure to causative agents more commonly takes place in industrial occupations. Pathologically, this condition is a result of apoptosis of melanocytes induced by oxidative stress after toxic exposure with an underlying genetic fragility of melanocytes.

Chemical leukoderma can affect any age group but is far more prevalent in adult patients, especially in the Western world where occupational exposure is the likely etiology. Pediatric cases of chemical leukoderma have been reported in developing countries where children have repeated exposure to common household objects containing the chemical agent.

"Chemical leukoderma syndrome" describes the spectrum of disease and includes patients with continued development of hypopigmented lesions despite avoidance of the causative toxin for more than a year.


L81.9 – Disorder of pigmentation, unspecified

297951005 – Skin depigmented

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Diagnostic Pearls

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Differential Diagnosis & Pitfalls

  • Vitiligo – Unlike chemical leukoderma, features trichome (area of intermediate pigment between hypopigmentation and normal-colored skin), leukotrichia (hypopigmentation of hair), and koebnerization (lesions favoring sites of trauma). Patients with vitiligo also lack a history of occupational exposure.
  • Pityriasis (tinea) versicolor – Scaly hypo- / hyperpigmented macules and patches with fungal elements visible on potassium hydroxide (KOH).
  • Pityriasis alba – Hypopigmentation frequently located on the face with fine pityriasiform scaling.
  • Post-inflammatory dyschromia / hypopigmentation – Presents in a patient with history of preceding dermatitis or other inflammatory dermatosis.
  • Idiopathic guttate hypomelanosis – Confetti-like macules on the extremities, particularly the forearm, calves, and shins.
  • Sarcoidosis – Generally presents as red-brown plaques with peripheral elevation and central hypopigmentation.
  • Tuberculoid leprosy – Presents with anesthetic hypopigmented macules and patches that are most prominent on the face and extremities.
  • Lepromatous leprosy – Can present with many widespread hypopigmented or slightly erythematous lesions. Lesions tend to be more prominent on the cooler parts of the body (eg, nose, earlobes, eyebrows, cheeks, ears, buttocks, and extensor and acral extremities).
  • Leishmaniasis (Old World, New World) – Lesions may heal without therapy, leaving a hypopigmented, atrophic scar. Active lesions usually develop central ulceration. Microscopy or biopsy should reveal parasite in most active cases.
  • Secondary syphilis – Presents as a papulosquamous, sometimes hypopigmented eruption involving the trunk and extremities, including palms and soles. History of primary chancre should raise concern for this diagnosis. Patients also usually present with systemic symptoms such as fever, headache, sore throat, and malaise.
  • Incontinentia pigmenti – Evolves from birth through childhood with hypopigmentation being the 4th (last) stage in the progression. Stages 1-3 present as vesicular stage, verrucous stage, and hyperpigmented stage.
  • Hypopigmented mycosis fungoides – Hypopigmented patches and plaques with fine scale and with local sensitivity. Generally located on the trunk, pelvic girdle, and lower limbs. Often associated with pruritus, poikiloderma, and ulceration.
  • Tuberous sclerosis – Often has hypopigmented macules or differing configurations.

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Management Pearls

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Drug Reaction Data

Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.

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Last Updated: 10/12/2018
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