Depigmentation

Depigmentation is the lightning of the skin, or loss of pigment. Depigmentation of the skin can be caused by a number of local and systemic conditions. The pigment loss can be partial (injury to the skin) or complete (caused by vitiligo). It can be temporary (from tinea versicolor) or permanent (from albinism).^[1]

Most commonly, depigmentation of the skin is linked to people born with vitiligo,which produces differing areas of light and dark skin. These individuals, if they so decided to use a lightning process to even out their skin tone, could apply a topical cream containing the organic compound monobenzone to lessen the remaining pigment. The brand drug incorporating 20% monobenzone is Benoquin, made by ICN.

Increasingly, people who are not afflicted with the vitiligo experiment with lower concentrations of monobenzone creams in the hope of lightning their skin tone evenly. An alternate method of lightning is to use the chemical mequinol over an extended period of time. Both monobenzone and mequinol produce dramatic skin whitening, but react very differently. Mequinol leaves the skin looking extremely pale. However, tanning is still possible. It is important to notice that the skin will not go back to its original color after the none treatment of mequinol. Mequinol should not be used by people that are allergic to any ingredient in mequinol, if you are pregnant, if you have eczema, irritated or inflamed skin, an increased number of white blood cells or if you are sensitive to sunlight or must be outside for prolonged periods of time.^[2] Mequinol is used in Europe in concentrations ranging from 2-20% and is approved in many countries for the treatment of solar lentigines.^[3] Monobenzone applied topically completely removes pigment in the long term and vigorous sun-safety must to be adhered to for life to avoid severe sun burn and melanomas. People using monobenzone without previously having vitiligo do so because standard products containing hydroquinone or other lightning agents are not effective for their skin and due to price and active ingredient strength. However, monobenzone is not recommended for skin conditions other than vitiligo.

For stubborn pigmented lesions the Q-switched ruby laser, cryotherapy or TCA peels can be used to ensure the skin remains pigment-free.

References

Pigmentation disorders/Dyschromia (L80–L81, 709.0)

Hypo-/
leucism

Loss of
melanocytes

Vitiligo	Quadrichrome vitiligo Vitiligo ponctué

Syndromic	Alezzandrini syndrome Vogt–Koyanagi–Harada syndrome

Melanocyte development	Piebaldism Waardenburg syndrome Tietz syndrome

Loss of melanin/
amelanism

Albinism	Oculocutaneous albinism Ocular albinism

Melanosome transfer	Hermansky–Pudlak syndrome Chédiak–Higashi syndrome Griscelli syndrome Elejalde syndrome Griscelli syndrome type 2 Griscelli syndrome type 3

Other	Cross syndrome ABCD syndrome Albinism–deafness syndrome Idiopathic guttate hypomelanosis Phylloid hypomelanosis Progressive macular hypomelanosis

Leukoderma w/o
hypomelanosis

Ungrouped

Hyper-

Melanin/
Melanosis/
Melanism

Reticulated	Dermatopathia pigmentosa reticularis Pigmentatio reticularis faciei et colli Reticulate acropigmentation of Kitamura Reticular pigmented anomaly of the flexures Naegeli–Franceschetti–Jadassohn syndrome Dyskeratosis congenita X-linked reticulate pigmentary disorder Galli–Galli disease Revesz syndrome

Diffuse/ circumscribed	Lentigo/Lentiginosis: Lentigo simplex Liver spot Centrofacial lentiginosis Generalized lentiginosis Inherited patterned lentiginosis in black persons Ink spot lentigo Lentigo maligna Mucosal lentigines Partial unilateral lentiginosis PUVA lentigines Melasma Erythema dyschromicum perstans Lichen planus pigmentosus Café au lait spot Poikiloderma (Poikiloderma of Civatte Poikiloderma vasculare atrophicans) Riehl melanosis

Linear	Incontinentia pigmenti Scratch dermatitis Shiitake mushroom dermatitis

Other/ ungrouped	Acanthosis nigricans Freckle Familial progressive hyperpigmentation Pallister–Killian syndrome Periorbital hyperpigmentation Photoleukomelanodermatitis of Kobori Postinflammatory hyperpigmentation Transient neonatal pustular melanosis

Other
pigments

Iron	Hemochromatosis Iron metallic discoloration Pigmented purpuric dermatosis Schamberg disease Majocchi's disease Gougerot–Blum syndrome Doucas and Kapetanakis pigmented purpura/Eczematid-like purpura of Doucas and Kapetanakis Lichen aureus Angioma serpiginosum Hemosiderin hyperpigmentation

Other metals	Argyria Chrysiasis Arsenic poisoning Lead poisoning Titanium metallic discoloration

Other	Carotenosis Tattoo Tar melanosis

Dyschromia