Vitiligo differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Differentiating Vitiligo from other Diseases

• Acquired macular hypomelanosis

• Seen in young adults and frequently referred to as a recalcitrant pityriasis versicolor; white macules are present on the trunk, with more marked involvement on the lower back and axillae; Propionibacterium acnes is a suspected cause of depigmentation

• Annular lichenoid dermatitis of youth
• Chemical leukoderma

• Certain chemicals, particularly aromatic derivatives of phenols and catechols, can destroy melanocytes, resulting in chemical leukoderma that may be differentiated from vitiligo by the history of toxin exposure, lesions with bizarre borders and scale, a “confetti-like” distribution, and symptomatic pruritus.

• Discoid lupus erythematosus
• Guttate hypomelanosis

• Presents with hypopig- mented macules in a photodistribution on a background of actinic damage primarily on the arms and legs; unlike vitiligo, the macules are usually 5 mm in diameter or less.

• Halo nevus
• Hypopigmented mycosis fungoides
• Idiopathic guttate hypomelanosis
• Ito's hypomelanosis

• Linear distribution, unilateral or bilateral pattern of hypopigmented streaks; sporadic; chromosomal or genetic mosaicism (involving blood or skin cells)

• Leprosy, indeterminate

• Manifested as hypochromic patches that are hypoesthetic to light touch

• Lichen sclerosus
• Melanoma

• Vitiligoid changes range from halo of depigmentation around a cutaneous melanoma (malignant Sutton’s phenomenon) to more widespread vitiligoid changes; under Wood’s lamp, the margins of such vitiligoid lesions are usually less distinct than in common vitiligo, and depigmentation is usually incomplete

• Melasma

May be confused with vitiligo when hyperpigmented facial lesions surround normal but hypochromic-looking skin; the pattern of relative hypopigmentation is usually different from that of vitiligo, and examination of other body sites allows a definitive diagnosis

• Mycosis fungoides

• May present with skin depigmentation in dark-skinned patients; clinical diagnosis may be difficult in the absence of signs of inflammation and skin infiltration; biopsy results are diagnostic

• Nevus anemicus
• Nevus depigmentosus
• Nevoid hypomelanosis
• Onchocerciasis
• Photodistributed vitiligo-like drug reaction in HIV patients
• Piebaldism

• White forelock, midline depigmentation of anterior body, bilateral shin depigmentation; autosomal dominance.

• Pinta
• Pityriasis alba

• Common in children with atopy; also may have fine scale, but lesions retain some pigment and are less sharply demarcated.

• Postinflammatory depigmentation
• Postinflammatory hypopigmentation

• A history of trauma or inflammation of the affected area will precede the loss of pigment; occurs in inflammatory disorders accompanied by increased epidermal turnover (e.g., psoriasis, atopic dermatitis), in lichenoid–cytotoxic infiltration of epidermal basal layer (e.g., lichen planus, toxic drug reactions), and in scleroderma; clinically distinguished by identification of the primary skin disease (e.g., scalp or plaque psoriasis, flexural dermatitis for atopic dermatitis, scleroderma plaques), but may coexist with primary disease; in genital areas, lichen sclerosus may resemble vitiligo or be associated with true vitiligo; biopsy is useful in cases that are difficult to diagnose

• Posttraumatic leukoderma

• May occur after deep burns or scarring in which hair follicles are removed entirely or in which the bulge area containing melanocyte precursors is destroyed; can be difficult to distinguish from true vitiligo when scarring is not obvious; may also occur after toxic epidermal necrolysis

• Sarcoidosis
• Scleroderma-related leukoderma
• Tinea versicolor

• May cause vitiligoid changes, generally after treatment in the absence of re-exposure to UV light; the distribution and shape of the lesions and the presence of scaling and green fluorescence of untreated lesions allow a definite diagnosis; may be differentiated by the presence of fine scale, positive potassium hydroxide preparation, and distribution primarily on the trunk and neck;

• Topical steroid leukoderma
• Tuberous sclerosis

• Ash-leaf white spots, typically later appearance of other cutaneous symptoms (e.g., shagreen patches, angiofibromas, periungual fibromas, or connective tissue nevi) and possibly neurological sequelae; autosomal dominance.

• Vitiligoid depigmentation

• May result from use of systemic drugs (e.g., chloroquine, fluphenazine, physostigmine, imatinib); in rare cases topical imiquimod may also cause vitiligoid depigmentation

• Vogt–Koyanagi–Harada syndrome
• Waardenburg’s syndrome

• White forelock, hypertelorism, deafness (varies according to genotype); possible association with con- genital megacolon (Hirschsprung’s disease)