Vitilago similar conditions

Disease name Presentation Diagnosis
Piebaldism Present at birth, non-progressive small lentiginous pigmentations within leukodermas. Clinical diagnosis.
Waardenburg’s syndrome Achromic patches present at birth, white forelock, heterochromia iridium, dystopia canthorum, deafness and other neurological symptoms, mental retardation. Clinical diagnosis.
Tuberculous sclerosis Typical ash-leaf-shaped hypopigmented macules, seizures, angiofibromas, and mental retardation.Occurs predominately on the thorax and legs. Hypomelanotic macules (ash leaf spots) are accentuated with Wood’s lamp (UV light).
Hypomelanosis of Ito Mosaic distribution of hypomelanotic macules and bands of speckled or mottled, greyish-brown to blue-black patches involving the skin, conjunctiva, sclera, tympanic membrane, and oral and nasal mucosa of the affected dermatomes.Hypochromic lesions in distinctive patterns (e.g., whirls, patches, streaks) on trunk, arms, legs, and face. Clinical diagnosis.
Incontinentia pigmenti Distribution along Blaschko’s lines, history of vesicular eruption perinatally, female gender. Genetic testing for NF-kappa-B essential modulator (NEMO) mutation.
Atopic dermatitis History of atopic trait in family, typical distribution pattern, severe pruritus.Inflammatory skin disease and associated pruritus, infiltration, scaling, crusting. Wood’s lamp findings of hypopigmentation, elevated totalIgE level, skin biopsy findings of adendritic epidermal cell population (Langerhans cells and mast cells), which carry IgE receptors and specific IgE.
Pityriasis alba Asymptomatic ill-defined small patches with fine scaling in children and adolescents, often with atopic trait. Clinical diagnosis.
Seborrhoic dermatitis Distribution pattern to seborrhoeic areas (e.g., scalp, forehead, eyebrow, nasolabial fold, periauricular, central chest, and back), greasy scales, dandruff. Clinical diagnosis.
Discoid lupus erythematosus Hyperpigmented, infiltrated rim around leukoderma, follicular plugging, scarring alopecia. Lesional biopsy positive for direct immunofluorescence (e.g., basement membrane).Hyperkeratosis with perivascular and periappendageal lymphocytic infiltrate in the dermis.
Psoriasis Hypopigmentation may have annular appearance. When the plaques are scraped pinpoint bleeding from the skin below is visible (Auspitz’s sign). Skin from a biopsy will show clubbed Rete pegs.
Pityriasis versicolour Polycyclic, well-demarcated, typical upper trunk and shoulder distribution. Pityrosporum orbiculare fluoresces yellow-green when exposed to Wood’s lamp examination.A scrape of skin scales reveals the organism on KOH wet mount.
Leprosy Distribution, hypoaesthesia, thickening of nerves, extended residence in or migration from endemic area. Tests for diagnosis include viral culture, serology, pp65 antigenaemia test, histopathology and nucleic acid amplification, and detection systems, most commonly PCR.
Chemically induced leukoderma Starts at sites of exposure to melanotoxic agentsMay progress to be clinically indistinguishable from vitiligo. Clinical diagnosis.
Melanoma –associated leucoderma May be indistinguishable from vitiligo; history of melanoma, leukoderma at an excision site, or melanoma or metastases found upon examination. Biopsy of suspicious melanocytic lesions characterised by loss of pigmentation in the primary lesion and an eccentrically placed hypopigmented macule.
Frost bite Well-defined leukoderma in areas of previous traumatic cold exposure. Clinical diagnosis.
Hypopigmented  T cell lymphoma Less well-circumscribed than vitiligo, mixed hypo- and depigmentation. Immunophenotype CD4 is positive, and CD7 negative; CD25 positivity is variable.
Hydroquinone-induced dermatopathy Ill-defined or patchy areas of hypopigmentation, history of using bleaching creams. Clinical diagnosis.
Corticosteroid-induced dermatopathy Ill-defined hypopigmentation, localised to area of topical or local corticosteroid therapy; associated dermal and epidermal atrophy, telangiectasia, purpura, acne. Clinical diagnosis.
Melanocyte receptor antagonist-induced dermatopathy Therapeutic agents (specifically with Imatinib mesilate and SU11428) targeting C-kit (receptor molecule in a signalling pathway essential for melanocyte development and survival) may trigger or worsen vitiligo, may also induce hypopigmentation of skin or hair. Clinical diagnosis.
Vogt-Koyanagi-Harada syndrome Acquired leukoderma associated with ocular and auditory compromise. Clinical diagnosis.
Idiopathic guttate hypomelanosis Small, often circular hypopigmented macules preferring lower extremities, slowly progressive accumulation of isolated lesions. Wood’s lamp findings of hypopigmentation and skin biopsy with epidermal atrophy, patchy decrease or absence of melanocytes and melanin, flat Rete ridges, and basket weave hyperkeratosis.
Progressive macular hypomelanosis Progressive hypopigmented patches on back and abdomen of young patients. Skin biopsy with diminished pigment in the epidermis and a normal-looking dermis. Electron microscopy shows a shift from large melanosomes in normal-looking skin to small aggregated, membrane-bound melanosomes in hypopigmented skin.