Vitiligo differential diagnosis: Difference between revisions

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{{Vitiligo}}
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==Overview==
==Overview==
There are numerous conditions that cause [[hypopigmentation]] from which vitiligo must be differentiated, and the most common are [[pityriasis alba]], postinflammatory hypopigmentation, [[tinea versicolor]], [[halo nevus]], [[tuberous sclerosis]] and [[albinism]].


==Differentiating Vitiligo from Other Diseases==
==Differentiating Vitiligo from Other Diseases==
The differential diagnoses of vitiligo include several conditions that should be considered during the diagnosis.<ref>{{Cite journal | doi = 10.1056/NEJMcp0804388 | issn = 1533-4406 | volume = 360 | issue = 2 | pages = 160–169 | last = Taïeb | first = Alain | coauthors = Mauro Picardo | title = Clinical practice. Vitiligo | journal = The New England Journal of Medicine | date = 2009-01-08 | pmid = 19129529 }}</ref><ref>{{cite book | last = Jackson | first = Scott | title = Differential diagnosis for the dermatologist | publisher = Springer | location = Berlin New York | year = 2012 | isbn = 3642280056 }}</ref><ref>{{Cite journal | issn = 0973-3922 | volume = 73 | issue = 3 | pages = 149–156 | last = Sehgal | first = Virendra N. | coauthors = Govind Srivastava | title = Vitiligo: compendium of clinico-epidemiological features | journal = Indian Journal of Dermatology, Venereology and Leprology | date = 2007-06 | pmid = 17558045 }}</ref><ref name="AlikhanFelsten2011">{{cite journal|last1=Alikhan|first1=Ali|last2=Felsten|first2=Lesley M.|last3=Daly|first3=Meaghan|last4=Petronic-Rosic|first4=Vesna|title=Vitiligo: A comprehensive overview|journal=Journal of the American Academy of Dermatology|volume=65|issue=3|year=2011|pages=473–491|issn=01909622|doi=10.1016/j.jaad.2010.11.061}}</ref>


The differential diagnoses of vitiligo include:<ref>{{Cite journal | doi = 10.1056/NEJMcp0804388 | issn = 1533-4406 | volume = 360 | issue = 2 | pages = 160–169 | last = Taïeb | first = Alain | coauthors = Mauro Picardo | title = Clinical practice. Vitiligo | journal = The New England Journal of Medicine | date = 2009-01-08 | pmid = 19129529 }}</ref><ref>{{cite book | last = Jackson | first = Scott | title = Differential diagnosis for the dermatologist | publisher = Springer | location = Berlin New York | year = 2012 | isbn = 3642280056 }}</ref><ref>{{Cite journal | issn = 0973-3922 | volume = 73 | issue = 3 | pages = 149–156 | last = Sehgal | first = Virendra N. | coauthors = Govind Srivastava | title = Vitiligo: compendium of clinico-epidemiological features | journal = Indian Journal of Dermatology, Venereology and Leprology | date = 2007-06 | pmid = 17558045 }}</ref>
====Autoimmune Disorders====


* Acquired macular hypomelanosis
* [[Vogt-Koyanagi-Harada syndrome|Vogt–Koyanagi–Harada syndrome]]
:* 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
:* Characterized by bilateral [[uveitis]] associated with variable auditory, neurological, and cutaneous manifestations due to [[T cell]]-mediated destruction of [[melanin]]-containing tissues.
* Annular lichenoid dermatitis of youth
 
* Chemical leukoderma
====Infections====
:* 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.
* Tuberculoid [[leprosy]]
* Discoid lupus erythematosus
:* Manifested as [[hypochromic]] patches that are hypoesthetic to light touch
* Guttate hypomelanosis
* [[Tinea versicolor]]
:* 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.
:* 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]];
* Halo nevus
* [[Pinta]]
* Hypopigmented mycosis fungoides
* [[Onchocerciasis]]
* Idiopathic guttate hypomelanosis
 
* Ito's hypomelanosis
====Genetic Syndromes====
:* Linear distribution, unilateral or bilateral pattern of hypopigmented streaks; sporadic; chromosomal or genetic mosaicism (involving blood or skin cells)
 
* Leprosy, indeterminate
* [[Incontinentia pigmenti achromians|Incontinentia pigmenti achromians (hypomelanosis of Ito)]]
:* Manifested as hypochromic patches that are hypoesthetic to light touch
:* Characterized by unilateral or bilateral [[macule|macular]] [[hypopigmentation|hypopigmented]] whorls, streaks, and patches corresponding to the [[Blaschko's lines]] that usually develop within the first two years of life; may be associated with other neurological, skeletal, and ocular symptoms.
* Lichen sclerosus et atrophicus
* [[Tuberous sclerosis]]
* Melanoma
:* Ash-leaf white spots, typically later appearance of other cutaneous symptoms (e.g., shagreen patches, [[angiofibroma]]s, periungual [[fibroma]]s, or connective tissue [[nevi]]) and possibly neurological sequelae; [[autosomal dominant|autosomal dominance]].
:* 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
* [[Waardenburg's syndrome]]
* Melasma
:* White forelock, [[hypertelorism]], [[deafness]] (varies according to [[genotype]]); possible association with [[congenital megacolon]] ([[Hirschsprung's disease]])
: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
* [[Piebaldism]]
* Mycosis fungoides
:* White forelock, midline depigmentation of anterior body, bilateral shin depigmentation; [[autosomal dominant|autosomal dominance]].
:* 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
* [[Menkes syndrome]]
* Nevus anemicus
:* [[X-linked recessive]] condition with diffuse hair and body [[hypopigmentation]], associated with neurodegenerative changes.
* Nevus depigmentosus
 
* Nevoid hypomelanosis
====Post-inflammatory Hypopigmentation====
* Onchocerciasis
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; [[skin biopsy|biopsy]] is useful in cases that are difficult to diagnose.  Other conditions include:
* Photodistributed vitiligo-like drug reaction in HIV patients
* [[Discoid lupus erythematosus]]
* Piebaldism
* [[Pityriasis alba]]
:* White forelock, midline depigmentation of anterior body, bilateral shin depigmentation; autosomal dominance.
:* Common in children with [[atopy]]; also may have fine scale, but lesions retain some pigment and are less sharply demarcated.
* 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/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
* 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
:* May occur after deep burns or scarring in which [[hair follicle]]s 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
* Topical steroid leukoderma
* Tuberous sclerosis
* Photodistributed vitiligo-like [[drug reaction]] in [[HIV]] patients
:* 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
* 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
:* 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
====Neoplasia====
:* White forelock, hypertelorism, deafness (varies according to genotype); possible association with con- genital megacolon (Hirschsprung’s disease)
* [[Halo nevus]]
* [[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
* [[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
 
====Idiopathic====
* 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
* [[Idiopathic guttate hypomelanosis]]
:* Presents with hypopigmented 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.
* [[Lichen sclerosus]] et atrophicus
* [[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
* [[Sarcoidosis]]
 
====Malformations====
* [[Nevus anemicus]]
* [[Nevus depigmentosus]]
 
====Other====
* Chemically-induced [[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]].


==References==
==References==

Latest revision as of 15:35, 27 June 2014

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]

Overview

There are numerous conditions that cause hypopigmentation from which vitiligo must be differentiated, and the most common are pityriasis alba, postinflammatory hypopigmentation, tinea versicolor, halo nevus, tuberous sclerosis and albinism.

Differentiating Vitiligo from Other Diseases

The differential diagnoses of vitiligo include several conditions that should be considered during the diagnosis.[1][2][3][4]

Autoimmune Disorders

  • Characterized by bilateral uveitis associated with variable auditory, neurological, and cutaneous manifestations due to T cell-mediated destruction of melanin-containing tissues.

Infections

  • Manifested as hypochromic patches that are hypoesthetic to light touch
  • 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;

Genetic Syndromes

  • Characterized by unilateral or bilateral macular hypopigmented whorls, streaks, and patches corresponding to the Blaschko's lines that usually develop within the first two years of life; may be associated with other neurological, skeletal, and ocular symptoms.
  • 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.
  • White forelock, midline depigmentation of anterior body, bilateral shin depigmentation; autosomal dominance.

Post-inflammatory 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. Other conditions include:

  • Common in children with atopy; also may have fine scale, but lesions retain some pigment and are less sharply demarcated.
  • 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.
  • Topical steroid leukoderma
  • Photodistributed vitiligo-like drug reaction in HIV patients
  • Vitiligoid depigmentation

Neoplasia

  • 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
  • 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

Idiopathic

  • Acquired macular hypomelanosis
  • Presents with hypopigmented 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.
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

Malformations

Other

  • 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.

References

  1. ↑ Taïeb, Alain (2009-01-08). "Clinical practice. Vitiligo". The New England Journal of Medicine. 360 (2): 160–169. doi:10.1056/NEJMcp0804388. ISSN 1533-4406. PMID 19129529. Unknown parameter |coauthors= ignored (help)
  2. ↑ Jackson, Scott (2012). Differential diagnosis for the dermatologist. Berlin New York: Springer. ISBN 3642280056.
  3. ↑ Sehgal, Virendra N. (2007-06). "Vitiligo: compendium of clinico-epidemiological features". Indian Journal of Dermatology, Venereology and Leprology. 73 (3): 149–156. ISSN 0973-3922. PMID 17558045. Unknown parameter |coauthors= ignored (help); Check date values in: |date= (help)
  4. ↑ Alikhan, Ali; Felsten, Lesley M.; Daly, Meaghan; Petronic-Rosic, Vesna (2011). "Vitiligo: A comprehensive overview". Journal of the American Academy of Dermatology. 65 (3): 473–491. doi:10.1016/j.jaad.2010.11.061. ISSN 0190-9622.
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