Vitiligo
Classification and external resources
Non-segmental vitiligo of the hand.
ICD-10 | L 80
ICD-9 | 709.01
OMIM | 193200
DiseasesDB | 13965
MedlinePlus | 000831
eMedicine | derm/453
MeSH | D014820

Vitiligo (/[unsupported input]ʔ v ʔ t ʔ ʔ l[unsupported input]ʔ[unsupported input]/) is a condition that causes depigmentation of sections of skin. It occurs when melanocytes, the cells responsible for skin pigmentation, die or are unable to function. The cause of vitiligo is unknown, but research suggests that it may arise from autoimmune, genetic, oxidative stress, neural, or viral causes.[1] The incidence worldwide is less than 1%.[2] The most common form is non-segmental vitiligo, which tends to appear in symmetric patches, sometimes over large areas of the body.

## Signs and symptoms[edit]

The most notable symptom of vitiligo is depigmentation of patches of skin that occurs on the extremities.[3][4] Although patches are initially small, they often enlarge and change shape.[1][3] When skin lesions occur, they are most prominent on the face, hands and wrists.[3][4] Depigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus.[3][4] Some lesions have hyperpigmentation around the edges.[5] Patients who are stigmatised for their condition may experience depression and similar mood disorders.[6]

## Treatment[edit]

There are a number of treatments for vitiligo. Treatment options generally fall into four groups:[7]

### UVB phototherapy[edit]

Exposing the skin to UVB light from UVB lamps is the most common treatment for vitiligo. The treatments can be done at home with a domestic UVB lamp or in a clinic. It is important to control the exposure time, so that the skin will not burn from over exposure. The UVB lamp should have a timer that turns off the lamp. Normally a small lamp is needed if the spot is small. Treatment can take a few weeks if the spots are on the neck and face and if they existed not more than 3 years. If the spots are on the hands and legs and have been there more than 3 years, it can take a few months. In a clinic the treatments are done 2?3 times a week, and at home every day, which makes the home treatments more effective. If the spots are on a large area of the body, full body treatment in a clinic or hospital will be needed. Both UVB broadband and UVB narrowband lamps can be used.[8][9] However these treatments are unreliable at best.[citation needed] There is no treatment that totally repigments the skin. Adding a psoralen, a photosensitizer, or an immunomodulant[10] that increases the effect of the UV light, can aid in partial repigmentation.

Studies have shown that immunomodulator creams such as Protopic and Elidel also cause repigmentation in some cases, when used with UVB narrowband treatments.[11][12] A 1997 report suggests that combining vitamin B12 and folic acid supplements with sun exposure caused repigmentation in 52% of cases.[13]

### PUVA phototherapy[edit]

Ultraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and ultraviolet A light (PUVA) treatment involves taking a drug which increases the skin's sensitivity to ultraviolet light. The skin is then exposed to high doses of ultraviolet A light. Treatment is required twice a week for 6?12 months or longer. Because of the high doses of UVA and psoralen, PUVA may cause side effects such as sunburn-type reactions or skin freckling.[7]

Narrowband ultraviolet B (UVB) phototherapy is now used more commonly than PUVA as it is less damaging to the skin. As with PUVA, treatment is carried out twice weekly in a clinic or every day at home, and there is no need to use psoralen.[7]

### Transplanting melanocytes[edit]

In October 1992, a scientific report was published of successfully transplanting melanocytes to vitiligo affected areas, effectively repigmenting the region.[14] The procedure involved taking a thin layer of pigmented skin from the patient's gluteal region. Melanocytes were then separated out to a cellular suspension that was expanded in culture. The area to be treated was then denuded with a dermabrader and the melanocytes graft applied. Between 70 and 85 percent of patients experienced nearly complete repigmentation of their skin. The longevity of the repigmentation differed from person to person.[15]

### Skin camouflage[edit]

In mild cases, vitiligo patches can be hidden with makeup or other cosmetic camouflage solutions. If the affected person is pale-skinned, the patches can be made less visible by avoiding both sunlight and the tanning of unaffected skin.[16]

### Reversal[edit]

The traditional treatment is the application of corticosteroid cream.[17]

### De-pigmenting[edit]

In cases of extensive vitiligo the option to de-pigment the unaffected skin with topical drugs like monobenzone, mequinol or hydroquinone may be considered to render the skin an even colour. The removal of all the skin pigment with monobenzone is permanent and vigorous. Sun-safety must be adhered to for life to avoid severe sun burn and melanomas. Depigmentation takes about a year to complete.[7]

### Non-segmental[edit]

In non-segmental vitiligo (NSV), there is usually some form of symmetry in the location of the patches of depigmentation. New patches also appear over time and can be generalized over large portions of the body or localized to a particular area. Vitiligo where little pigmented skin remains is referred to as vitiligo universalis. NSV can come about at any age, unlike segmental vitiligo, which is far more prevalent in teenage years.[5]

Classes of non-segmental vitiligo include:

- Generalized Vitiligo: the most common pattern, wide and randomly distributed areas of depigmentation[16]
- Universal Vitiligo: depigmentation encompasses most of the body[16]
- Focal Vitiligo: one or a few scattered macules in one area, most common in children[16]
- Acrofacial Vitiligo: fingers and periorificial areas[16]
- Mucosal Vitiligo: depigmentation of only the mucous membranes[16]

### Segmental[edit]

Segmental vitiligo (SV) differs in appearance, etiology and prevalence from associated illnesses. Its treatment is different from that of NSV. It tends to affect areas of skin that are associated with dorsal roots from the spine and is most often unilateral. It spreads much more rapidly than NSV and, without treatment, it is much more stable/ static in course and is not associated with auto-immune diseases. It is a very treatable condition that responds to topical treatment.[5]

- Vitiligo on lighter skin

- Vitiligo on darker skin

## Differential diagnosis[edit]

Conditions with similar symptoms include:

- Pityriasis alba
- Tuberceloid Leprosy
- Postinflammatory hypopigmentation
- Tinea versicolor[16]
- Albinism
- piebaldism[16]
- idiopathic guttate hypomelanosis[16]
- progressive macular hypomelanosis[16]
- Primary Adrenal Insufficiency

## Pathogenesis[edit]

Vitiligo is a disorder characterized by patchy loss of skin pigmentation due to immune attacks on melanocytes. Although there is no significant proof or evidence, many doctors believe that it can be caused by defects in many genes[citation needed]. Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo. The immune system genes are associated with other autoimmune disorders.

In one case, the gene TYR, which makes the melanocyte more susceptible to the immune system in vitiligo, also makes the melanocyte more susceptible to the immune system in the skin cancer malignant melanoma. So people with vitiligo caused by the TYR gene are less likely to have malignant melanoma.

A genomewide association study found 10 independent susceptibility loci for generalized vitiligo, responsible for 7.4% of the genetic risk. Some patients had vitiligo alone; others had generalized vitiligo with other autoimmune diseases. Most loci were associated with both forms. (The exception was PTPN22, which was only associated with generalized vitiligo.) In the MHC region, which controls the immune system, major association signals were identified in the class I gene region (between HLA-A and HLA-HGC9) and class II gene region (between HLA-DRB1 and HLA-DQA1). Outside the MHC region, association signals were identified near RERE, PTPN22, LPP, IL2RA, GZMB, UBASH3A and C1QTNF6 genes, which are associated with other autoimmune diseases. TYR encodes tyrosinase, which is not a component of the immune system, but is an enzyme of the melanocyte that catalyzes melanin biosynthesis, and a major autoantigen in generalized vitiligo. The major alleles of TYR are associated with vitiligo, and the minor alleles are associated with malignant melanoma. Vitiligo-associated 402R tyrosinase may be more efficiently presented to the immune system. Melanoma-associated 402Q may fail to be identified by the immune system.[18]

The transcriptional profile of melanocytes from vitiligo patients have been studied. Oligonucleotide microarrays containing approximately 16,000 unique genes were used to analyse mRNA expression in melanocytes from vitiligo patients and age-matched healthy controls. In total, 859 genes were identified as differentially expressed.[19]

Vitiligo is sometimes associated with autoimmune and inflammatory diseases,[20] commonly thyroid overexpression and underexpression. A study comparing 656 people with and without vitiligo in 114 families found several mutations (single-nucleotide polymorphisms) in the NALP1 gene. The NALP1 gene, which is on chromosome 17 located at 17p13, is on a cascade that regulates inflammation and cell death, including myeloid and lymphoid cells, which are white cells that are part of the immune response. NALP1 is expressed at high levels in T cells and Langerhan cells, white blood cells that are involved in skin autoimmunity. Polymorphisms of CD4 were shown to be associated with the vitiligo and other autoimmune diseases like type I Diabetes Mellitus.[21]

Among the inflammatory products of NALP1 are caspase 1 and caspase 7, which activate the inflammatory cytokine interleukin-1?. Interleukin-1? is expressed at high levels in patients with vitiligo. There are compounds which inhibit caspase and interleukin-1?, and so might be useful drugs for vitiligo and associated autoimmune diseases. In one of the mutations, the amino acid leucine in the NALP1 protein was replaced by histidine (Leu155->His). The original protein and sequence is highly conserved in evolution, and found in humans, chimpanzee, rhesus monkey, and bush baby, which means that it is an important protein and an alteration is likely to be harmful. Addison's disease (typically an autoimmune destruction of the adrenal glands) may cause vitiligo.[22][23]

## Notable cases[edit]

Michael Jackson claimed that he was diagnosed with vitiligo universalis. Here, apparently pictured in the early stages of the disease.

- Michael Jackson stated that he was diagnosed with vitiligo in 1986. In a 90-minute interview with Oprah Winfrey in February 1993, Jackson claimed that he didn't bleach his skin, stating for the first time that he had vitiligo.
- Graham Norton, Irish television personality.[24]
- Lee Thomas, a news anchor and entertainment reporter for WJBK (Fox) Detroit.[25][26][27]
- Francesco Cossiga, Italian politician, former President of Italian Republic[28]
- Yvette Fielding, British TV presenter, has had vitiligo from age 11; her mother developed it at age 24.[29][30]
- John Wiley Price, Dallas County Commissioner.[31]
- Amitabh Bachchan, Bollywood actor.[32]
- Scott Jorgensen, UFC fighter.[33]
- Daniel Bryan, professional wrestler, WWE superstar.[34]
- Jon Hamm, actor best known for his role in Mad Men.[35]
- John Henson, one of the hosts of ABC's Wipeout, has vitiligo that has caused a white patch of hair on the right side of his head.[36]
- Michaela DePrince, ballet dancer[37]
- Hedvig Lindahl, goalkeeper for Sweden women's national football team, has been diagnosed with vilitigo since the age of 5.[38]
- Krizz Kaliko, American hip hop artist who named his debut album after the condition (Vitiligo) and refers to his condition in numerous songs.

## See also[edit]

- Albinism, uniform absence of melanin
- Alphos, a non-contagious leprosy formerly referred to as "vitiligo"
- Amelanism, lack of pigmentation
- Chimera (genetics)
- Coloboma
- Erythrism, excessive red pigmentation
- Heterochromia iridum, another condition characterized by pigment variations
- Leucism, reduced pigmentation
- Leukoderma
- List of cutaneous conditions
- Melanism, uniform saturation of melanin
- Nevus depigmentosus
- Piebaldism
- Pityriasis alba
- Quadrichrome vitiligo, characterized by patches of reduced but not absent pigment
- Selective ultraviolet phototherapy
- Uvb_lamps
- Xanthochromism
- Melanising agents

## References[edit]

1. ^ a b Halder, RM; Chappell, JL (2009). "Vitiligo update". Seminars in cutaneous medicine and surgery 28 (2): 86?92. doi:10.1016/j.sder.2009.04.008. PMID 19608058.
2. ^ Nath SK, Majumder PP, Nordlund JJ (1994). "Genetic epidemiology of vitiligo: multilocus recessivity cross-validated". American Journal of Human Genetics 55 (5): 981?90. PMC 1918341. PMID 7977362.
3. ^ a b c d National Institute of Arthritis and Musculoskeletal and Skin Diseases (March 2007). "What Is Vitiligo? Fast Facts: An Easy-to-Read Series of Publications for the Public Additional". Retrieved 2010-07-18.
4. ^ a b c Halder RM, et al. (2007). "72. Vitiligo". In Wolff K, Freedberg IM, Fitzpatrick TB (eds). Fitzpatrick's dermatology in general medicine (7th ed.). New York: McGraw-Hill Professional. ISBN 978-0-07-146690-5. OCLC 154751587.
5. ^ a b c Huggins RH, Schwartz RA, Janniger CK (2005). "Vitiligo". Acta Dermatovenerologica Alpina, Panonica, et Adriatica 14 (4): 137?42, 144?5. PMID 16435042.
6. ^ Picardi A, Pasquini P, Cattaruzza MS, Gaetano P, Melchi CF, Baliva G, Camaioni D, Tiago A, Abeni D, Biondi M (2003). "Stressful life events, social support, attachment security and alexithymia in vitiligo. A case-control study". Psychotherapy and Psychosomatics 72 (3): 150?8. doi:10.1159/000069731. PMID 12707482.
7. ^ a b c d Anon. "What are the treatment options for vitiligo?". Patient UK. EMIS PiP. Retrieved 2010-02-01.
8. ^ Scherschun, L; Kim, JJ; Lim, HW (2001). "Narrow-band ultraviolet B is a useful and well-tolerated treatment for vitiligo". Journal of the American Academy of Dermatology 44 (6): 999?1003. doi:10.1067/mjd.2001.114752. PMID 11369913.
9. ^ Don, Philip; Iuga, Aurel; Dacko, Anne; Hardick, Kathleen (2006). "Treatment of vitiligo with broadband ultraviolet B and vitamins". International Journal of Dermatology 45 (1): 63?5. doi:10.1111/j.1365-4632.2005.02447.x. PMID 16426381.
10. ^ Nistic? S, Chiricozzi A, Saraceno R, Schipani C, Chimenti S (Jan 2012). "Vitiligo treatment with monochromatic excimer light and tacrolimus: results of an open randomized controlled study". Photomed Laser Surg. 30 (1): 26?30. doi:10.1089/pho.2011.3029. PMID 22054204.
11. ^ Tanghetti EA (2003). "Tacrolimus ointment 0.1% produces repigmentation in patients with vitiligo: results of a prospective patient series". Cutis 71 (2): 158?62. PMID 12635898.
12. ^ Silverberg NB, Lin P, Travis L, et al. (2004). "Tacrolimus ointment promotes repigmentation of vitiligo in children: a review of 57 cases". Journal of the American Academy of Dermatology 51 (5): 760?6. doi:10.1016/j.jaad.2004.05.036. PMID 15523355.
13. ^ Juhlin L, Olsson MJ (1997). "Improvement of vitiligo after oral treatment with vitamin B12 and folic acid and the importance of sun exposure". Acta Derm. Venereol. 77 (6): 460?2. PMID 9394983.
14. ^ Olsson MJ, Juhlin L (1992). "Melanocyte transplantation in vitiligo". Lancet 340 (8825): 981. doi:10.1016/0140-6736(92)92875-G. PMID 1357390.
15. ^ Olsson MJ, Juhlin L (2002). "Long-term follow-up of leucoderma patients treated with transplants of autologous cultured melanocytes, ultrathin epidermal sheets and basal cell layer suspension". The British Journal of Dermatology 147 (5): 893?904. doi:10.1046/j.1365-2133.2002.04837.x. PMID 12410698.
16. ^ a b c d e f g h i j Halder RM, et al. Vitiligo. In: Wolff K, et al. Fitzpatrick's Dermatology in General Medicine. 7th ed. New York, N.Y.: McGraw-Hill Professional; 2007
17. ^ Kwinter J, Pelletier J, Khambalia A, Pope E (2007). "High-potency steroid use in children with vitiligo: a retrospective study". Journal of the American Academy of Dermatology 56 (2): 236?41. doi:10.1016/j.jaad.2006.08.017. PMID 17224367.
18. ^ Jin Y, Birlea SA, Fain PR, et al. (2010). "Variant of TYR and Autoimmunity Susceptibility Loci in Generalized Vitiligo". N. Engl. J. Med. 362 (18): 1686?97. doi:10.1056/NEJMoa0908547. PMC 2891985. PMID 20410501.
19. ^ Str?mberg S, Bj?rklund MG, Asplund A, et al. (2008). "Transcriptional profiling of melanocytes from patients with vitiligo vulgaris". Pigment Cell Melanoma Research 21 (2): 162?71. doi:10.1111/j.1755-148X.2007.00429.x. PMID 18426409.
20. ^ Hedstrand H, Ekwall O, Olsson MJ, et al. (2001). "The transcription factors SOX9 and SOX10 are vitiligo autoantigens in autoimmune polyendocrine syndrome type I". The Journal of Biological Chemistry 276 (38): 35390?5. doi:10.1074/jbc.M102391200. PMID 11423552.
21. ^ Mashaghi A et al. (2010). "Possible association of the CD4 gene polymorphism with vitiligo". Clin Exp Dermatol 35 (5): 521?4. doi:10.1111/j.1365-2230.2009.03667.x.
22. ^ Gregersen PK (2007). "Modern genetics, ancient defenses, and potential therapies". The New England Journal of Medicine 356 (12): 1263?6. doi:10.1056/NEJMe078017. PMID 17377166.
23. ^ Jin Y, Mailloux CM, Gowan K, et al. (2007). "NALP1 in vitiligo-associated multiple autoimmune disease". The New England Journal of Medicine 356 (12): 1216?25. doi:10.1056/NEJMoa061592. PMID 17377159.
24. ^ Barber, Lynn (28 October 2001). "Glad to be Graham". The Guardian (London). Retrieved 2010-04-09.
25. ^ 'I'm a black man turning white on television'", BrisbaneTimes, 18 December 2007
26. ^ "Turning White". Turning White. Retrieved 2011-01-31.
27. ^ "FOX TV Reporter Refuses to Give In to Skin Disorder Turning Him White". Fox News Channel. Associated Press. 17 December 2007. Retrieved 2009-02-09. "'I'm a black man turning white on television and people can see it,' says Thomas, an anchor and entertainment reporter for the local Fox Broadcasting Company affiliate. 'If you've watched me over the years, you've seen my hands completely change from brown to white.'"
28. ^ (Italian)Famous persons with vitiligo
29. ^ Baxter, Biddy; Barnes, Edward (1989). "9. Crest of a Wave". Blue Peter: The Inside Story. Letchworth: Ringpress. pp. 214?216. ISBN 0-948955-50-3.
30. ^ Epstein, Angela; Fielding, Yvette (6 May 2003). "My skin colour changed from dark olive to a bleach white". Daily Mail (London: Associated Newspapers). p. 39. ISSN 0307-7578.
31. ^ Atkinson, Jim (1 March 1996). "Pale by Comparison". Texas Monthly. Retrieved 2011-01-31.
32. ^ "Famous People Vitiligo". Vitiligos.com. 12 February 2010. Retrieved 2011-01-31.
33. ^ "Scott Jorgensen talks about rare skin condition". Fiveknuckles.com. Retrieved 2011-01-31.
34. ^ "Daniel Bryan tweets about his skin condition". Twitter. Retrieved 2011-07-29.
35. ^ "Mad Men star's stress disease". The Age (Australia). 6 September 2010.
36. ^ John Henson. Vitiligoguide.com (11 July 1967). Retrieved 2012-07-08.
37. ^ Smith, David (16 July 2012). "Sierra Leone war orphan returns to Africa en pointe for ballet debut". The Guardian. Archived from the original on 2012-07-20. Retrieved 2012-07-17.
38. ^ [1]. Hedviglindahl.com. Retrieved 2012-08-29.

## External links[edit]

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- API at the Open Directory Project

Diseases of the skin and appendages by morphology
Growths |
Epidermal | wart callus seborrheic keratosis acrochordon molluscum contagiosum actinic keratosis squamous cell carcinoma basal cell carcinoma merkel cell carcinoma nevus sebaceous trichoepithelioma
Pigmented | Freckles lentigo melasma nevus melanoma
Dermal and subcutaneous | epidermal inclusion cyst hemangioma dermatofibroma keloid lipoma neurofibroma xanthoma Kaposi's sarcoma infantile digital fibromatosis granular cell tumor leiomyoma lymphangioma circumscriptum myxoid cyst
Rashes |
With epidermal involvement |
Eczematous | contact dermatitis atopic dermatitis seborrheic dermatitis stasis dermatitis lichen simplex chronicus Darier's disease glucagonoma syndrome langerhans cell histiocytosis lichen sclerosus pemphigus foliaceus Wiskott-Aldrich syndrome Zinc deficiency
Scaling | psoriasis tinea (corporis cruris pedis manuum faciei) pityriasis rosea secondary syphilis mycosis fungoides systemic lupus erythematosus pityriasis rubra pilaris parapsoriasis ichthyosis
Blistering | herpes simplex herpes zoster varicella bullous impetigo acute contact dermatitis pemphigus vulgaris bullous pemphigoid dermatitis herpetiformis porphyria cutanea tarda epidermolysis bullosa simplex
Papular | scabies insect bite reactions lichen planus miliaria keratosis pilaris lichen spinulosus transient acantholytic dermatosis lichen nitidus pityriasis lichenoides et varioliformis acuta
Pustular | acne vulgaris acne rosacea folliculitis impetigo candidiasis gonococcemia dermatophyte coccidioidomycosis subcorneal pustular dermatosis
Hypopigmented | tinea versicolor vitiligo pityriasis alba postinflammatory hyperpigmentation tuberous sclerosis idiopathic guttate hypomelanosis leprosy hypopigmented mycosis fungoides
Without epidermal involvement |
Red |
Blanchable Erythema |
Generalized | drug eruptions viral exanthems toxic erythema systemic lupus erythematosus
Localized | cellulitis abscess boil erythema nodosum carcinoid syndrome fixed drug eruption
Specialized | urticaria erythema (multiforme migrans gyratum repens annulare centrifugum ab igne)
Nonblanchable Purpura |
Macular | thrombocytopenic purpura actinic purpura
Papular | disseminated intravascular coagulation vasculitis
Indurated | scleroderma/morphea granuloma annulare lichen sclerosis et atrophicus necrobiosis lipoidica
Miscellaneous disorders |
Ulcers |
Hair | telogen effluvium androgenic alopecia trichotillomania alopecia areata systemic lupus erythematosus tinea capitis loose anagen syndrome lichen planopilaris folliculitis decalvans acne keloidalis nuchae
Nail | onychomycosis psoriasis paronychia ingrown nail
Mucous membrane | aphthous stomatitis oral candidiasis lichen planus leukoplakia pemphigus vulgaris mucous membrane pemphigoid cicatricial pemphigoid herpesvirus coxsackievirus syphilis systemic histoplasmosis squamous cell carcinoma

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 | Vasospastic macule · Woronoff's ring · Nevus anemicus
Ungrouped | ungrouped: Nevus depigmentosus · Postinflammatory hypopigmentation · Pityriasis alba · Vagabond's leukomelanoderma · Yemenite deaf-blind hypopigmentation syndrome · Wende–Bauckus syndrome
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 (Acral acanthotic anomaly) · 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
Dyschromatoses | Dyschromatosis symmetrica hereditaria · Dyschromatosis universalis hereditaria
M: INT, SF, LCT | anat/phys/devp | noco (i/b/d/q/u/r/p/m/k/v/f)/cong/tumr (n/e/d), sysi/epon | proc, drug (D2/3/4/5/8/11)