vitiligo

Summary

Summary: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.

Top Publications

  1. Dell Anna M, Cario Andre M, Bellei B, Taieb A, Picardo M. In vitro research on vitiligo: strategies, principles, methodological options and common pitfalls. Exp Dermatol. 2012;21:490-6 pubmed publisher
    Understanding the cellular and molecular mechanisms leading to melanocyte loss in vitiligo is a mandatory step in improving the overall management of vitiligo patients...
  2. Toosi S, Orlow S, Manga P. Vitiligo-inducing phenols activate the unfolded protein response in melanocytes resulting in upregulation of IL6 and IL8. J Invest Dermatol. 2012;132:2601-9 pubmed publisher
    b>Vitiligo is characterized by depigmented skin patches caused by loss of epidermal melanocytes. Oxidative stress may have a role in vitiligo onset, while autoimmunity contributes to disease progression...
  3. Zhou L, Li K, SHI Y, Hamzavi I, Gao T, Henderson M, et al. Systemic analyses of immunophenotypes of peripheral T cells in non-segmental vitiligo: implication of defective natural killer T cells. Pigment Cell Melanoma Res. 2012;25:602-11 pubmed publisher
    Although it is widely believed that non-segmental vitiligo (NSV) results from the autoimmune destruction of melanocytes, a clear understanding of defects in immune tolerance, which mediate this uncontrolled self-reactivity, is still ..
  4. Kotobuki Y, Tanemura A, Yang L, Itoi S, Wataya Kaneda M, Murota H, et al. Dysregulation of melanocyte function by Th17-related cytokines: significance of Th17 cell infiltration in autoimmune vitiligo vulgaris. Pigment Cell Melanoma Res. 2012;25:219-30 pubmed publisher
    The aim of this study was to determine whether CD4(+) IL-17A(+) Th17 cells infiltrate vitiligo skin and to investigate whether the proinflammatory cytokines related to Th17 cell influence melanocyte enzymatic activity and cell fate...
  5. van Geel N, Speeckaert R, Mollet I, De Schepper S, De Wolf J, Tjin E, et al. In vivo vitiligo induction and therapy model: double-blind, randomized clinical trial. Pigment Cell Melanoma Res. 2012;25:57-65 pubmed publisher
    In this study, we developed an in vivo vitiligo induction model to explore the underlying mechanisms leading to Koebner's phenomenon and to evaluate the efficacy of therapeutic strategies...
  6. Alikhan A, Felsten L, Daly M, Petronic Rosic V. Vitiligo: a comprehensive overview Part I. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work-up. J Am Acad Dermatol. 2011;65:473-491 pubmed publisher
    b>Vitiligo is an acquired pigmentary disorder of unknown etiology that is clinically characterized by the development of white macules related to the selective loss of melanocytes...
  7. Ricard A, Pain C, Daubos A, Ezzedine K, Lamrissi Garcia I, Bibeyran A, et al. Study of CCN3 (NOV) and DDR1 in normal melanocytes and vitiligo skin. Exp Dermatol. 2012;21:411-6 pubmed publisher
    We have hypothesised that melanocytes disappear in vitiligo because they are weakly attached to the epidermal basal membrane (melanocytorrhagy)...
  8. Zhu K, Lv Y, Yin X, Wang Z, Sun L, He S, et al. Psoriasis regression analysis of MHC loci identifies shared genetic variants with vitiligo. PLoS ONE. 2011;6:e23089 pubmed publisher
    ..More importantly we find that rs9468925 in HLA-C/HLA-B is associated with both psoriasis and vitiligo, providing first important evidence that two major skin diseases share a common genetic locus in the MHC, and a ..
  9. Akbas H, Dertlioglu S, Dilmec F, Balkan M. No association between catalase (CAT) gene polymorphisms and susceptibility to vitiligo in a Turkish population. Clin Ter. 2013;164:e173-7 pubmed publisher
    b>Vitiligo is an acquired hypomelanotic skin disorder resulting from the loss of functional melanocytes from the cutaneous epidermis...

More Information

Publications62

  1. Jin Y, Birlea S, Fain P, Ferrara T, Ben S, Riccardi S, et al. Genome-wide association analyses identify 13 new susceptibility loci for generalized vitiligo. Nat Genet. 2012;44:676-80 pubmed publisher
    We previously reported a genome-wide association study (GWAS) identifying 14 susceptibility loci for generalized vitiligo. We report here a second GWAS (450 individuals with vitiligo (cases) and 3,182 controls), an independent replication ..
  2. Gregg R, Nichols L, Chen Y, Lu B, Engelhard V. Mechanisms of spatial and temporal development of autoimmune vitiligo in tyrosinase-specific TCR transgenic mice. J Immunol. 2010;184:1909-17 pubmed publisher
    Generalized vitiligo is thought to have an autoimmune etiology and has been correlated with the presence of CD8 T cells specific for melanocyte differentiation Ag...
  3. Bulut H, Pehlivan M, Alper S, Tomatir A, Onay H, Yüksel S, et al. Lack of association between catalase gene polymorphism (T/C exon 9) and susceptibility to vitiligo in a Turkish population. Genet Mol Res. 2011;10:4126-32 pubmed publisher
    ..of hydrogen peroxide (H(2)O(2)) and low catalase (CAT) activity have been demonstrated in the epidermis of vitiligo patients...
  4. Narahari S, Ryan T, Bose K, Prasanna K, Aggithaya G. Integrating modern dermatology and Ayurveda in the treatment of vitiligo and lymphedema in India. Int J Dermatol. 2011;50:310-34 pubmed publisher
    ..Three-hundred eighty-one vitiligo patients were examined and treated to understand the clinical presentations and treatment options in Ayurveda...
  5. Ben Ahmed M, Zaraa I, Rekik R, Elbeldi Ferchiou A, Kourda N, Belhadj Hmida N, et al. Functional defects of peripheral regulatory T lymphocytes in patients with progressive vitiligo. Pigment Cell Melanoma Res. 2012;25:99-109 pubmed publisher
    Auto-reactive cytotoxic T lymphocytes play a key role in the progressive loss or destruction of melanocytes in vitiligo but the mechanism underlying the loss of self-tolerance is unknown...
  6. Byrne K, Turk M. New perspectives on the role of vitiligo in immune responses to melanoma. Oncotarget. 2011;2:684-94 pubmed
    Melanoma-associated vitiligo is the best-studied example of the linkage between tumor immunity and autoimmunity...
  7. Rao A, Gupta S, Dinda A, Sharma A, Sharma V, Kumar G, et al. Study of clinical, biochemical and immunological factors determining stability of disease in patients with generalized vitiligo undergoing melanocyte transplantation. Br J Dermatol. 2012;166:1230-6 pubmed publisher
    Stability is considered the most important parameter before performing any melanocyte transplantation procedure in vitiligo; however, current criteria rely on the history given by the patients.
  8. Dwivedi M, Laddha N, Begum R. Correlation of increased MYG1 expression and its promoter polymorphism with disease progression and higher susceptibility in vitiligo patients. J Dermatol Sci. 2013;71:195-202 pubmed publisher
    ..The promoter polymorphism was shown to be associated with vitiligo in Caucasian population...
  9. Li K, Shi Q, Yang L, Li X, Liu L, Wang L, et al. The association of vitamin D receptor gene polymorphisms and serum 25-hydroxyvitamin D levels with generalized vitiligo. Br J Dermatol. 2012;167:815-21 pubmed publisher
    b>Vitiligo is an acquired depigmentation autoimmune disorder that has been described as being associated with lower levels of 25-hydroxyvitamin D [25(OH)D]...
  10. Feily A, Pazyar N. Why vitiligo is associated with fewer risk of skin cancer?: providing a molecular mechanism. Arch Dermatol Res. 2011;303:623-4 pubmed publisher
    b>Vitiligo is an acquired clinical conundrum, characterized by white areas on the skin due to loss of functional melanocytes...
  11. Shi F, Erf G. IFN-?, IL-21, and IL-10 co-expression in evolving autoimmune vitiligo lesions of Smyth line chickens. J Invest Dermatol. 2012;132:642-9 pubmed publisher
    The Smyth line (SL) of chicken is an excellent animal model for human autoimmune vitiligo. In SL vitiligo (SLV), postnatal loss of melanocytes in feathers appears to be due to cell-mediated immunity...
  12. Bassiouny D, Khorshied M. Glutathione S-transferase M1 and T1 genetic polymorphism in Egyptian patients with nonsegmental vitiligo. Clin Exp Dermatol. 2013;38:160-3 pubmed publisher
    Oxidative stress and accumulation of free radicals might play a role in the pathogenesis of vitiligo. Glutathione S-transferase (GST) is a multigene family of enzymes that detoxify oxidative stress products...
  13. Newman M, Silverberg N. Once-daily application of calcipotriene 0.005%-betamethasone dipropionate 0.064% ointment for repigmentation of facial vitiligo. Cutis. 2011;88:256-9 pubmed
    b>Vitiligo vulgaris is an autoimmune pigmentary disorder with no universally efficacious therapeutic options. Separate applications of calcipotriene ointment 0...
  14. Qiao J, Zhou G, Ding Y, Zhu D, Fang H. Multiple paraneoplastic syndromes: myasthenia gravis, vitiligo, alopecia areata, and oral lichen planus associated with thymoma. J Neurol Sci. 2011;308:177-9 pubmed publisher
    ..We describe a thymoma patient with diagnoses of myasthenia gravis, vitiligo, alopecia areata, and oral lichen planus associated with a thymoma...
  15. Imran M, Laddha N, Dwivedi M, Mansuri M, Singh J, Rani R, et al. Interleukin-4 genetic variants correlate with its transcript and protein levels in patients with vitiligo. Br J Dermatol. 2012;167:314-23 pubmed publisher
    b>Vitiligo is an acquired pigmentary disorder resulting from loss of melanocytes...
  16. Schallreuter K, Salem M, Gibbons N, Martinez A, Slominski R, Lüdemann J, et al. Blunted epidermal L-tryptophan metabolism in vitiligo affects immune response and ROS scavenging by Fenton chemistry, part 1: Epidermal H2O2/ONOO(-)-mediated stress abrogates tryptophan hydroxylase and dopa decarboxylase activities, leading to low se. FASEB J. 2012;26:2457-70 pubmed publisher
    b>Vitiligo is characterized by a progressive loss of inherited skin color. The cause of the disease is still unknown...
  17. Hong W, Hu D, Qian G, McCormick S, Xu A. Ratio of size of recipient and donor areas in treatment of vitiligo by autologous cultured melanocyte transplantation. Br J Dermatol. 2011;165:520-5 pubmed publisher
    Autologous melanocytes can be expanded in vitro, allowing the treatment of large lesions of vitiligo in one session...
  18. Laddha N, Dwivedi M, Begum R. Increased Tumor Necrosis Factor (TNF)-? and its promoter polymorphisms correlate with disease progression and higher susceptibility towards vitiligo. PLoS ONE. 2012;7:e52298 pubmed publisher
    ..of melanocytes, which plays a critical role in the pathogenesis of several autoimmune diseases including vitiligo, as abnormal immune responses have frequently been observed in vitiligo patients...
  19. Zhang X, Chen J, Liu J. The genetic concept of vitiligo. J Dermatol Sci. 2005;39:137-46 pubmed
    b>Vitiligo is a relatively common, acquired pigmentary disorder characterized by areas of depigmented skin resulting from loss of epidermal melanocytes. The prevalence of this disease varies from 0.1 to 2% in various global populations...
  20. Levy E, Neven B, Entz Werle N, Cribier B, Lipsker D. [Post-thymus transplant vitiligo in a child with Foxn1 deficiency]. Ann Dermatol Venereol. 2012;139:468-71 pubmed publisher
    ..Foxn1 transcription factor deficit leads to immune deficiency, with hair and nail abnormalities. We report the case of a patient also presenting localized leucoderma...
  21. Jin Y, Birlea S, Fain P, Gowan K, Riccardi S, Holland P, et al. Genome-wide analysis identifies a quantitative trait locus in the MHC class II region associated with generalized vitiligo age of onset. J Invest Dermatol. 2011;131:1308-12 pubmed publisher
    Generalized vitiligo is a common autoimmune disease in which acquired patchy depigmentation of skin, hair, and mucous membranes results from loss of melanocytes from involved areas...
  22. Ghajarzadeh M, Ghiasi M, Kheirkhah S. Associations between skin diseases and quality of life: a comparison of psoriasis, vitiligo, and alopecia areata. Acta Med Iran. 2012;50:511-5 pubmed
    The goal of this study was to compare depression and quality of life in three auto immune diseases: psoriasis, vitiligo, and alopecia areata...
  23. Spritz R. Recent progress in the genetics of generalized vitiligo. J Genet Genomics. 2011;38:271-8 pubmed publisher
    b>Vitiligo is an acquired disease characterized principally by patchy depigmentation of skin and overlying hair...
  24. Song G, Kim J, Lee Y. The CTLA-4 +49 A/G, CT60 A/G and PTPN22 1858 C/T polymorphisms and susceptibility to vitiligo: a meta-analysis. Mol Biol Rep. 2013;40:2985-93 pubmed publisher
    ..A/G, and protein tyrosine phosphatase nonreceptor 22 (PTPN22) 1858 C/T polymorphisms confer susceptibility to vitiligo. A meta-analysis was conducted of the associations between the CTLA-4 +49 A/G, CT60 and PTPN22 1858 C/T ..
  25. Harris J, Harris T, Weninger W, Wherry E, Hunter C, Turka L. A mouse model of vitiligo with focused epidermal depigmentation requires IFN-? for autoreactive CD8? T-cell accumulation in the skin. J Invest Dermatol. 2012;132:1869-76 pubmed publisher
    b>Vitiligo is an autoimmune disease of the skin causing disfiguring patchy depigmentation of the epidermis and, less commonly, hair. Therapeutic options for vitiligo are limited, reflecting in part limited knowledge of disease pathogenesis...
  26. Shi F, Kong B, Song J, Lee J, Dienglewicz R, Erf G. Understanding mechanisms of vitiligo development in Smyth line of chickens by transcriptomic microarray analysis of evolving autoimmune lesions. BMC Immunol. 2012;13:18 pubmed publisher
    The Smyth line (SL) of chicken is an excellent avian model for human autoimmune vitiligo. The etiology of vitiligo is complicated and far from clear...
  27. Mosenson J, Zloza A, Klarquist J, Barfuss A, Guevara Patino J, Poole I. HSP70i is a critical component of the immune response leading to vitiligo. Pigment Cell Melanoma Res. 2012;25:88-98 pubmed publisher
    ..Next, we demonstrated that HSP70i was necessary and sufficient to accelerate depigmentation in vitiligo-prone Pmel-1 mice, accompanied by lasting phenotypic changes in dendritic cell subpopulations...
  28. Huggins R, Henderson M, Mulekar S, Ozog D, Kerr H, Jabobsen G, et al. Melanocyte-keratinocyte transplantation procedure in the treatment of vitiligo: the experience of an academic medical center in the United States. J Am Acad Dermatol. 2012;66:785-93 pubmed publisher
    b>Vitiligo is a disfiguring disease with limited treatment options. Surgical treatment is underused in the United States because of perceived risk of infection, costs, and difficulty of the procedure...
  29. Cheong K, Kim N, Noh M, Lee A. Three new single nucleotide polymorphisms identified by a genome-wide association study in Korean patients with vitiligo. J Korean Med Sci. 2013;28:775-9 pubmed publisher
    Genetic susceptibility is involved in the pathogenesis of vitiligo. Association studies with a whole genome-based approach instead of a single or a few candidate genes may be useful for discovering new susceptible genes...
  30. Tang X, Zhang Z, Hu D, Xu A, Zhou H, Sun L, et al. Association analyses identify three susceptibility Loci for vitiligo in the Chinese Han population. J Invest Dermatol. 2013;133:403-10 pubmed publisher
    To identify susceptibility loci for vitiligo, we extended our previous vitiligo genome-wide association study with a two-staged replication study that included 6,857 cases and 12,025 controls from the Chinese Han population...
  31. Sandoval Cruz M, Garcia Carrasco M, Sanchez Porras R, Mendoza Pinto C, Jiménez Hernández M, Munguía Realpozo P, et al. Immunopathogenesis of vitiligo. Autoimmun Rev. 2011;10:762-5 pubmed publisher
    b>Vitiligo is a common depigmenting disorder which may have devastating psychological and social consequences and is characterized by the presence of circumscribed white macules in the skin due to the destruction of melanocytes in the ..
  32. Wang X, Li K, Guo S, Qiang H, Liu L, Song P, et al. The association of functional polymorphisms in the aryl hydrocarbon receptor (AHR) gene with the risk of vitiligo in Han Chinese populations. Br J Dermatol. 2012;166:1081-7 pubmed publisher
    b>Vitiligo is an acquired depigmentation disorder resulting from selective destruction of melanocytes...
  33. Teulings H, Overkamp M, Ceylan E, Nieuweboer Krobotova L, Bos J, Nijsten T, et al. Decreased risk of melanoma and nonmelanoma skin cancer in patients with vitiligo: a survey among 1307 patients and their partners. Br J Dermatol. 2013;168:162-71 pubmed publisher
    b>Vitiligo is a common skin disease characterized by autoimmune melanocyte destruction...
  34. Schallreuter K, Salem M, Holtz S, Panske A. Basic evidence for epidermal H2O2/ONOO(-)-mediated oxidation/nitration in segmental vitiligo is supported by repigmentation of skin and eyelashes after reduction of epidermal H2O2 with topical NB-UVB-activated pseudocatalase PC-KUS. FASEB J. 2013;27:3113-22 pubmed publisher
    Nonsegmental vitiligo (NSV) is characterized by loss of inherited skin color...
  35. Elassiuty Y, Klarquist J, Speiser J, Yousef R, El Refaee A, Hunter N, et al. Heme oxygenase-1 expression protects melanocytes from stress-induced cell death: implications for vitiligo. Exp Dermatol. 2011;20:496-501 pubmed publisher
    ..of melanocytes from stress-induced cell death by heme oxygenases during depigmentation and repigmentation in vitiligo, expression of isoforms 1 and 2 was studied in cultured control and patient melanocytes and normal skin explants ..
  36. Vrijman C, Kroon M, Limpens J, Leeflang M, Luiten R, van der Veen J, et al. The prevalence of thyroid disease in patients with vitiligo: a systematic review. Br J Dermatol. 2012;167:1224-35 pubmed publisher
    Thyroid disease has been suggested to be associated with vitiligo. However, the outcomes of prevalence studies on thyroid disease in vitiligo vary widely...
  37. Ezzedine K, Lim H, Suzuki T, Katayama I, Hamzavi I, Lan C, et al. Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference. Pigment Cell Melanoma Res. 2012;25:E1-13 pubmed publisher
    During the 2011 International Pigment Cell Conference (IPCC), the Vitiligo European Taskforce (VETF) convened a consensus conference on issues of global importance for vitiligo clinical research...
  38. Byrne K, Côté A, Zhang P, Steinberg S, Guo Y, Allie R, et al. Autoimmune melanocyte destruction is required for robust CD8+ memory T cell responses to mouse melanoma. J Clin Invest. 2011;121:1797-809 pubmed publisher
    ..In the present study we have found that vitiligo, the autoimmune destruction of melanocytes, generates self antigen required for mounting persistent and ..
  39. Singh A, Sharma P, Kar H, Sharma V, Tembhre M, Gupta S, et al. HLA alleles and amino-acid signatures of the peptide-binding pockets of HLA molecules in vitiligo. J Invest Dermatol. 2012;132:124-34 pubmed publisher
    b>Vitiligo is a depigmenting disorder of the skin that is characterized by the loss of functional melanocytes from the lesional sites...
  40. Dwivedi M, Laddha N, Mansuri M, Marfatia Y, Begum R. Association of NLRP1 genetic variants and mRNA overexpression with generalized vitiligo and disease activity in a Gujarat population. Br J Dermatol. 2013;169:1114-25 pubmed publisher
    ..suggested that NLRP1 is involved in susceptibility to a wide range of autoimmune diseases including generalized vitiligo (GV)...
  41. Huang Y, Yi X, Jian Z, Wei C, Li S, Cai C, et al. A single-nucleotide polymorphism of miR-196a-2 and vitiligo: an association study and functional analysis in a Han Chinese population. Pigment Cell Melanoma Res. 2013;26:338-47 pubmed publisher
    Recent evidence indicates that oxidative stress and genetic factors play an important role in the pathogenesis of vitiligo. SNPs in miRNAs involved in oxidative stress could potentially influence the development of vitiligo...
  42. Nunes D, Esser L. Vitiligo epidemiological profile and the association with thyroid disease. An Bras Dermatol. 2011;86:241-8 pubmed
    b>Vitiligo is considered the most frequent acquired hypomelanosis. Although its pathogenesis is uncertain, it is believed that autoimmune etiology is the most plausible...
  43. Boissy R, Nordlund J. Vitiligo: current medical and scientific understanding. G Ital Dermatol Venereol. 2011;146:69-75 pubmed
    b>Vitiligo is a relatively common acquired skin depigmentary disease with a complex presentation, therapy, and etiology. Both the prognosis and therapeutic response for patients with vitiligo is unpredictable...
  44. Wang C, Cruz Inigo A, Fuentes Duculan J, Moussai D, Gulati N, Sullivan Whalen M, et al. Th17 cells and activated dendritic cells are increased in vitiligo lesions. PLoS ONE. 2011;6:e18907 pubmed publisher
    b>Vitiligo is a common skin disorder, characterized by progressive skin de-pigmentation due to the loss of cutaneous melanocytes...
  45. Levandowski C, Mailloux C, Ferrara T, Gowan K, Ben S, Jin Y, et al. NLRP1 haplotypes associated with vitiligo and autoimmunity increase interleukin-1? processing via the NLRP1 inflammasome. Proc Natl Acad Sci U S A. 2013;110:2952-6 pubmed publisher
    ..NLRP1 is genetically associated with risk of several autoimmune diseases including generalized vitiligo, Addison disease, type 1 diabetes, rheumatoid arthritis, and others...
  46. Seif El Nasr H, Shaker O, Fawzi M, El Hanafi G. Basic fibroblast growth factor and tumour necrosis factor alpha in vitiligo and other hypopigmented disorders: suggestive possible therapeutic targets. J Eur Acad Dermatol Venereol. 2013;27:103-8 pubmed publisher
    ..of basic fibroblast growth factor (bFGF) and tumour necrosis factor alpha (TNF-?) mRNA levels in lesional skin of vitiligo, hypopigmented mycosis fungoides and hypopigmented tinea versicolor...
  47. Rätsep R, Kingo K, Karelson M, Reimann E, Raud K, Silm H, et al. Gene expression study of IL10 family genes in vitiligo skin biopsies, peripheral blood mononuclear cells and sera. Br J Dermatol. 2008;159:1275-81 pubmed publisher
    b>Vitiligo is a pigmentation disorder, the cause of which is complex and not yet fully understood...
  48. Abanmi A, Al Harthi F, Al Baqami R, Al Assaf S, Zouman A, Arfin M, et al. Association of HLA loci alleles and antigens in Saudi patients with vitiligo. Arch Dermatol Res. 2006;298:347-52 pubmed
    ..b>Vitiligo, a commonly acquired dermatological disorder, has been associated with different HLA antigens in different ethnic ..
  49. Soylu S, Gul U, Gonul M, Kilic A, Cakmak S, Demiriz M. An uncommon presentation of the co-existence of morphea and vitiligo in a patient with chronic hepatitis B virus infection: is there a possible association with autoimmunity?. Am J Clin Dermatol. 2009;10:336-8 pubmed publisher
    ..The patient had also had vitiligo for 3.5 years, and hepatitis B virus (HBV) infection and cirrhosis for a 2-year period...
  50. Canton I, Akhtar S, Gavalas N, Gawkrodger D, Blomhoff A, Watson P, et al. A single-nucleotide polymorphism in the gene encoding lymphoid protein tyrosine phosphatase (PTPN22) confers susceptibility to generalised vitiligo. Genes Immun. 2005;6:584-7 pubmed
    b>Vitiligo is an acquired hypomelanotic skin disorder resulting from the loss of functional melanocytes from the cutaneous epidermis and autoimmunity has been suggested to play a part in its pathogenesis...
  51. Gavalas N, Gottumukkala R, Gawkrodger D, Watson P, Weetman A, Kemp E. Mapping of melanin-concentrating hormone receptor 1 B cell epitopes predicts two major binding sites for vitiligo patient autoantibodies. Exp Dermatol. 2009;18:454-63 pubmed publisher
    The melanin-concentrating hormone receptor 1 (MCHR1) has been identified as a B cell autoantigen in vitiligo with antibodies to the receptor detectable in binding and function-blocking assays...
  52. Tsuboi H, Yonemoto K, Katsuoka K. Vitiligo with inflammatory raised borders with hepatitis C virus infection. J Dermatol. 2006;33:577-8 pubmed
  53. Tavares Bello R. Capecitabine-induced hand-foot syndrome and cutaneous hyperpigmentation in an elderly vitiligo patient. J Eur Acad Dermatol Venereol. 2007;21:1434-5 pubmed