Physiopathology and genetics of vitiligo

Passeron, Thierry; Ortonne, Jean‐Paul

doi:10.1016/j.jaut.2005.10.001

Cited by 135 publications

(118 citation statements)

References 53 publications

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“…As vitiligo may be a cytotoxic T lymphocyte-mediated autoimmune disease, it is likely that imiquimod could contribute to the elimination of melanocytes by inducing acquired immunity through the induction of cytokines [16]. This mechanism may be comparable with interferon-induced vitiligo cases [18]. However, localized nature of the depigmentation to the site of application with imiquimod suggests that imiquimod may have direct eVects on melanocytes.…”

Section: Introductionmentioning

confidence: 99%

Imiquimod induces apoptosis of human melanocytes

et al. 2009

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Development of vitiligo-like hypopigmentary lesions associated with topical imiquimod has been reported. We hypothesized that mode of action of imiquimod in melanocytes may include triggering of apoptosis resulted in loss of cells, which may be a possible mechanism of imiquimod-induced hypopigmentary lesions. Therefore, we investigated whether imiquimod induces apoptosis of human melanocytes and also whether it modulates expression of apoptosis-related molecules in human melanocytes. Imiquimod treatment induced apoptosis of melanocytes, which was observed by TUNEL assay and Hoechst 33258 staining. Imiquimod-induced apoptosis was further shown by measuring mitochondrial membrane potential in melanocytes. The apoptotic activity of imiquimod was associated with caspase-3, Bcl-2 and mitogenactivated protein kinase expression in melanocytes. These results indicated that imiquimod induces apoptosis of melanocytes. These Wndings may provide a clue to understand pathogenesis of imiquimod-induced vitiligo-like hypopigmentary lesions.

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Section: Introductionmentioning

confidence: 99%

Imiquimod induces apoptosis of human melanocytes

et al. 2009

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“…There are several hypotheses explaining the development of different components of APS III [1,[10][11][12][13][14][15][16]. The most widely accepted is the autoimmune genetic hypothesis, assuming involvement of genes associated with immune regulation [17].…”

Section: Discussionmentioning

confidence: 99%

Przypadek pokrzywki autoimmunologicznej współistniejącej z autoimmunologicznym zespołem wielogruczołowym typu III związanym z chorobą Hashimoto, cukrzycą typu 1 i bielactwem

Kasznicki¹,

Drzewoski²

2014

Endokrynologia Polska

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We present a case of autoimmune polyglandular syndrome type III (APS III) associated with Hashimoto's disease, type 1 diabetes mellitus, vitiligo and autoimmune urticaria. This rare genetic disorder occurs with unknown frequency in the Polish population. It is characterised by endocrine tissue destruction resulting in the malfunction of multiple organs. Several cases of APS III associated with organ-specific autoimmune diseases such as coeliac disease, hypogonadism and myasthenia gravis, as well as organ-nonspecific or systemic autoimmune diseases such as sarcoidosis, Sjögren syndrome, and rheumatoid arthritis have been described. To the best of our knowledge, we here describe the first case of APS III associated with autoimmune thyroiditis, type 1 diabetes mellitus, vitiligo and autoimmune urticaria in an adult patient.

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“…The pathogenesis of melanocyte loss in vitiligo is not completely understood but an autoimmune reaction against melanocytes is likely involved [5,6]. Several mechanisms have been suggested to explain how HIV-induced immunodeficiency can result in vitiligo [1].…”

Section: Commentmentioning

confidence: 99%

HIV-Associated Vitiligo Totalis with Minimal Repigmentation and Alopecia Areata Diffusa During Immune-Reconstitution

Sack¹,

Rojhirunsakool²,

Bhawan³

et al. 2008

TODJ

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Abstract:Background: Cutaneous findings in the setting of HIV infection encompass a broad spectrum of diseases. Only few cases of vitiligo or alopecia areata have been described in HIV/AIDS patients and it remains unclear whether there is a causal relationship between HIV/AIDS and these two conditions.Observations: Our patient initially presented with diffuse generalized pruritic hypo-and depigmented macules and patches. She was diagnosed with advanced HIV/AIDS at that time. There was progression to vitiligo totalis followed by partial repigmentation and generalized alopecia areata diffusa with immune-reconstitution.Conclusions: This is, to our knowledge, the first case of rapidly progressing vitiligo totalis in a patient with advanced HIV/AIDS. We conclude that this, together with the observation of repigmentation during immune-reconstitution, suggests a causal relation between vitiligo and HIV/AIDS. The different time course of the also observed alopecia areata diffusa, with first manifestation during immune-reconstitution, may be due to differences in the immune-pathogenesis between vitiligo and alopecia areata. CASE REPORTA 50-year-old Haitian female presented with a two month history of a progressive eruption of symmetric pruritic ill-defined hypo-and depigmented macules and patches. The eruption had begun on the face and later involved the trunk and upper and lower extremities. There was no known family history of vitiligo or other autoimmune diseases. A punch biopsy from the right arm showed reduced epidermal melanin, focal lymphocytic exocytosis, absence of melanocytes (confirmed by lack of staining with Mel-5), a sparse superficial perivascular lymphocytic infiltrate and melanophages; findings consistent with vitiligo. Topical corticosteroid therapy was supplemented with narrow-band UVB phototherapy. This combination effectively controlled the pruritus but, despite a six month three times weekly course, did not halt the progressive pigment loss. The patient was diagnosed with HIV/AIDS (Initial CD4+ cells 11/mm 3 ; viral load 39313 copies/ml). Post initiation of HAART (Emtricitabine/Tenofovir, Efavirenz), with subsequent rising number of CD4+ cells and falling HIV viral load, she continued to rapidly depigment and was completely depigmented within five months (Fig. 1). With recovery of CD4 counts to 161/mm 3 , small foci of repigmentation were noted (Fig. 2) and, with continued improvement of CD4 counts up to 300/mm 3 , additional macular repigmentation was evident. This repigmentation developed over eight months and involved the posterior upper arms, left shin and inner thighs.*Address correspondence to this author at the Sudbury Skin Clinic, 885 Regent Street, Suite 300, Sudbury, ON P3E 5M4, Canada; Tel: 705 669 0002; Fax: 705 669 1771; E-mail : jasonsack55@hotmail.com Nevertheless, repigmentation was minimal, involving less than 1 % of the total body surface area. Despite the enormous psychological impact vitiligo presents for most patients, our patient is happy with her "new skin color" and wishes no...

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Physiopathology and genetics of vitiligo

Cited by 135 publications

References 53 publications

Imiquimod induces apoptosis of human melanocytes

Imiquimod induces apoptosis of human melanocytes

Przypadek pokrzywki autoimmunologicznej współistniejącej z autoimmunologicznym zespołem wielogruczołowym typu III związanym z chorobą Hashimoto, cukrzycą typu 1 i bielactwem

HIV-Associated Vitiligo Totalis with Minimal Repigmentation and Alopecia Areata Diffusa During Immune-Reconstitution

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