Vitiligo Vulgaris

Nordlund, James J.; Caroline, I.; Boissy, Raymond E.

doi:10.1007/978-1-84800-165-7_38

Cited by 27 publications

(39 citation statements)

References 300 publications

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“…Melanocyte loss in generalized vitiligo occurs primarily on an autoimmune basis (7,(30)(31)(32), although the triggers of the autoimmune response remain unknown. Many patients have circulating antibodies to various melanocyte components, most frequently tyrosinase (33), the key enzyme of melanin biosynthesis (34), as well as circulating skin-homing melanocytespecific cytotoxic T-lymphocytes (35).…”

Section: Epidemiology Of Generalized Vitiligo and Associated Autoimmumentioning

confidence: 99%

“…The most prevalent are the autoimmune thyroid diseases (AITD), principally Hashimoto's disease and Graves' disease (2)(3)(4), characterized by infiltration of the thyroid by thyroid-reactive T and B cells and by the production of thyroid autoantibodies (5,6). Perhaps the most recognizable autoimmune disease is generalized vitiligo, with descriptions of its visually striking clinical manifestations dating back several millennia (7).…”

Section: Introductionmentioning

confidence: 99%

“…Generalized vitiligo is characterized clinically by acquired patches of white skin and overlying hair, usually multifocal and often bilateral (7,8) (Fig. 1), resulting from progressive autoimmune loss of melanocytes from the involved areas.…”

Section: Introductionmentioning

confidence: 99%

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Shared Genetic Relationships Underlying Generalized Vitiligo and Autoimmune Thyroid Disease

Spritz

2010

Thyroid

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Section: Epidemiology Of Generalized Vitiligo and Associated Autoimmumentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Shared Genetic Relationships Underlying Generalized Vitiligo and Autoimmune Thyroid Disease

Spritz

2010

Thyroid

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“…The time lag between improvement in MG and improvement in vitiligo may have led to the erroneous conclusion that treatment has no effect on vitiligo. As the patient had a family history of vitiligo vulgaris, the immunological factors associated with MG may have had a strong impact on the genetic factors involved in the autoimmune melanocyte destruction 3. In other words, if melanocyte destruction was accelerated by the exacerbation of MG due to thymoma enlargement, it can be assumed that treatment of MG through the removal of the thymoma and steroid administration led to the deceleration of melanocyte destruction.…”

Section: Discussionmentioning

confidence: 99%

“…A number of aetiologic hypotheses are suggested for vitiligo, which is caused by the destruction of melanocytes. One such hypothesis assumes that environmental, genetic, and immunological factors affect melanocyte destruction induced via an autoimmune mechanism 3. The condition is known to have a genetic aspect, with 20% of the patients with the condition having a family history 4…”

Section: Introductionmentioning

confidence: 99%

A case of vitiligo vulgaris showing a pronounced improvement after treatment for myasthenia gravis

Nakamagoe

Furuta²,

Shioya³

et al. 2009

Case Reports

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This is a report of a 64 year-old male patient whose myasthenia gravis (MG) was accompanied by vitiligo vulgaris. Depigmentation of the face, trunk, and hands was noted. He was diagnosed with vitiligo vulgaris according to macroscopic findings and a skin biopsy. He was also found to have blepharoptosis, and proximal dominant muscle weakness of the extremities. He was anti-acetylcholine receptor antibody-positive, with repetitive nerve stimulation showing a waning phenomenon and chest computed tomography showing invasive thymoma, which led to the diagnosis of generalised MG. His myasthenic symptoms were relieved by the use of steroids and the removal of the thymoma. His vitiligo vulgaris began to improve a month after the relief of myasthenic symptoms. Such improvement was pronounced during the next several months. The clinical or immunological relationship between MG and vitiligo vulgaris is still not known, but these findings might indicate clinical correlation between MG and vitiligo vulgaris.

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Mechanisms underlying the dysfunction of melanocytes in vitiligo epidermis: role of SCF/KIT protein interactions and the downstream effector, MITF‐M

Kitamura

Tsukamoto

Harada

et al. 2004

The Journal of Pathology

117

118

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Little is known about the mechanisms involved in the dysfunction of melanocytes in vitiligo epidermis. It is hypothesized that some cytokine/receptor interactions may be affected, resulting in dysfunction and/or loss of melanocytes. This study has compared the expression of endothelin (ET)-1, the ET-1 receptor (ET(B)R), granulocyte macrophage colony stimulating factor (GM-CSF), stem cell factor (SCF), the SCF receptor (KIT protein), tyrosinase, and S100 alpha between lesional and non-lesional vitiligo epidermis. Analysis by reverse transcription-polymerase chain reaction (RT-PCR) and by western blotting for ET-1 and SCF unexpectedly demonstrated up-regulated expression of these cytokines in lesional vitiligo epidermis. Immunohistochemistry with antibodies to melanocyte markers revealed that at the edge of the lesional epidermis, melanocytes remain and express tyrosinase, S100 alpha and ET(B)R, but not KIT protein or melanocyte-specific microphthalmia-associated transcription factor (MITF-M). Quantitation of the staining revealed a slight or moderate decrease in the number of S100 alpha, tyrosinase, and ET(B)R-positive cells at the edge of the lesional epidermis. In contrast, the number of cells expressing KIT protein was markedly decreased at the edge of the lesional epidermis compared with the non-lesional epidermis. At the centre of the lesional epidermis, there was complete loss of melanocytes expressing KIT protein, S100 alpha, ET(B)R, and/or tyrosinase. Western blotting revealed down-regulated expression of c-kit and MITF-M proteins at the edge of the lesional epidermis in vitiligo. These findings suggest that reduction in the expression of KIT protein by melanocytes and its downstream effectors, including MITF-M, may be associated with the dysfunction and/or loss of melanocytes in vitiligo epidermis.

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Vitiligo Vulgaris

Cited by 27 publications

References 300 publications

Shared Genetic Relationships Underlying Generalized Vitiligo and Autoimmune Thyroid Disease

Shared Genetic Relationships Underlying Generalized Vitiligo and Autoimmune Thyroid Disease

A case of vitiligo vulgaris showing a pronounced improvement after treatment for myasthenia gravis

Mechanisms underlying the dysfunction of melanocytes in vitiligo epidermis: role of SCF/KIT protein interactions and the downstream effector, MITF‐M

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