Etanercept in the Treatment of Vitiligo

Rigopoulos, Dimitrios; Gregoriou, Stamatis; Larios, George; Moustou, E; Belayeva-Karatza, Elena; Kalogeromitros, D.

doi:10.1159/000102044

Cited by 38 publications

(26 citation statements)

References 12 publications

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“…TNF-α has been shown to inhibit melanogenesis and promote melanocyte apoptosis (Swope et al, 1991;Kim et al, 2007). Cases of vitiligo treated with TNF-α inhibitors, although achieving mixed results, have been reported as well (Rigopoulos et al, 2007;Campanati et al, 2010). A recent study has shown that the anti-TNF-α agent etanercept can stop vitiligo progression and induce repigmentation in some cases (Kim et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with vitiligo

Al-Harthi

Zouman²,

Arfin³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Vitiligo is an acquired depigmentary disorder of the skin, characterized by multiple susceptibility loci and genetic heterogeneity. The etiology of vitiligo is unknown but several hypotheses, including an autoimmune origin, have been proposed. Tumor necrosis factor (TNF)-α, a pleiotropic proinflammatory cytokine, has been shown to play a critical role in several autoimmune diseases including vitiligo. The aim of present study was to determine the association of TNF-α and -β gene polymorphisms with vitiligo in Saudi patients. TNF-α and -β genes were amplified in 123 Saudi patients and 200 matched controls using polymerase chain reaction to search for polymorphisms involved at positions -308, and intron 1 +252. The frequency of the TNF-α (-308) GA genotype was higher and the frequencies of the GG and AA genotypes were significantly lower in vitiligo patients compared to controls. These findings suggested that genotype GA-positive individuals at position -308 of TNF-α are susceptible to vitiligo, whereas the GG and AA genotypes might exert a protective effect. The frequency of allele A (TNF-α 2-allele) was significantly higher and that of allele G (TNF-α 1-allele) was lower in vitiligo patients compared to controls, indicating an association of allele A with susceptibility to TNF-α and -β polymorphisms in vitiligo vitiligo in Saudi patients. The results of our examination of TNF-β (intron 1 +252) polymorphisms showed a significant increase in the frequency of the GG genotype and allele G (TNF-b 1-allele) in vitiligo patients, suggesting a susceptibility of the GG genotype and allele G for vitiligo. By contrast, the high frequency of the GA genotype in controls might indicate a protective effect. The results of the present study strongly support a link between TNF-α (-308) and -β (intron 1 +252) polymorphisms and vitiligo in Saudi patients.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with vitiligo

Al-Harthi

Zouman²,

Arfin³

et al. 2013

Genet. Mol. Res.

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“…Elevated levels of TNF-α and IL-6 have been found in vitiligo skin when compared to adjacent uninvolved skin [18,19,20,21]. Acute GVHD appeared to be induced by a synergistic interaction of IL-6, γ-interferon and TNF-α.…”

Section: Discussionmentioning

confidence: 99%

Vitiligo after Hematopoietic Cell Transplantation: Six Cases and Review of the Literature

et al. 2008

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Aim: To investigate the prevalence and clinical characteristics of vitiligo after allogeneic hematopoietic cell transplantation (AHCT). Methods: The development of vitiligo was analyzed among 421 patients who underwent AHCT in Ibni Sina Hospital (University of Ankara) between 1988 and 2004. Results: Among 421 patients, we describe 6 with generalized vitiligo occurring after AHCT for chronic myelogenous leukemia. Five of them had severe chronic graft-versus-host disease (GVHD). Vitiligo was accompanied by alopecia areata and acquired ichthyosis in 2 patients with GVHD. Conclusion: Melanocyte destruction caused by the autoimmune reactions triggered by chronic GVHD as well as a genetic predisposition might have played a role in the development of vitiligo in our patients. These data support the hypothesis that vitiligo is an autoimmune entity.

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“…An association between vitiligo and spondyloarthropathies has been described [2]. In addition, a preliminary study suggested that anti-TNF-α blocking could be a potential alternative in treating vitiligo [3]. Here we describe the effect of infliximab on vitiligo in a patient with AS.…”

Section: Introductionmentioning

confidence: 87%

Vitiligo Improvement in a Patient with Ankylosing Spondylitis Treated with Infliximab

Simón¹,

Burgos‐Vargas

2008

Dermatology

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Ankylosing spondylitis (AS) is a disabling disease affecting the enthesis and joints of the spine and peripheral sites. Tumour necrosis factor α (TNF-α) is a proinflammatory mediator which plays a significant role in the pathogenesis of AS. Infliximab (a chimeric monoclonal antibody which blocks the activity of TNF-α) is one of the most effective therapies of AS thus far. Vitiligo is a depigmenting disorder of the skin of unknown aetiology affecting 0.5–1% of the population. Here we describe the effect of infliximab on vitiligo in a patient with AS.

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Etanercept in the Treatment of Vitiligo

Cited by 38 publications

References 12 publications

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with vitiligo

Tumor necrosis factor-α and -β genetic polymorphisms as a risk factor in Saudi patients with vitiligo

Vitiligo after Hematopoietic Cell Transplantation: Six Cases and Review of the Literature

Vitiligo Improvement in a Patient with Ankylosing Spondylitis Treated with Infliximab

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