Segmental vitiligo after infliximab use for rheumatoid arthritis - A case report

Carvalho, Clarissa Luiza Dalla Bernardina; Ortigosa, Luciena Cegatto Martins

doi:10.1590/abd1806-4841.20142887

Cited by 18 publications

(15 citation statements)

References 11 publications

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“…There are also 18 reported patients who developed de novo vitiligo after initiating therapy with a TNF‐α antagonist for nonvitiligo conditions. Seven of these patients are detailed in case reports, with an additional eight patients in one case series and three reported in observational studies . In two observational studies looking at adverse cutaneous events that developed during TNF‐α antagonist treatment for rheumatological conditions, one of 5437 patients developed vitiligo in one study, and one of 435 patients developed vitiligo in another .…”

Section: Mixed Results For Tumour Necrosis Factor‐α Antagonists In Thmentioning

confidence: 99%

Tumour necrosis factor-α inhibition can stabilize disease in progressive vitiligo

et al. 2015

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TNF-α, a proinflammatory cytokine central to many autoimmune diseases, has been implicated in the depigmentation process in vitiligo. We reviewed its role in vitiligo by exploring its pro- and anti-inflammatory properties and examined the effects of blocking its actions with TNF-α antagonist therapeutics in reports available in the literature. We found that TNF-α inhibition halts disease progression in patients with progressive vitiligo but that, paradoxically, treatment can be associated with de novo vitiligo development in some patients when used to treat other autoimmune conditions, particularly when using adalimumab and infliximab. These studies reinforce the importance of stating appropriate outcomes measures as most pilot trials proposed to measure repigmentation, whereas halting depigmentation was commonly overlooked as a measure of success. We conclude that TNF inhibition was useful for patients with progressive vitiligo, where TNF-α inhibition is able to quash cytotoxic T cell-mediated melanocyte destruction. However, a lingering concern for initiating de novo disease will likely prevent a more widespread application of TNF inhibitors to treat vitiligo.

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Section: Mixed Results For Tumour Necrosis Factor‐α Antagonists In Thmentioning

confidence: 99%

Tumour necrosis factor-α inhibition can stabilize disease in progressive vitiligo

et al. 2015

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“…The role of TNF-α in the pathogenesis of vitiligo is less clear (30)(31)(32)(33); in the skin of vitiligo patients, TNF-α is produced by perilesional T cells and is involved in the development of cytotoxic T lymphocytes (34). However, treatment with TNF-α blocking agents, such as adalimumab and infliximab, can be paradoxically associated with de novo vitiligo development in patients with other autoimmune conditions (30)(31)(32)(33)35).…”

Section: Discussionmentioning

confidence: 99%

MHC class II super-enhancer increases surface expression of HLA-DR and HLA-DQ and affects cytokine production in autoimmune vitiligo

Cavalli

Hayashi

Jin

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Genetic risk for autoimmunity in HLA genes is most often attributed to structural specificity resulting in presentation of self-antigens. Autoimmune vitiligo is strongly associated with the MHC class II region. Here, we fine-map vitiligo MHC class II genetic risk to three SNPs only 47 bp apart, located within a predicted super-enhancer in an intergenic region between HLA-DRB1 and HLA-DQA1, localized by a genomewide association study of 2,853 Caucasian vitiligo patients. The superenhancer corresponds to an expression quantitative trait locus for expression of HLA-DR and HLA-DQ RNA; we observed elevated surface expression of HLA-DR (P = 0.008) and HLA-DQ (P = 0.02) on monocytes from healthy subjects homozygous for the high-risk SNP haplotype. Unexpectedly, pathogen-stimulated peripheral blood mononuclear cells from subjects homozygous for the high-risk super-enhancer haplotype exhibited greater increase in production of IFN-γ and IL-1β than cells from subjects homozygous for the low-risk haplotype. Specifically, production of IFN-γ on stimulation of dectin-1, mannose, and Toll-like receptors with Candida albicans and Staphylococcus epidermidis was 2.5-and 2.9-fold higher in high-risk subjects than in low-risk subjects, respectively (P = 0.007 and P = 0.01). Similarly, production of IL-1β was fivefold higher in high-risk subjects than in low-risk subjects (P = 0.02). Increased production of immunostimulatory cytokines in subjects carrying the high-risk haplotype may act as an "adjuvant" during the presentation of autoantigens, tying together genetic variation in the MHC with the development of autoimmunity. This study demonstrates that for risk of autoimmune vitiligo, expression level of HLA class II molecules is as or more important than antigen specificity.A utoimmune diseases are a group of over 80 disorders that together affect 3-5% of the United States population (1, 2). Many autoimmune diseases are associated with genetic variation in the HLA class I and class II gene regions of the major histocompatibility complex (MHC) on chromosome 6p21.3. HLA class I molecules present peptide antigens on the surface of almost all cells, whereas HLA class II molecules present antigens on the surface of antigen-presenting cells, such as dendritic cells, mononuclear phagocytes, and B cells. Contributions of HLA molecules to autoimmunity have almost exclusively focused on antigenic diversity and specificity. Although polymorphisms in intergenic regions of the MHC might additionally affect the complex transcriptional regulation of HLA genes, the potential role of these noncoding regions in the pathogenesis of autoimmune diseases has received much less attention.Vitiligo is an autoimmune disease in which white spots of skin and overlying hair result from progressive destruction of melanocytes by autoreactive T cells (3). In previous genome-wide association studies of autoimmune vitiligo in European-derived Caucasian (EUR) populations, we have identified association with 27 different loci (4-6), most strongly with MHC class II r...

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“…The ANA prevalence in the normal population varies greatly between reports, but is generally < 5% . ANA could be a serological hallmark of patients with cutaneous and systemic autoimmune disease . Detection can also provide further diagnostic and prognostic data for patients who have minimal symptoms or who have clinical features of more than one autoimmune disease .…”

Section: Discussionmentioning

confidence: 99%

“…18 ANA could be a serological hallmark of patients with cutaneous and systemic autoimmune disease. 19 Detection can also provide further diagnostic and prognostic data for patients who have minimal symptoms or who have clinical features of more than one autoimmune disease. 20 The higher positivity rate of this autoantibody in both NSV and SV compared with the normal population supports the autoimmune background of vitiligo.…”

Section: Discussionmentioning

confidence: 99%

Positivity rates of antithyroid antibody, antinuclear antibody and thyroid peroxidase antibody in different types of vitiligo

et al. 2015

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Segmental vitiligo after infliximab use for rheumatoid arthritis - A case report

Cited by 18 publications

References 11 publications

Tumour necrosis factor-α inhibition can stabilize disease in progressive vitiligo

Tumour necrosis factor-α inhibition can stabilize disease in progressive vitiligo

MHC class II super-enhancer increases surface expression of HLA-DR and HLA-DQ and affects cytokine production in autoimmune vitiligo

Positivity rates of antithyroid antibody, antinuclear antibody and thyroid peroxidase antibody in different types of vitiligo

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