Vasculitis, Vitiligo, Thyroiditis, and Altered Hormone Levels After Anti-Tumor Necrosis Factor Therapy

Lahita, Robert G.; Vernace, Melchiore A.

doi:10.3899/jrheum.100968

Cited by 20 publications

(8 citation statements)

References 9 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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“…It is demonstrated for the first time, in the segmental form and nationwide, in this report. 3,4,5,6,9 …”

Section: Introductionmentioning

confidence: 99%

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

Carvalho

Ortigosa

2014

An. Bras. Dermatol.

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The tumor necrosis factor alpha is a cytokine related to immune and inflammatory processes by acting on different parts of the body. It is secreted by several cell types including macrophages, lymphocytes, monocytes, neutrophils, dendritic cells, among others. Infliximab is a chimeric monoclonal antibody that specifically binds to soluble and transmembrane tumor necrosis factor alpha form blocking its action. In rheumatoid arthritis it is used because the cytokines that cause inflammation in this disease are regulated by tumor necrosis factor alpha and IL-1. We report the case of a 46-year-old patient with rheumatoid arthritis who developed segmental vitiligo after two months using infliximab. The event aims to alert to the existence of this adverse effect that can be induced with the use of this medication.

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“…[39][40][41][42] Recently, the incidence rate of newly developed vitiligo was shown to be significantly elevated in patients receiving anti-TNF therapy compared with those treated with conventional medications. There has been an increasing number of cases in which patients exhibit newly onset vitiligo and vitiligo progression following anti-TNF therapy.…”

Section: Discussionmentioning

confidence: 99%

“…There has been an increasing number of cases in which patients exhibit newly onset vitiligo and vitiligo progression following anti-TNF therapy. [39][40][41][42] Recently, the incidence rate of newly developed vitiligo was shown to be significantly elevated in patients receiving anti-TNF therapy compared with those treated with conventional medications. [43] Although the pathophysiology is not clarified, anti-TNF therapy may facilitate vitiligo pathogenesis by reversing TNF-α-mediated inhibitory effects on Fas-mediated melanocyte apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Fas‐FasL interaction in cytotoxic T cell‐mediated vitiligo: The role of lesional expression of tumor necrosis factor‐α and interferon‐γ in Fas‐mediated melanocyte apoptosis

Jimbo

Nagai

Fujiwara

et al. 2019

Experimental Dermatology

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Vitiligo is an acquired skin depigmentation disorder resulting from the selective loss of epidermal melanocytes, and previous studies have suggested that a T lymphocyte‐mediated mechanism has a role in melanocyte loss. Although Fas‐Fas ligand (FasL) interactions are important for T lymphocytes to mediate cytotoxicity, there are only few reports examining the involvement of the Fas‐FasL pathway in vitiligo using in vivo mouse models. In addition, there have been no reports concerning Fas‐mediated apoptosis in human melanocytes in vitro. In this study, we found that the Fas‐mediated pathway is involved in cytotoxic T lymphocyte (CTL)‐dependent vitiligo in a mouse model and FasL‐induced apoptosis of human melanocytes. Tumor necrosis factor (TNF)‐α and interferon (IFN)‐γ, the expression levels of which have been reported to be elevated in lesional skin of patients with vitiligo, synergistically upregulated Fas expression on human melanocytes but inhibited the Fas‐mediated apoptosis. Treatment with TNF‐α and IFN‐γ synergistically upregulated the expression of the anti‐apoptotic genes, c‐IAP2, c‐FLIP and MCL1. A siRNA knock‐down study showed that c‐FLIP and MCL1, but not c‐IAP2, were involved in inducing synergistic inhibitory effects on Fas‐mediated apoptosis. Furthermore, we found that FasL and TNF‐related apoptosis‐inducing ligand (TRAIL) synergistically induced apoptosis on human melanocytes. In conclusion, our results suggest that the Fas‐FasL pathway is involved in CTL‐dependent vitiligo and the elevated expression levels of TNF‐α and IFN‐γ in lesional skin may act synergistically on melanocytes to suppress Fas‐mediated apoptosis.

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Vasculitis, Vitiligo, Thyroiditis, and Altered Hormone Levels After Anti-Tumor Necrosis Factor Therapy

Cited by 20 publications

References 9 publications

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

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

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

Fas‐FasL interaction in cytotoxic T cell‐mediated vitiligo: The role of lesional expression of tumor necrosis factor‐α and interferon‐γ in Fas‐mediated melanocyte apoptosis

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