Infliximab-induced autoantibodies: a multicenter study

Vaz, João Luiz Pereira; Fernandes, Vander; Nogueira, Felipe; Arnóbio, Adriano; Levy, Roger A.

doi:10.1007/s10067-015-3140-6

Cited by 24 publications

(13 citation statements)

References 22 publications

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“…IFX is a chimeric anti-human TNF monoclonal antibody [124] use to treat autoimmune diseases [125]. In rheumatoid arthritis patients, IFX lowers circulating TNF levels and improves sleep [126].…”

Section: Sleep/wake Effects Of Prescribed Tnf-active Substancesmentioning

confidence: 99%

Tumor necrosis factor alpha in sleep regulation

Rockstrom

Chen

Taishi

et al. 2018

Sleep Medicine Reviews

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This review details tumor necrosis factor alpha (TNF) biology and its role in sleep, and describes how TNF medications influence sleep/wake activity. Substantial evidence from healthy young animals indicates acute enhancement or inhibition of endogenous brain TNF respectively promotes and inhibits sleep. In contrast, the role of TNF in sleep in most human studies involves pathological conditions associated with chronic elevations of systemic TNF and disrupted sleep. Normalization of TNF levels in such patients improves sleep. A few studies involving normal healthy humans and their TNF levels and sleep are consistent with the animal studies but are necessarily more limited in scope. TNF can act on established sleep regulatory circuits to promote sleep and on the cortex within small networks, such as cortical columns, to induce sleep-like states. TNF affects multiple synaptic functions, e.g., its role in synaptic scaling is firmly established. The TNF-plasticity actions, like its role in sleep, can be local network events suggesting that sleep and plasticity share biochemical regulatory mechanisms and thus may be inseparable from each other. We conclude that TNF is involved in sleep regulation acting within an extensive tightly orchestrated biochemical network to niche-adapt sleep in health and disease.

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Section: Sleep/wake Effects Of Prescribed Tnf-active Substancesmentioning

confidence: 99%

Tumor necrosis factor alpha in sleep regulation

Rockstrom

Chen

Taishi

et al. 2018

Sleep Medicine Reviews

View full text Add to dashboard Cite

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“…One patient developed drug-induced lupus erythematosus. Vaz et al 38 reported in a multicenter study that infliximab for various diseases induced a significant increase in the number of patients with antinuclear antibody and anti-dsDNA. Momen et al 39 recently reviewed 80 patients who developed TNF-a inhibitor-induced lupus.…”

Section: Lupusmentioning

confidence: 99%

Safety of biologics in psoriasis

Kamata

Tada

2017

The Journal of Dermatology

107

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The advent of biologics brought a paradigm shift in ways to treat psoriatic patients because they have dramatic efficacy. At the same time, safety concerns about biologics have been raised. In this paper, we focus on the safety profile of biologics for psoriasis. As of 2017, six biologics are available in Japan. Two tumor necrosis factor-a inhibitors; infliximab and adalimumab, one anti-interleukin (IL)-12/23p40 antibody; ustekinumab, and IL-17 inhibitors; secukinumab, ixekizumab and brodalumab. Secukinumab and ixekizumab are anti-IL-17A antibodies. Brodalumab is an anti-IL17RA antibody. In this review, we pick up topics which have drawn attention regarding the safety of biologics and discuss them with recent published work.

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“…However, tumour necrosis factor (TNF)‐α inhibitor therapy in severe lichenoid dermatitis resulting from cancer immunotherapy should be used with caution, as some of these cases may represent early‐stage autoimmune disease. TNF‐α inhibitors impact the formation of lupus autoantibodies and can induce or exacerbate cutaneous autoimmune disease . Treatment with infliximab may have perpetuated SCLE in our second patient and contributed to her positive serologies.…”

Section: Discussionmentioning

confidence: 78%

Subacute cutaneous lupus erythematosus and dermatomyositis associated with anti‐programmed cell death 1 therapy

et al. 2018

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Summary Programmed cell death 1 (PD‐1) blockade has rapidly emerged as an effective therapy for a wide variety of metastatic malignancies. It has been associated with multiple immune‐related adverse effects, including cutaneous eruptions. We describe two patients with clinical and histological findings that were consistent with subacute cutaneous lupus erythematosus (SCLE) after receiving PD‐1 inhibitor therapy for metastatic lung cancer. We successfully treated our first patient with systemic and topical steroids, photoprotection and hydroxychloroquine. However, he subsequently developed dermatomyositis after continuing PD‐1 inhibitor therapy. Our second patient presented with a protracted course of a cutaneous eruption in spite of discontinuation of anti‐PD‐1 therapy and treatment with systemic corticosteroids and infliximab. This patient's SCLE resolved after the addition of topical steroids and photoprotection and discontinuation of anti‐tumour necrosis factor therapy. She and her oncology team decided to pursue non‐PD‐1 inhibitor treatment for lung cancer owing to a lack of tumour response. We add SCLE and dermatomyositis to the growing list of autoimmune complications of PD‐1 blockade. Our cases raise a number of questions, particularly in relation to the viability of continuing anti‐PD‐1 therapy after developing SCLE and the role of immunosuppressive therapy in patients with PD‐1 inhibitor‐associated connective tissue disease. What's already known about this topic? Programmed cell death 1 (PD‐1) blockade, which is rapidly emerging as a therapy for a wide variety of metastatic malignancies, has been associated with multiple immune‐related adverse effects. These include systemic autoimmune diseases such as colitis and thyroiditis in addition to numerous cutaneous adverse events. Cutaneous side‐effects of PD‐1 inhibitors most commonly reported in clinical trials include lichenoid reactions, eczematous dermatitis and vitiligo. What does this study add? We report two cases of PD‐1 inhibitor‐associated subacute cutaneous lupus erythematosus (SCLE), with one patient progressing to dermatomyositis with continued PD‐1 inhibitor treatment. In addition to being a novel cutaneous adverse event, we also demonstrate the possibility of development of multiple autoimmune diseases in one patient, which is different from classic drug‐related SCLE. We discuss the treatment challenges for patients with autoimmune skin disease receiving PD‐1 inhibitor therapy.

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Infliximab-induced autoantibodies: a multicenter study

Cited by 24 publications

References 22 publications

Tumor necrosis factor alpha in sleep regulation

Tumor necrosis factor alpha in sleep regulation

Safety of biologics in psoriasis

Subacute cutaneous lupus erythematosus and dermatomyositis associated with anti‐programmed cell death 1 therapy

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