Demyelination and other neurological adverse events after anti-TNF therapy

Kaltsonoudis, Evripidis; Voulgari, Paraskevi V.; Konitsiotis, Spyridon; Drosos, Alexandros A.

doi:10.1016/j.autrev.2013.09.002

Cited by 162 publications

(107 citation statements)

References 51 publications

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“…As anti-TNF agents used in systemic autoimmune diseases are not specific for TNFR1, their administration could, indeed, induce such phenomenology. Overall, in patients with a history of MS, CIDP, or other demyelinating diseases, TNF inhibitors should be avoided, and patients receiving these agents should be closely monitored for the onset of neurological manifestations [198]. In our clinic, we have seen and followed 2 patients who developed multiple mononeuritis multiplex and CIDP after anti-TNF inhibitors requiring treatment with IVIg and rituximab.…”

Section: Cns and Pns Demyelination Caused By Anti-tnf Agentsmentioning

confidence: 99%

Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity

et al. 2016

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Neurological involvement is relatively common in the majority of systemic autoimmune diseases and may lead to severe morbidity and mortality, if not promptly treated. Treatment options vary greatly, depending on the underlying systemic pathophysiology and the associated neurological symptoms. Selecting the appropriate therapeutic scheme is further complicated by the lack of definite therapeutic guidelines, the necessity to differentiate primary neurological syndromes from those related to the underlying systemic disease, and to sort out adverse neurological manifestations caused by immunosuppressants or the biological agents used to treat the primary disease. Immunotherapy is a sine qua non for treating most, if not all, neurological conditions presenting in the context of systemic autoimmunity. Specific agents include classical immune modulators such as corticosteroids, cyclophosphamide, intravenous immunoglobulin, and plasma exchange, as well as numerous biological therapies, for example antitumor necrosis factor agents and monoclonal antibodies that target various immune pathways such as B cells, cytokines, and co-stimulatory molecules. However, experience regarding the use of these agents in neurological complications of systemic diseases is mainly empirical or based on small uncontrolled studies and case series. The aim of this review is to present the state-of-the-art therapies applied in various neurological manifestations encountered in the context of systemic autoimmune diseases; evaluate all treatment options on the basis of existing guidelines; and compliment these data with our personal experience derived from a large number of patients.

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Section: Cns and Pns Demyelination Caused By Anti-tnf Agentsmentioning

confidence: 99%

Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity

et al. 2016

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“…TNF blockade may also offer a potential avenue for the treatment of acute neuromyelitis optica (NMO) and/or NMO spectrum disorders (NMOSD) [5]. However, the use of currently available anti-TNF therapeutics is limited by their association with new onset or exacerbation of neuroinflammatory demyelinating disorders, including multiple sclerosis (MS), optic neuritis (ON), and acute transverse myelitis [2]. The precise mechanisms that predispose patients who receive anti-TNF treatment to benefit or increase risk of central nervous system (CNS) demyelination are not well-understood, but several theories have been proposed.…”

Section: Sex; Microbiomementioning

confidence: 99%

“…Tumor necrosis factor-α (TNF), a double-edged sword with both pro-inflammatory and anti-inflammatory properties, is one of the most widespread clinically targeted cytokines [1][2][3][4]. Anti-TNF therapies, such as infliximab, adalimumab, golimumab, and certolizumab, are central to the treatment of several autoimmune diseases, including rheumatoid arthritis (RA), inflammatory bowel disease (IBD), ankylosing spondylitis (SpA), and psoriasis.…”

Section: Sex; Microbiomementioning

confidence: 99%

TNF Blockade, CNS Autoimmunity, Sex, and the Microbiome

Cm¹,

Em²

2016

J Mult Scler

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“…Anti-TNFα antibodies (e.g. etanercept and infliximab) have been reported to induce central nervous system (CNS) demyelination or worsen the preexisting demyelinating disease [Kaltsonoudis et al 2014]. These monoclonal antibodies can induce a drug-induced lupus syndrome with clinical and laboratory features different from traditional druginduced lupus, including a higher incidence of rash, anti-DNA antibodies, leukopenia and thrombocytopenia, and a lower incidence of antihistone antibodies [Chang and Gershwin, 2011].…”

Section: Isoniazid and Autoimmunitymentioning

confidence: 99%

Isoniazid in autoimmunity: a trigger for multiple sclerosis?

Nourbakhsh

Stüve

2014

Ther Adv Neurol Disord

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Isoniazid (INH) is a prodrug activated by the mycobacterial enzyme KatG, a multifunctional catalase peroxidase. KatG converts INH to reactive antimycobacterial species. For decades, an association between INH and drug-induced lupus erythematosus has been recognized. We present the case of a patient with primary progressive multiple sclerosis whose disease commenced weeks after initiating INH therapy for prevention of tuberculosis. Possible mechanisms by which INH may trigger autoimmunity in humans are discussed.

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Demyelination and other neurological adverse events after anti-TNF therapy

Cited by 162 publications

References 51 publications

Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity

Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity

TNF Blockade, CNS Autoimmunity, Sex, and the Microbiome

Isoniazid in autoimmunity: a trigger for multiple sclerosis?

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