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Autoimmun Rev. 2014 Jan;13(1):54-8. doi: 10.1016/j.autrev.2013.09.002. Epub 2013 Sep 12.

Demyelination and other neurological adverse events after anti-TNF therapy.

Author information

1
Rheumatology Clinic, Department of Internal Medicine, Medical School, University of Ioannina, Ioannina, Greece.

Abstract

Tumor necrosis factor (TNF) α inhibitors are an essential therapeutic option for several inflammatory diseases, like rheumatoid arthritis, spondyloarthropathies and inflammatory bowel diseases. As TNFα antagonists have become increasingly utilized, there have been a number of reports of neurological adverse events in patients receiving anti-TNFα therapy. The frequency of central nervous system adverse events after initiation of anti-TNFα therapy is unknown. However, questions have been raised about a possible causal association. Although several hypotheses have been proposed in an attempt to explain the possible relationship between TNFα antagonist and demyelination, none is considered to be adequate. Thus, in this report we deal with the implication of TNFα in multiple sclerosis and we discuss the possible relationship of TNFα antagonist and demyelinating diseases.

KEYWORDS:

BBB; CNS; DMARDs; EAE; IL; INF-γ; MS; Multiple sclerosis; NOD; Neurological adverse events; RA; SpA; TACE; TNF receptor; TNFR1,2; TNFR2; TNFα; TNFα antagonists; TNFα converting enzyme; blood brain barrier; central nervous system; disease modifying anti-rheumatic drugs; experimental autoimmune encephalomyelitis; interferon γ; interleukin; monomeric type-2 transmembrane precursor protein; multiple sclerosis; nonobese diabetic; rheumatoid arthritis; sTNF; sTNFα; soluble form of cytokine; spondyloarthropathies; tmTNF; tmTNFα; tumor necrosis factor α

PMID:
24035809
DOI:
10.1016/j.autrev.2013.09.002
[Indexed for MEDLINE]

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