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Tumour necrosis factor alpha (TNFα) is a key cytokine in inflammatory rheumatic diseases but is also implicated in multiple sclerosis (MS) where TNFα is elevated in demyelinating plaques. However, TNFα inhibitors (TNFi) have opposite effects: they have revolutionised the treatment of chronic rheumatic diseases but may cause flares of MS.1 Several studies have suggested an association between TNFi use and occurrence of demyelinating disorders.2 3 Their incidence is estimated up to 4% after 18 months of treatment in a recent prospective study with systematic neurological examination before and after treatment initiation.4
In addition, two TNF receptor superfamily 1 (TNFRSF1A) single nucleotide polymorphisms, (SNPs) rs1800693 and rs4149584 (TNFRSF1A R92Q), have been shown to increase the risk of developing MS.5 The rs1800693*G allele leads to a dysfunctional TNFα soluble receptor that inhibits TNFα signalling.6 Rare variants of TNFRSF1A locus have also been implicated …
Handling editor Josef S Smolen
Contributors SB, CM-R, RS and XM designed the study. All authors acquired the data. SB, CM-R, RS, XM, PAJ, CV and PD analysed the data. All authors gave final approval to the paper.
Funding This study was funded by Pfizer (10.13039/100004319) and grant number: Passerelle.
Competing interests None declared.
Patient consent Not required.
Ethics approval This study was approved by the local institutional review board named CPP Île de France VII under number PP 12-030.
Provenance and peer review Not commissioned; externally peer reviewed.
Presented at This work has already been presented at the European League Against Rheumatism and published as a conference abstract .