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ARTYKUŁ REDAKCYJNY
Tumor necrosis factor alpha inhibitors and demyelinating disease: what is behind it?
 
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Ukryj
1
Department of Internal Medicine, Rheumatology and Clinical Immunology, Medical University of Silesia, Katowice, Poland
 
 
Data publikacji online: 27-04-2021
 
 
Reumatologia 2021;59(2):65-67
 
STRESZCZENIE
The development of tumor necrosis factor alpha (TNF-) inhibitors is probably one of the most significant advancement in the management of a number of inflammatory rheumatic disorders to date. High efficacy of the treatment is associated with relatively rare and very heterogeneous adverse reactions. The reactions are gradually recognized with an increase in number of the patients receiving medication and prolonged period of the drug usage. Neurological adverse events in patients receiving TNF- inhibitors are not common. This finding emergence a question of coincidental occurrence of the nervous system involvements as opposite to suggestion of induction of the nervous system disease or unmasking of latent disease due to the drug administration. Potential association of anti-TNF- therapy with demyelination is one of neurological adverse reaction, and is an important concern for every day clinical practice of rheumatologist as well as is an interesting problem from pathophysiological point of view.
REFERENCJE (10)
1.
Kopp TI, Delcoigne B, Arkema EV, et al. Risk of neuroinflammatory events in arthritis patients treated with tumor necrosis factor alpha inhibitors: collaborative population-based cohort study form Denmark and Sweden. Ann Rheum Dis 2020; 79: 566–572, DOI: 10.1136/annrheumdis-2019-216693.
 
2.
Bernatsky S, Renoux C, Suissa S. Demyelinating events in rheumatoid arthritis after drug exposures. Ann Rheum Dis 2010; 69: 1691–1693, DOI: 10.1136/ard.2009.111500.
 
3.
Etminan M, Sodhi M, Samii A, et al. Tumor necrosis factor inhibitors and risk of peripheral neuropathy in patients with rheumatic diseases. Semin Arthritis Rheum 2019; 49: 1083–1086, DOI: 10.1016/j.semarthrit.2018.09.006.
 
4.
Bosch X, Saiz A, Ramos-Casals M, BIOGEAS Study Group. Monoclonal antibody therapy-associated neurological disorders. Nature Rev Neurol 2011; 7: 165–172, DOI: 10.1038/nrneurol.2011.1.
 
5.
Kaltsonoudis E, Voulgari PV, Konitsiotis S, Drosos AA. Demyelination and other neurological adverse events after anti-TNF therapy. Autoimm Rev 2014; 13: 54–58, DOI: 10.1016/j.autrev. 2013.09.002.
 
6.
Zhu TH, Nakamura M, Abrouk M, et al. Demyelinating disorders secondary to TNF-inhibitor therapy for psoriasis: a review. J Dermatol Treat 2016; 27: 406–413, DOI: 10.3109/ 09546634. 2015.1136385.
 
7.
Bitoun S, Miceli-Richard C, Verstuyft C, et al. Frequency of tumor necrosis factor alpha receptor superfamily 1A multiple sclerosis-associated variants in patients with rheumatoid arthritis with anti-tumor necrosis factor therapy-related demyelinating complications. Ann Rheum Dis 2018; 77: 1835–1836, DOI: 10.1136/annrheumdis-2018-213183.
 
8.
Seror R, Richez C, Sordet C, et al. Pattern of demyelination occurring during anti-TNF- therapy: a French national survey. Rheumatology (Oxford) 2013; 52: 868–874, DOI: 10.1093/rheumatology/kes375.
 
9.
Cortese R, Prosperini L, Stasolla A, et al. Clinical course of central nervous system demyelinating neurological events associated with anti-TNF-therapy. J Neurol 2021, DOI: 10.1007/s00415-021-10460-6 [Online ahead of print].
 
10.
Kotyla P, Śliwińska-Kotyla B, Kucharz EJ. Treatment with inflixi­mab may contribute to the development of peripheral neuro­pathy among the patients with rheumatoid arthritis. Clin Rheumatol 2007; 26: 1595–1596, DOI: 10.1007/s10067-007-0657-3.
 
Copyright: © Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w Warszawie. This is an Open Access journal, all articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (https://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
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ISSN:0034-6233
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