Научная статья на тему 'Demyelination and other neurological side effects after anti-TNF-α treatment'

Demyelination and other neurological side effects after anti-TNF-α treatment Текст научной статьи по специальности «Медицинские технологии»

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Ключевые слова
TNFα antagonists / neurological adverse events / multiple sclerosis / tmTNFα / sTNFα / TNFR1 / 2

Аннотация научной статьи по медицинским технологиям, автор научной работы — Eyripidis Kaltsonoudis, Paraskevi Β. Voulgari, Spyridon Konitsiotis, Alexandros Α. Drossos

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.

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Текст научной работы на тему «Demyelination and other neurological side effects after anti-TNF-α treatment»

mediterranean journal 26

of RHEUMATOLOGY 1

EAAHNIKH PEYMATQAOriA 2015

AnoMueAivwon Kai aAAeQ veupoAoYiKeQ aveni9uMnieQ evepYeieQ Meia anö avTi-TNF-a 9epaneia

EupiniöriQ KaAioovouöriQ, MD, napaoKeun B. BouAYapn, MD, PhD, Inuplöwv KovrroiwiriQ1, MD, PhD, AXe^avöpoq A. Apöooq, MD, PhD

PeuMaToXoyiKn KAiviKn, ToMeaq naBoAoYlaq, Kai 1NeupoXoyiKn KAiviKn, laipiKn ^xoAn, navenioinMio Iwavvlvwv

nEPIAHYH

Oi avTi-TNF-a (napaYoviaQ veKpwonQ öykwv) npooöiöouv onMaviiKö nAeoveKinMa oin 9epaneia inQ peuMaioeiöouQ ap9piiiöaQ (PA), iwv onovöuAoap9piiiöwv (SpA), Ka9üQ Kai aAAwv 0ÄeYMovw6üv voonMaiwv. 'Exei ano6eix9ei, öii oi napaYovieQ auioi eivai nio anoieAeoMaiiKoi anö ö,ii 1a napaöooiaKa ipononoiniiKa inQ vöoou 0apMaKa (DMARDs), Kai öii Mnopei va napeMnoöioouv nio anoieAeoMaiiKa inv avaniu^n öomikhq ßAaßnQ iwv ap9püoewv. Qoiöoo, n au^nM^vn xpnon touq Kaia in öiapKeia inQ ieAeuiaiaQ öeKaeiiaQ, exei anoKaAu^ei Mia oeipa anö aveni9üMnieQ evepYeieQ öiaMeooAaßouMeveQ anö to avooonoiniiKö ouoinMa. 'Exouv Aoinöv ava0ep9ei onMeia Kai ouMniÜMaia auioavoowv voonMaiwv, önwQ Kviöwon, ^wpiaon, oüvöpoMa oav Aukoq, oaKxapüönQ öiaßninQ iünou I Kai aAAa.

EninAeov, ¿xouv önMooieuiei noAuapi9MeQ ava0opeQ Kai oeipeQ nepiniüoewv anö veupoAoYiKeQ aveni9ÜMnieQ evepYeieQ, iiq onoieQ anoöiöouv oinv avaoioAn iou TNF-a. Oi veupoAoYiKeQ auieQ aveni9uMnieQ eninAoKeQ Meia^ü aAAwv nepiAaMßavouv inv anoMueAivwiiKn vöoo, inv oniiKH veupiiiöa, in xpövia 0AeYMovüön anoMueAivwiiKn noAuveupona9eia, inv noAAanAn MovoveupiiiöaQ, to ouvöpoMo Guillain - Barre Kai aAAa. Qoiöoo, eYeipoviai epwinMaia oxeiiKa Me inv ni9avn aiiioAoYiKn ouoxeiion.

'Eioi, av Kai exouv npoia9ei 6ia0opeQ uno9eoeiQ oe Mia npoona9eia va epMnveuoouv inv ni9avn oxeon Meia^u iwv TNF-a aviaYwvioiüv Kai inQ anoMueAivwiiKHQ vöoou, KaMia öev 9ewpeiiai enapKHQ. napopMouMevoi anö to YeYovöQ auiö, oinv napouoa avaoKönnon 9a avaZninoouMe iiq ni9aveQ eniniüoeiQ iou TNF-a oinv noAAanAn oKAnpuvon Kai 9a epeuvqoouMe inv ni9avn oxeon iwv anoKAeioiüv iou TNF-a oiiQ anoMueAivwiiKeQ na9qoeiQ.

Mediterr J Rheumatol 2015; 26(1): 70-71

Ynsu8uvoq aAAr|Aoypa0iac;

AAe^avSpoQ A. ÄpöaoQ, Ka8nvnTnQ na8oAoYiaQ/PeupaToAoYiaQ. PeupaxoAoyiKn KAiviKri, TopeaQ na8oAoYiK|Q AvaTopiaQ, laTpiKii ^xoAq naveniCTTHMiou luavvivuv, 45110, Iwävviva

TqA. 2651007503, Fax. 2651007054,

email: adrosos@cc.uoi.gr, www.rheumatology.gr

Corresponding author:

Alexandros A. Drossos,

Professor of Internal Medicine/Rheumatology,

Rheumatology Clinic, Department of Internal Medicine,

School of Medicine, University of loannina,

45110, loannina, Greece

Ae^eiQ-KAeiöiä: TNF-a avraYuvioreQ, veupoAoYiKeQ eKÖnAüoeiQ, noAAanAn oKAnpuvon, tmTNFa, sTNFa, TNFR1,2

AnOMYEAINQIH KAIAAAEXNEYROAORIKEX ANEniQYMHTEI ENEREEIEI META AnO ANTI-TNF-A QERAnEIA DEMYELiNATiON AND OTHER NEUROLOGiCAL SiDE EFFECTS AFTER ANTi-TNF-A TREATMENT

Demyelination and other neurological side effects after anti-TNF-a treatment

Eyripidis Kaltsonoudis,MD, Paraskevi B. Voulgari, MD,PhD, Spyridon Konitsiotis1, MD, PhD, Alexandros A. Drossos, MD,PhD Rheumatology Clinic, Department of Medicine, and 1 Neurology Clinic, School of Medicine, University of loannina

ABSTRACT

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

Mediterr J Rheumatol 2015; 26(1): 70-71

Keywords: TNFa antagonists; neurological adverse events; multiple sclerosis; tmTNFa; sTNFa; TNFR1,2.

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