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Biological treatments in giant cell arteritis & Takayasu arteritis.

Identifieur interne : 001470 ( Main/Exploration ); précédent : 001469; suivant : 001471

Biological treatments in giant cell arteritis & Takayasu arteritis.

Auteurs : Maxime Samson [Espagne] ; Georgina Espígol-Frigolé [Espagne] ; Nekane Terrades-García [Espagne] ; Sergio Prieto-González [Espagne] ; Marc Corbera-Bellalta [Espagne] ; Roser Alba-Rovira [Espagne] ; José Hernández-Rodríguez [Espagne] ; Sylvain Audia [France] ; Bernard Bonnotte [France] ; Maria C. Cid [Espagne]

Source :

RBID : pubmed:29146018

Descripteurs français

English descriptors

Abstract

Giant cell arteritis (GCA) and Takayasu arteritis (TAK) are the two main large vessel vasculitides. They share some similarities regarding their clinical, radiological and histological presentations but some pathogenic processes in GCA and TAK are activated differently, thus explaining their different sensitivity to biological therapies. The treatment of GCA and TAK essentially relies on glucocorticoids. However, thanks to major progress in our understanding of their pathogenesis, the role of biological therapies in the treatment of these two vasculitides is expanding, especially in relapsing or refractory diseases. In this review, the efficacy, the safety and the limits of the main biological therapies ever tested in GCA and TAK are discussed. Briefly, anti TNF-α agents appear to be effective in treating TAK but not GCA. Recent randomized placebo-controlled trials have reported on the efficacy and safety of abatacept and mostly tocilizumab in inducing and maintaining remission of GCA. Abatacept was not effective in TAK and robust data are still lacking to draw any conclusions concerning the use of tocilizumab in TAK. Furthermore, ustekinumab appears promising in relapsing/refractory GCA whereas rituximab has been reported to be effective in only a few cases of refractory TAK patients. If a biological therapy is indicated, and in light of the data discussed in this review, the first choice would be tocilizumab in GCA and anti-TNF-α agents (mainly infliximab) in TAK.

DOI: 10.1016/j.ejim.2017.11.003
PubMed: 29146018


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Le document en format XML

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<front>
<div type="abstract" xml:lang="en">Giant cell arteritis (GCA) and Takayasu arteritis (TAK) are the two main large vessel vasculitides. They share some similarities regarding their clinical, radiological and histological presentations but some pathogenic processes in GCA and TAK are activated differently, thus explaining their different sensitivity to biological therapies. The treatment of GCA and TAK essentially relies on glucocorticoids. However, thanks to major progress in our understanding of their pathogenesis, the role of biological therapies in the treatment of these two vasculitides is expanding, especially in relapsing or refractory diseases. In this review, the efficacy, the safety and the limits of the main biological therapies ever tested in GCA and TAK are discussed. Briefly, anti TNF-α agents appear to be effective in treating TAK but not GCA. Recent randomized placebo-controlled trials have reported on the efficacy and safety of abatacept and mostly tocilizumab in inducing and maintaining remission of GCA. Abatacept was not effective in TAK and robust data are still lacking to draw any conclusions concerning the use of tocilizumab in TAK. Furthermore, ustekinumab appears promising in relapsing/refractory GCA whereas rituximab has been reported to be effective in only a few cases of refractory TAK patients. If a biological therapy is indicated, and in light of the data discussed in this review, the first choice would be tocilizumab in GCA and anti-TNF-α agents (mainly infliximab) in TAK.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Espagne</li>
<li>France</li>
</country>
<region>
<li>Bourgogne</li>
<li>Bourgogne-Franche-Comté</li>
<li>Catalogne</li>
</region>
<settlement>
<li>Barcelone</li>
<li>Dijon</li>
</settlement>
</list>
<tree>
<country name="Espagne">
<region name="Catalogne">
<name sortKey="Samson, Maxime" sort="Samson, Maxime" uniqKey="Samson M" first="Maxime" last="Samson">Maxime Samson</name>
</region>
<name sortKey="Alba Rovira, Roser" sort="Alba Rovira, Roser" uniqKey="Alba Rovira R" first="Roser" last="Alba-Rovira">Roser Alba-Rovira</name>
<name sortKey="Cid, Maria C" sort="Cid, Maria C" uniqKey="Cid M" first="Maria C" last="Cid">Maria C. Cid</name>
<name sortKey="Corbera Bellalta, Marc" sort="Corbera Bellalta, Marc" uniqKey="Corbera Bellalta M" first="Marc" last="Corbera-Bellalta">Marc Corbera-Bellalta</name>
<name sortKey="Espigol Frigole, Georgina" sort="Espigol Frigole, Georgina" uniqKey="Espigol Frigole G" first="Georgina" last="Espígol-Frigolé">Georgina Espígol-Frigolé</name>
<name sortKey="Hernandez Rodriguez, Jose" sort="Hernandez Rodriguez, Jose" uniqKey="Hernandez Rodriguez J" first="José" last="Hernández-Rodríguez">José Hernández-Rodríguez</name>
<name sortKey="Prieto Gonzalez, Sergio" sort="Prieto Gonzalez, Sergio" uniqKey="Prieto Gonzalez S" first="Sergio" last="Prieto-González">Sergio Prieto-González</name>
<name sortKey="Terrades Garcia, Nekane" sort="Terrades Garcia, Nekane" uniqKey="Terrades Garcia N" first="Nekane" last="Terrades-García">Nekane Terrades-García</name>
</country>
<country name="France">
<region name="Bourgogne-Franche-Comté">
<name sortKey="Audia, Sylvain" sort="Audia, Sylvain" uniqKey="Audia S" first="Sylvain" last="Audia">Sylvain Audia</name>
</region>
<name sortKey="Bonnotte, Bernard" sort="Bonnotte, Bernard" uniqKey="Bonnotte B" first="Bernard" last="Bonnotte">Bernard Bonnotte</name>
</country>
</tree>
</affiliations>
</record>

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