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Biological treatments in giant cell arteritis & Takayasu arteritis

  • Maxime Samson
    Correspondence
    Corresponding author at: Service de Médecine Interne et Immunologie Clinique, Hôpital François Mitterrand, CHU de Dijon, 2, Bd Mal de Lattre de Tassigny, 21000 Dijon, France.
    Affiliations
    Department of Internal Medicine and Clinical Immunology, François Mitterrand Hospital, Dijon University Hospital, Dijon, France

    INSERM, UMR1098, University of Bourgogne Franche-Comté, FHU INCREASE, Dijon, France

    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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  • Georgina Espígol-Frigolé
    Affiliations
    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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  • Nekane Terrades-García
    Affiliations
    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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  • Sergio Prieto-González
    Affiliations
    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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  • Marc Corbera-Bellalta
    Affiliations
    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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  • Roser Alba-Rovira
    Affiliations
    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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  • José Hernández-Rodríguez
    Affiliations
    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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  • Sylvain Audia
    Affiliations
    Department of Internal Medicine and Clinical Immunology, François Mitterrand Hospital, Dijon University Hospital, Dijon, France

    INSERM, UMR1098, University of Bourgogne Franche-Comté, FHU INCREASE, Dijon, France
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  • Bernard Bonnotte
    Affiliations
    Department of Internal Medicine and Clinical Immunology, François Mitterrand Hospital, Dijon University Hospital, Dijon, France

    INSERM, UMR1098, University of Bourgogne Franche-Comté, FHU INCREASE, Dijon, France
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  • Maria C. Cid
    Affiliations
    Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain
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Published:November 13, 2017DOI:https://doi.org/10.1016/j.ejim.2017.11.003

      Highlights

      • Glucocorticoids remain the cornerstone of remission-induction in GCA and TAK
      • Biologics are often used in clinical practice as second- or third-line therapies
      • In case a biological treatment is necessary:
        • abatacept and mainly tocilizumab are effective in maintaining remission in GCA
        • anti-TNF-α agents are probably the best choice in TAK patients

      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.

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