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Vasculitis therapy refines vasculitis mechanistic classification

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Vasculitis therapy refines vasculitis mechanistic classification. / Torp, Christopher Kirkegaard; Brüner, Mads; Keller, Kresten Krarup; Brouwer, Elisabeth; Hauge, Ellen-Margrethe; McGonagle, Dennis; Kragstrup, Tue Wenzel.

I: Autoimmunity Reviews, Bind 20, Nr. 6, 102829, 06.2021.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisReviewForskningpeer review

Harvard

Torp, CK, Brüner, M, Keller, KK, Brouwer, E, Hauge, E-M, McGonagle, D & Kragstrup, TW 2021, 'Vasculitis therapy refines vasculitis mechanistic classification', Autoimmunity Reviews, bind 20, nr. 6, 102829. https://doi.org/10.1016/j.autrev.2021.102829

APA

CBE

Torp CK, Brüner M, Keller KK, Brouwer E, Hauge E-M, McGonagle D, Kragstrup TW. 2021. Vasculitis therapy refines vasculitis mechanistic classification. Autoimmunity Reviews. 20(6):Article 102829. https://doi.org/10.1016/j.autrev.2021.102829

MLA

Vancouver

Torp CK, Brüner M, Keller KK, Brouwer E, Hauge E-M, McGonagle D o.a. Vasculitis therapy refines vasculitis mechanistic classification. Autoimmunity Reviews. 2021 jun;20(6). 102829. https://doi.org/10.1016/j.autrev.2021.102829

Author

Torp, Christopher Kirkegaard ; Brüner, Mads ; Keller, Kresten Krarup ; Brouwer, Elisabeth ; Hauge, Ellen-Margrethe ; McGonagle, Dennis ; Kragstrup, Tue Wenzel. / Vasculitis therapy refines vasculitis mechanistic classification. I: Autoimmunity Reviews. 2021 ; Bind 20, Nr. 6.

Bibtex

@article{f6af5f8a9964408b8152d828420c82a0,
title = "Vasculitis therapy refines vasculitis mechanistic classification",
abstract = "The primary vasculitides constitute a heterogeneous group of immune mediated diseases of incompletely understood pathogenesis currently classified by the size of blood vessels affected (Chapel Hill classification). In recent years, several drugs with well-characterized immunological targets have been tested in clinical trials in large vessel vasculitis and small vessel vasculitis. Such trials provide {"}reverse translational{"} or bedside to bench information about underlying pathogenic mechanisms. Therefore, the aim of this systematic literature review was to examine the evidence base for a more refined mechanistic immunological classification of vasculitis. A total of 40 studies (20 randomized controlled trials (RCTs), 16 prospective studies, 1 retrospective cohort study and 3 case series) were included for full qualitative assessment. RCTs concerning biologic therapy for large vessel vasculitis mainly supports interleukin 6 receptor inhibition (tocilizumab). RCTs concerning biologic therapy for granulomatosis with polyangiitis and microscopic polyangiitis mainly support anti-CD20 treatment (rituximab) and complement inhibition with a small molecule C5a receptor antagonist (avacopan) is an emerging treatment option. The biologic treatment of eosinophilic granulomatosis with polyangiitis is centered around interleukin 5 inhibition (mepolizumab). Studies on tumor necrosis factor alpha inhibition (adalimumab, infliximab, and etanercept) showed negative results in giant cell arteritis but some effect in Takayasu arteritis. Taken together, clinical studies with cytokine and cell specific drugs are dissecting the heterogeneous immunopathogenic mechanisms of vasculitis and support a mechanistic immunological classification. Especially, cytokine antagonism is pointing towards immunological distinctions between eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis/microscopic polyangiitis and differences between giant cell arteritis and Takayasu arteritis.",
keywords = "Abatacept, Adlimumab, Antineutrophil cytoplasmic antibody-associated vasculitis, Avacopan, Churg-Strauss, Eosinophilic granulomatosis with polyangiitis, Etanercept, Giant cell arteritis, Granulomatosis with polyangiitis, Infliximab, Large vessel vasculitis, Mepolizumab, Microscopic polyangiitis, Rituximab, Secukinumab, Small vessel vasculitis, Takayasu arteritis, Temporal arteritis, Tocilizumab, Ustekinumab, Wegeners granulomatosis",
author = "Torp, {Christopher Kirkegaard} and Mads Br{\"u}ner and Keller, {Kresten Krarup} and Elisabeth Brouwer and Ellen-Margrethe Hauge and Dennis McGonagle and Kragstrup, {Tue Wenzel}",
note = "Copyright {\textcopyright} 2021. Published by Elsevier B.V.",
year = "2021",
month = jun,
doi = "10.1016/j.autrev.2021.102829",
language = "English",
volume = "20",
journal = "Autoimmunity Reviews",
issn = "1568-9972",
publisher = "Elsevier Inc.",
number = "6",

}

RIS

TY - JOUR

T1 - Vasculitis therapy refines vasculitis mechanistic classification

AU - Torp, Christopher Kirkegaard

AU - Brüner, Mads

AU - Keller, Kresten Krarup

AU - Brouwer, Elisabeth

AU - Hauge, Ellen-Margrethe

AU - McGonagle, Dennis

AU - Kragstrup, Tue Wenzel

N1 - Copyright © 2021. Published by Elsevier B.V.

PY - 2021/6

Y1 - 2021/6

N2 - The primary vasculitides constitute a heterogeneous group of immune mediated diseases of incompletely understood pathogenesis currently classified by the size of blood vessels affected (Chapel Hill classification). In recent years, several drugs with well-characterized immunological targets have been tested in clinical trials in large vessel vasculitis and small vessel vasculitis. Such trials provide "reverse translational" or bedside to bench information about underlying pathogenic mechanisms. Therefore, the aim of this systematic literature review was to examine the evidence base for a more refined mechanistic immunological classification of vasculitis. A total of 40 studies (20 randomized controlled trials (RCTs), 16 prospective studies, 1 retrospective cohort study and 3 case series) were included for full qualitative assessment. RCTs concerning biologic therapy for large vessel vasculitis mainly supports interleukin 6 receptor inhibition (tocilizumab). RCTs concerning biologic therapy for granulomatosis with polyangiitis and microscopic polyangiitis mainly support anti-CD20 treatment (rituximab) and complement inhibition with a small molecule C5a receptor antagonist (avacopan) is an emerging treatment option. The biologic treatment of eosinophilic granulomatosis with polyangiitis is centered around interleukin 5 inhibition (mepolizumab). Studies on tumor necrosis factor alpha inhibition (adalimumab, infliximab, and etanercept) showed negative results in giant cell arteritis but some effect in Takayasu arteritis. Taken together, clinical studies with cytokine and cell specific drugs are dissecting the heterogeneous immunopathogenic mechanisms of vasculitis and support a mechanistic immunological classification. Especially, cytokine antagonism is pointing towards immunological distinctions between eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis/microscopic polyangiitis and differences between giant cell arteritis and Takayasu arteritis.

AB - The primary vasculitides constitute a heterogeneous group of immune mediated diseases of incompletely understood pathogenesis currently classified by the size of blood vessels affected (Chapel Hill classification). In recent years, several drugs with well-characterized immunological targets have been tested in clinical trials in large vessel vasculitis and small vessel vasculitis. Such trials provide "reverse translational" or bedside to bench information about underlying pathogenic mechanisms. Therefore, the aim of this systematic literature review was to examine the evidence base for a more refined mechanistic immunological classification of vasculitis. A total of 40 studies (20 randomized controlled trials (RCTs), 16 prospective studies, 1 retrospective cohort study and 3 case series) were included for full qualitative assessment. RCTs concerning biologic therapy for large vessel vasculitis mainly supports interleukin 6 receptor inhibition (tocilizumab). RCTs concerning biologic therapy for granulomatosis with polyangiitis and microscopic polyangiitis mainly support anti-CD20 treatment (rituximab) and complement inhibition with a small molecule C5a receptor antagonist (avacopan) is an emerging treatment option. The biologic treatment of eosinophilic granulomatosis with polyangiitis is centered around interleukin 5 inhibition (mepolizumab). Studies on tumor necrosis factor alpha inhibition (adalimumab, infliximab, and etanercept) showed negative results in giant cell arteritis but some effect in Takayasu arteritis. Taken together, clinical studies with cytokine and cell specific drugs are dissecting the heterogeneous immunopathogenic mechanisms of vasculitis and support a mechanistic immunological classification. Especially, cytokine antagonism is pointing towards immunological distinctions between eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis/microscopic polyangiitis and differences between giant cell arteritis and Takayasu arteritis.

KW - Abatacept

KW - Adlimumab

KW - Antineutrophil cytoplasmic antibody-associated vasculitis

KW - Avacopan

KW - Churg-Strauss

KW - Eosinophilic granulomatosis with polyangiitis

KW - Etanercept

KW - Giant cell arteritis

KW - Granulomatosis with polyangiitis

KW - Infliximab

KW - Large vessel vasculitis

KW - Mepolizumab

KW - Microscopic polyangiitis

KW - Rituximab

KW - Secukinumab

KW - Small vessel vasculitis

KW - Takayasu arteritis

KW - Temporal arteritis

KW - Tocilizumab

KW - Ustekinumab

KW - Wegeners granulomatosis

UR - http://www.scopus.com/inward/record.url?scp=85104607565&partnerID=8YFLogxK

U2 - 10.1016/j.autrev.2021.102829

DO - 10.1016/j.autrev.2021.102829

M3 - Review

C2 - 33872767

VL - 20

JO - Autoimmunity Reviews

JF - Autoimmunity Reviews

SN - 1568-9972

IS - 6

M1 - 102829

ER -