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Giant cell arteritis: From pathogenesis to new therapeutic targets
被引:0
|作者:
Samson, M.
[1
,2
]
Greigert, H.
[1
,2
]
Ghesquiere, T.
[1
,2
]
Bonnotte, B.
[1
,2
]
机构:
[1] CHU Dijon Bourgogne, Hop Francois Mitterrand, Serv Med Interne & Immunol Clin, F-21000 Dijon, France
[2] Univ Bourgogne Franche Comte, UMR1098, EFS BFC, INSERM, F-21000 Dijon, France
来源:
BULLETIN DE L ACADEMIE NATIONALE DE MEDECINE
|
2020年
/
204卷
/
01期
关键词:
Giant cell arteritis;
Ustekinumab;
Abatacept;
VARICELLA-ZOSTER-VIRUS;
PLACEBO-CONTROLLED TRIAL;
REGULATORY T-CELLS;
INTERLEUKIN-6 RECEPTOR BLOCKADE;
POLYMYALGIA-RHEUMATICA;
DOUBLE-BLIND;
TEMPORAL ARTERITIS;
DENDRITIC CELLS;
VESSEL;
LESIONS;
D O I:
10.1016/j.banm.2019.10.016
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Giant cell arteritis (GCA) is the most common vasculitis in adults. GCA is a granulomatous large-vessel vasculitis involving the aorta and its major branches in people > 50 years. Glucocorticoids (GC) remain the cornerstone of GCA treatment. Prednisone is usually started at 0.7 or 1 mg/kg/day depending on the occurrence of ischemic complications. GC is very efficient but relapses often occur when the dose is tapered so that the risk of GC-related side effects increases. That is the main reason why GC-sparing strategies have to be developed to improve GCA-patient care. The pathogenesis of GCA is not fully understood but major advances have been achieved in the recent years. Although the trigger of GCA is still not identified, several mechanisms inducing granulomatous inflammation of the arterial wall and vascular remodeling leading to the occurrence of ischemic events have been deciphered. Thanks to these advances, new therapeutic targets have emerged such as blockade of T cell activation or inhibition of the interleukin-6 (IL-6), IL-12/23 or IL-1 beta pathways and in the next future strategies to better prevent vascular remodeling. (C) 2019 l'Acadernie nationale de medecine. Published by Elsevier Masson SAS. All rights reserved.
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页码:18 / 28
页数:11
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