The association of serum interleukin-6 levels with clinical outcomes in antineutrophil cytoplasmic antibody-associated vasculitis.
Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
/ blood
Antibodies, Antineutrophil Cytoplasmic
/ immunology
Azathioprine
/ therapeutic use
B-Lymphocytes
/ drug effects
Cyclophosphamide
/ therapeutic use
Cytoplasm
/ immunology
Double-Blind Method
Drug Therapy, Combination
Female
Humans
Immunosuppressive Agents
/ therapeutic use
Interleukin-6
/ blood
Longitudinal Studies
Male
Middle Aged
Myeloblastin
/ immunology
Neutrophils
/ drug effects
Peroxidase
/ immunology
Remission Induction
/ methods
Rituximab
/ therapeutic use
ANCA-Associated vasculitis
ANCA-type
Cytokines
IL-6
Interleukin-6
RAVE
Journal
Journal of autoimmunity
ISSN: 1095-9157
Titre abrégé: J Autoimmun
Pays: England
ID NLM: 8812164
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
20
05
2019
revised:
04
07
2019
accepted:
08
07
2019
pubmed:
20
7
2019
medline:
28
7
2020
entrez:
20
7
2019
Statut:
ppublish
Résumé
To investigate serum IL-6 (sIL-6) levels during active disease, complete remission (CR), and relapse in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), and to explore the association of changes in sIL-6 with clinical outcomes. sIL-6 levels were measured at baseline and longitudinally over 18 months, in 78 patients with AAV enrolled in a randomized controlled trial comparing treatment with either rituximab (RTX) or cyclophosphamide (CYC)/azathioprine (AZA). Outcome variables included baseline clinical features, ANCA specificity, disease activity (active disease versus CR), time to relapse events, B cell repopulation, and ANCA titer increases. At baseline, sIL6 levels were detectable in 81% of patients; 73% (n = 57) of subjects were proteinase 3 (PR3)-ANCA positive, sIL-6 levels were higher in subjects with PR3-ANCAs and positively correlated with their levels (r At baseline, sIL-6 concentrations correlate with PR3-ANCA titers and are associated with specific clinical manifestations of AAV. Baseline sIL6 concentrations do not predict CR at 6 months, but the increase in sIL-6 concentrations during CR is associated with subsequent severe relapse among RTX-treated patients. Further investigation into the mechanistic role of IL6 in AAV might lead to identifying this pathway as a potential therapeutic target in this disease.
Identifiants
pubmed: 31320177
pii: S0896-8411(19)30334-8
doi: 10.1016/j.jaut.2019.07.001
pmc: PMC7217333
mid: NIHMS1535295
pii:
doi:
Substances chimiques
Antibodies, Antineutrophil Cytoplasmic
0
IL6 protein, human
0
Immunosuppressive Agents
0
Interleukin-6
0
Rituximab
4F4X42SYQ6
Cyclophosphamide
8N3DW7272P
Peroxidase
EC 1.11.1.7
Myeloblastin
EC 3.4.21.76
Azathioprine
MRK240IY2L
Types de publication
Journal Article
Multicenter Study
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
102302Subventions
Organisme : NCRR NIH HHS
ID : UL1 RR025005
Pays : United States
Organisme : NIAMS NIH HHS
ID : K23 AR052820
Pays : United States
Organisme : NCRR NIH HHS
ID : M01 RR000533
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR025771
Pays : United States
Organisme : NIAMS NIH HHS
ID : K24 AR002224
Pays : United States
Organisme : NIAMS NIH HHS
ID : P60 AR047785
Pays : United States
Organisme : NCRR NIH HHS
ID : U54 RR019497
Pays : United States
Organisme : NINDS NIH HHS
ID : U54 NS064808
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR024150
Pays : United States
Organisme : NIAMS NIH HHS
ID : U54 AR057319
Pays : United States
Organisme : NIAMS NIH HHS
ID : RC1 AR058303
Pays : United States
Organisme : NIAID NIH HHS
ID : N01 AI015416
Pays : United States
Organisme : NIAMS NIH HHS
ID : K24 AR049185
Pays : United States
Organisme : NIAMS NIH HHS
ID : P30 AR072571
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.
Références
Clin Infect Dis. 2000 Oct;31 Suppl 5:S178-84
pubmed: 11113021
Rheumatology (Oxford). 2011 Oct;50(10):1928-30
pubmed: 21719417
Ann Rheum Dis. 2013 Aug;72(8):1342-50
pubmed: 22975753
Arthritis Rheum. 2001 Apr;44(4):912-20
pubmed: 11318006
Arthritis Rheum. 1988 Jun;31(6):784-8
pubmed: 3260102
Clin Exp Nephrol. 2011 Aug;15(4):596-601
pubmed: 21360022
Arthritis Rheumatol. 2014 Feb;66(2):428-32
pubmed: 24504815
Mediators Inflamm. 2004 Aug;13(4):275-83
pubmed: 15545059
Arthritis Rheum. 2000 May;43(5):1041-8
pubmed: 10817557
Arthritis Rheum. 2004 Feb;50(2):581-8
pubmed: 14872502
Nat Rev Rheumatol. 2017 Jul;13(7):399-409
pubmed: 28615731
Nat Rev Rheumatol. 2014 Dec;10(12):720-7
pubmed: 25136784
Semin Arthritis Rheum. 2015 Aug;45(1):48-54
pubmed: 25841802
J Am Soc Nephrol. 1999 Jul;10(7):1506-15
pubmed: 10405206
Microbiol Immunol. 2013 Sep;57(9):640-50
pubmed: 23829825
Ann Intern Med. 2009 May 19;150(10):670-80
pubmed: 19451574
Mod Rheumatol. 2016 Nov;26(6):900-907
pubmed: 26934300
J Exp Med. 1988 Feb 1;167(2):332-44
pubmed: 3258006
Clin Immunol Immunopathol. 1989 Mar;50(3):394-8
pubmed: 2783897
J Exp Med. 2009 Jan 16;206(1):69-78
pubmed: 19139170
Clin Nephrol. 1993 Nov;40(5):256-64
pubmed: 8281714
Arthritis Rheumatol. 2018 Jul;70(7):1114-1121
pubmed: 29693324
Intern Med. 1993 Feb;32(2):189-92
pubmed: 8507933
Autoimmunity. 2005 Aug;38(5):359-67
pubmed: 16227151
Ann N Y Acad Sci. 1989;557:230-8, discussion 239
pubmed: 2786697
Nephrol Dial Transplant. 2017 Feb 1;32(2):254-264
pubmed: 28186568
Chem Immunol. 1992;51:153-80
pubmed: 1567541
Ciba Found Symp. 1992;167:5-16; discussion 16-23
pubmed: 1425018
Nat Rev Rheumatol. 2013 Dec;9(12):731-40
pubmed: 24189842
Arthritis Rheumatol. 2016 Jul;68(7):1700-10
pubmed: 26882078
N Engl J Med. 2013 Aug 1;369(5):417-27
pubmed: 23902481
N Engl J Med. 2010 Jul 15;363(3):221-32
pubmed: 20647199
Nat Clin Pract Rheumatol. 2006 Nov;2(11):619-26
pubmed: 17075601