Changes of Metabolic Biomarker Levels upon One-Year Anti-TNF-α Therapy in Rheumatoid Arthritis and Ankylosing Spondylitis: Associations with Vascular Pathophysiology.
Adult
Aged
Aged, 80 and over
Arthritis, Rheumatoid
/ blood
Aryldialkylphosphatase
/ blood
Biomarkers
/ blood
C-Reactive Protein
/ metabolism
Carboxylic Ester Hydrolases
/ blood
Carotid Intima-Media Thickness
Certolizumab Pegol
/ administration & dosage
Etanercept
/ administration & dosage
Female
Heart Disease Risk Factors
Humans
Lipid Metabolism
/ drug effects
Lipids
/ blood
Male
Middle Aged
Obesity
/ blood
Peroxidase
/ blood
Spondylitis, Ankylosing
/ blood
Tumor Necrosis Factor-alpha
/ antagonists & inhibitors
adipokines
ankylosing spondylitis
biologic therapy
lipids
metabolic biomarkers
rheumatoid arthritis
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
18 10 2021
18 10 2021
Historique:
received:
26
07
2021
revised:
15
10
2021
accepted:
15
10
2021
entrez:
23
10
2021
pubmed:
24
10
2021
medline:
20
1
2022
Statut:
epublish
Résumé
Cardiovascular (CV) morbidity, mortality, and metabolic syndrome are associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Here, lipids and other metabolic markers in relation to vascular function and clinical markers were evaluated in RA and AS patients undergoing one-year anti-TNF therapy. Fifty-three patients including 36 RA patients treated with either etanercept (ETN) or certolizumab pegol (CZP) and 17 AS patients treated with ETN were included in a 12-month follow-up study. Various lipids, paraoxonase (PON) and arylesterase (ARE) activities, myeloperoxidase (MPO) and adipokine levels were determined overtime. Ultrasonography was performed to determine flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT), and arterial pulse-wave velocity (PWV) in all patients. All assessments were performed at baseline and 6 and 12 months after treatment initiation. Anti-TNF therapy decreased ARE activity, MPO, adiponectin, and chemerin levels after 12 months ( Assessment of various metabolic parameters together with disease activity, CRP, and ultrasound-based techniques may exert additional value in determining CV burden and in monitoring the effects of biologics on preclinical vascular pathophysiology.
Sections du résumé
BACKGROUND
Cardiovascular (CV) morbidity, mortality, and metabolic syndrome are associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Here, lipids and other metabolic markers in relation to vascular function and clinical markers were evaluated in RA and AS patients undergoing one-year anti-TNF therapy.
PATIENTS AND METHODS
Fifty-three patients including 36 RA patients treated with either etanercept (ETN) or certolizumab pegol (CZP) and 17 AS patients treated with ETN were included in a 12-month follow-up study. Various lipids, paraoxonase (PON) and arylesterase (ARE) activities, myeloperoxidase (MPO) and adipokine levels were determined overtime. Ultrasonography was performed to determine flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT), and arterial pulse-wave velocity (PWV) in all patients. All assessments were performed at baseline and 6 and 12 months after treatment initiation.
RESULTS
Anti-TNF therapy decreased ARE activity, MPO, adiponectin, and chemerin levels after 12 months (
CONCLUSIONS
Assessment of various metabolic parameters together with disease activity, CRP, and ultrasound-based techniques may exert additional value in determining CV burden and in monitoring the effects of biologics on preclinical vascular pathophysiology.
Identifiants
pubmed: 34680168
pii: biom11101535
doi: 10.3390/biom11101535
pmc: PMC8533731
pii:
doi:
Substances chimiques
Biomarkers
0
Lipids
0
Tumor Necrosis Factor-alpha
0
C-Reactive Protein
9007-41-4
Peroxidase
EC 1.11.1.7
Carboxylic Ester Hydrolases
EC 3.1.1.-
arylesterase
EC 3.1.1.2
Aryldialkylphosphatase
EC 3.1.8.1
Etanercept
OP401G7OJC
Certolizumab Pegol
UMD07X179E
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Références
J Rheumatol. 2011 Apr;38(4):723-9
pubmed: 21239756
Ann Rheum Dis. 2017 Jan;76(1):17-28
pubmed: 27697765
Vasa. 2017 Aug;46(5):370-376
pubmed: 28602123
Eur J Clin Pharmacol. 2004 Dec;60(10):685-91
pubmed: 15490140
Cerebrovasc Dis. 2008;25(1-2):122-8
pubmed: 18073465
BMC Musculoskelet Disord. 2014 Nov 19;15:379
pubmed: 25406539
Ann Rheum Dis. 2015 Mar;74(3):480-9
pubmed: 25561362
Ann Rheum Dis. 2014 Jan;73(1):124-31
pubmed: 23482473
Nat Rev Rheumatol. 2013 Sep;9(9):513-23
pubmed: 23774906
Rheumatol Int. 2013 Jun;33(6):1487-94
pubmed: 23239038
Arthritis Rheum. 1995 Jan;38(1):44-8
pubmed: 7818570
Clin Biochem. 2016 Aug;49(12):862-7
pubmed: 27129797
Ann Rheum Dis. 1994 Jan;53(1):24-9
pubmed: 8311550
J Rheumatol. 1994 Dec;21(12):2286-91
pubmed: 7699630
Arthritis Res Ther. 2013;15(6):R194
pubmed: 24245495
Life Sci. 2003 May 9;72(25):2877-85
pubmed: 12697270
J Rheumatol. 2010 Jan;37(1):161-6
pubmed: 19955053
Clin Exp Rheumatol. 2009 Mar-Apr;27(2):222-8
pubmed: 19473561
Best Pract Res Clin Rheumatol. 2016 Oct;30(5):851-869
pubmed: 27964792
Arthritis Res Ther. 2011;13(5):R158
pubmed: 21959042
Nat Rev Rheumatol. 2011 Aug 02;7(9):528-36
pubmed: 21808287
Eur Heart J. 2015 Feb 21;36(8):482-9c
pubmed: 25433021
Clin Biochem. 2008 May;41(7-8):532-7
pubmed: 18280811
Ann Rheum Dis. 2006 Sep;65(9):1198-201
pubmed: 16414972
Metabolism. 2007 Nov;56(11):1542-9
pubmed: 17950106
J Cell Mol Med. 2014 Jul;18(7):1313-20
pubmed: 24702860
Wien Klin Wochenschr. 2020 Mar;132(5-6):150-154
pubmed: 31974766
J Clin Lab Anal. 2021 Mar;35(3):e23666
pubmed: 33231330
Nat Rev Rheumatol. 2009 Dec;5(12):677-84
pubmed: 19901918
Curr Opin Hematol. 2000 Jan;7(1):53-8
pubmed: 10608505
Nat Rev Rheumatol. 2015 Dec;11(12):693-704
pubmed: 26282082
Ann Rheum Dis. 2016 Oct;75(10):1806-12
pubmed: 26613768
J Rheumatol. 2006 May;33(5):921-3
pubmed: 16541480
Nat Rev Rheumatol. 2014 Nov;10(11):691-6
pubmed: 25090948
PLoS One. 2019 Aug 5;14(8):e0220531
pubmed: 31381601
Nat Rev Rheumatol. 2012 Feb 21;8(4):224-34
pubmed: 22349611
J Rheumatol. 2008 Mar;35(3):398-406
pubmed: 18203326
PLoS One. 2013;8(2):e57802
pubmed: 23460910
Arthritis Rheum. 2007 Sep;56(9):2905-12
pubmed: 17763428
Sci Rep. 2020 Oct 8;10(1):16848
pubmed: 33033318
Clin Rev Allergy Immunol. 2020 Feb;58(1):1-14
pubmed: 30259381
Clin Rheumatol. 2007 Mar;26(3):342-8
pubmed: 16642406
Am J Hum Genet. 1983 Mar;35(2):214-27
pubmed: 6301268
Ann Rheum Dis. 2011 Apr;70(4):576-82
pubmed: 21109516
J Rheumatol. 2014 Sep;41(9):1746-54
pubmed: 25028378
Ann Rheum Dis. 2009 Jun;68(6):868-72
pubmed: 18635596
Mediators Inflamm. 2013;2013:710928
pubmed: 23431244
Clin Invest Med. 2011 Aug 01;34(4):E225
pubmed: 21810380
Curr Atheroscler Rep. 2005 Mar;7(2):127-31
pubmed: 15727728
Atherosclerosis. 2008 Mar;197(1):363-7
pubmed: 17624354
Clin Exp Rheumatol. 2019 Mar-Apr;37(2):293-300
pubmed: 30148441
Arthritis Res Ther. 2016 Oct 20;18(1):239
pubmed: 27765067
Curr Vasc Pharmacol. 2020;18(5):431-446
pubmed: 31258091
Br J Dermatol. 2013 May;168(5):984-9
pubmed: 23614561
Rheumatol Int. 2012 Jun;32(6):1605-9
pubmed: 21331575
Rheumatology (Oxford). 2012 Oct;51(10):1796-803
pubmed: 22814531
Rheumatol Int. 2020 Mar;40(3):427-436
pubmed: 31848735
Ann Rheum Dis. 2011 Mar;70(3):482-7
pubmed: 21216812
Ann Rheum Dis. 2007 Jul;66(7):958-61
pubmed: 17314120
Arthritis Rheumatol. 2017 Jan;69(1):46-57
pubmed: 27483410