Document Detail

Effect of 1-year anti-TNF-α therapy on aortic stiffness, carotid atherosclerosis, and calprotectin in inflammatory arthropathies: a controlled study.
MedLine Citation:
PMID:  22378036     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Premature arterial stiffening and atherosclerosis are increased in patients with inflammatory arthropathies such as rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA). The proinflammatory protein calprotectin is associated with inflammatory arthropathies, vascular pathology, and acute coronary events. We examined the long-term effects of treatment with tumor necrosis factor (TNF)-α antagonists on aortic stiffness and carotid intima media thickness (CIMT) in patients with inflammatory arthropathies, and the relationships to the levels of calprotectin.
METHODS: Fifty-five patients with RA, AS, or PsA and a clinical indication for anti-TNF-α therapy were included and followed with regular examinations for 1 year. Thirty-six patients starting with anti-TNF-α therapy were compared with a nontreatment group of 19 patients. Examinations included assessments of aortic stiffness (aortic pulse wave velocity, aPWV), CIMT, and plasma calprotectin.
RESULTS: After 1 year, aPWV (mean (s.d.)) was improved in the treatment group, but not in the control group (-0.54 [0.79] m/s vs. 0.06 [0.61] m/s, respectively; P = 0.004), and CIMT progression (median (quartile cut-points, 25th and 75th percentiles)) was reduced in the treatment group compared to the control group (-0.002 [-0.038, 0.030] mm vs. 0.030 [0.011, 0.043] mm, respectively; P = 0.01). In multivariable analyses, anti-TNF-α therapy over time was associated with improved aPWV (P = 0.02) and reduced CIMT progression (P = 0.04), and calprotectin was longitudinally associated with aPWV (P = 0.02).
CONCLUSIONS: Long-term anti-TNF-α therapy improved aortic stiffness and CIMT progression in patients with inflammatory arthropathies. Calprotectin may be a soluble biomarker reflecting aortic stiffening in these patients.
Kristin Angel; Sella A Provan; Magne K Fagerhol; Petter Mowinckel; Tore K Kvien; Dan Atar
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Publication Detail:
Type:  Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-03-01
Journal Detail:
Title:  American journal of hypertension     Volume:  25     ISSN:  1941-7225     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-05-17     Completed Date:  2012-10-23     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  United States    
Other Details:
Languages:  eng     Pagination:  644-50     Citation Subset:  IM    
Department of Cardiology B, Oslo University Hospital Ullevaal, Oslo, Norway.
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MeSH Terms
Antirheumatic Agents / pharmacology,  therapeutic use*
Arthritis, Psoriatic / drug therapy*,  physiopathology
Arthritis, Rheumatoid / drug therapy*,  physiopathology
Blood Pressure / drug effects,  physiology
Carotid Artery Diseases / drug therapy*,  physiopathology
Carotid Intima-Media Thickness
Disease Progression
Leukocyte L1 Antigen Complex / blood,  drug effects,  physiology*
Longitudinal Studies
Middle Aged
Prospective Studies
Spondylitis, Ankylosing / drug therapy*,  physiopathology
Treatment Outcome
Tumor Necrosis Factor-alpha / antagonists & inhibitors*
Vascular Stiffness / drug effects,  physiology*
Reg. No./Substance:
0/Antirheumatic Agents; 0/Leukocyte L1 Antigen Complex; 0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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