Document Detail


Clinical improvement in rheumatoid arthritis is associated with healthier microvascular function in patients who respond to antirheumatic therapy.
MedLine Citation:
PMID:  20080919     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Rheumatoid arthritis (RA) is associated with increased cardiovascular (CV) mortality. Microvascular endothelial dysfunction occurs early in the development of CV disease and is worsened by inflammation. The effect of drug treatment for RA on microvascular function has been poorly studied. We assessed the effect of antirheumatic treatment on microvascular endothelial function in patients with RA, particularly to examine responders versus nonresponders to therapy.
METHODS: Fifty-one patients with active RA and no previous history of CV disease were assessed at baseline and after 2 and 4 months' therapy with either anti-tumor necrosis factor-alpha drugs (etanercept, n = 27, adalimumab, n = 3) or methotrexate, n = 21. RA disease activity, inflammatory measures, and skin microvascular responses, measured using laser Doppler imaging after iontophoretic delivery of acetylcholine (ACh) and sodium nitroprusside (SNP), were assessed at each study visit.
RESULTS: Disease Activity Score (DAS28) decreased significantly from baseline to visit 2 and 3 (6.04 +/- 1.2, 4.34 +/- 1.3, 4 +/- 1.3, respectively; p < 0.0001). Endothelium-dependent (ACh) and independent (SNP) responses for the whole cohort did not improve significantly after drug treatment (p = 0.250, p = 0.062, respectively). When patients who responded to antirheumatic therapy (n = 31) were analyzed, there were significant improvements in both ACh (p = 0.028) and SNP responses (p = 0.019).
CONCLUSION: Microvascular endothelial function improves in patients who respond to antirheumatic therapy. These results support the importance of effective therapy for RA patients in terms of CV effects, which might extrapolate to reduced CV events in the future. Clinical trial registration no. ISRCTN57761809.
Authors:
Bernat Galarraga; Jill J F Belch; Tom Pullar; Simon Ogston; Faisel Khan
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-15
Journal Detail:
Title:  The Journal of rheumatology     Volume:  37     ISSN:  0315-162X     ISO Abbreviation:  J. Rheumatol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-03     Completed Date:  2010-05-20     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  7501984     Medline TA:  J Rheumatol     Country:  Canada    
Other Details:
Languages:  eng     Pagination:  521-8     Citation Subset:  IM    
Affiliation:
Vascular and Inflammatory Diseases Research Unit, Centre for Cardiovascular and Lung Biology, Division of Medical Sciences, Ninewells Hospital and Medical School, Dundee, DD1 9SY, Scotland.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Antibodies, Monoclonal / therapeutic use
Antibodies, Monoclonal, Humanized
Antirheumatic Agents / therapeutic use*
Arthritis, Rheumatoid / complications,  drug therapy*,  physiopathology*
Cardiovascular Diseases / epidemiology
Dose-Response Relationship, Drug
Endothelium, Vascular / physiopathology*
Female
Follow-Up Studies
Humans
Immunoglobulin G / therapeutic use
Male
Methotrexate / therapeutic use
Microcirculation / physiology*
Middle Aged
Receptors, Tumor Necrosis Factor / therapeutic use
Risk Factors
Treatment Outcome
Tumor Necrosis Factor-alpha / antagonists & inhibitors
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antibodies, Monoclonal, Humanized; 0/Antirheumatic Agents; 0/Immunoglobulin G; 0/Receptors, Tumor Necrosis Factor; 0/Tumor Necrosis Factor-alpha; 185243-69-0/TNFR-Fc fusion protein; 59-05-2/Methotrexate; FYS6T7F842/adalimumab

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


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