Rheumatoid arthritis: links with cardiovascular disease and the receptor for advanced glycation end products

Carroll, Lisa, Hannawi, Suad, Marwick, Thomas and Thomas, Ranjeny (2006) Rheumatoid arthritis: links with cardiovascular disease and the receptor for advanced glycation end products. Wiener Medizinische Wochenschrift, 156 1-2: 42-52. doi:10.1007/s10354-005-0242-9


Author Carroll, Lisa
Hannawi, Suad
Marwick, Thomas
Thomas, Ranjeny
Title Rheumatoid arthritis: links with cardiovascular disease and the receptor for advanced glycation end products
Journal name Wiener Medizinische Wochenschrift   Check publisher's open access policy
ISSN 0043-5341
1563-258X
Publication date 2006
Sub-type Article (original research)
DOI 10.1007/s10354-005-0242-9
Volume 156
Issue 1-2
Start page 42
End page 52
Total pages 11
Editor H. Kurz
Place of publication Austria
Publisher Springer-Verlag Wien
Collection year 2006
Language eng
Subject C1
321028 Rheumatology and Arthritis
730106 Cardiovascular system and diseases
1102 Cardiovascular Medicine and Haematology
110322 Rheumatology and Arthritis
Abstract Cardiovascular (CV) disease is increased in patients with chronic inflammatory disease, including rheumatoid arthritis (RA). Furthermore it has become clear at a pathophysiological level, that atherosclerosis has striking similarities with autoimmune disease. This realization has come at a time of paradigm shift in how rheumatologists manage RA, with the availability of biological agents targeting key inflammatory cytokines. This review will focus on the possible causes of increased vascular disease in RA, including the role of traditional CV risk factors. Mechanisms potentially at play, such as C-reactive protein (CRP), altered coagulation, and cyclooxygenase (COX) -2 inhibitors will be covered in brief. The Receptor for Advanced Glycation End Products (RAGE) has been identified as a candidate molecule influencing response to ongoing inflammation and autoimmunity. There will be a focus on the role of RAGE in CV disease and RA. As has been the case with many novel molecules, functional polymorphisms are thought to alter disease expression and assist us in coming to terms with the biological activities of the parent molecule. The review will conclude with a discussion of the potential role of the RAGE Glycine 82 Serine polymorphism
Keyword Arthritis Rheumatoid
Cardiovascular Diseases
Advanced Glycation End-Product Receptor
Polymorphism
Genetic
Inflammation
C-Reactive Protein
Hyperlipidaemia
Coagulation
Q-Index Code C1

 
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Created: Wed, 15 Aug 2007, 10:01:51 EST