scholarly journals The role of inflammation and cardiovascular disease risk on microvascular and macrovascular endothelial function in patients with rheumatoid arthritis: a cross-sectional and longitudinal study

2012 ◽  
Vol 14 (3) ◽  
pp. R117 ◽  
Author(s):  
Aamer Sandoo ◽  
George D Kitas ◽  
Douglas Carroll ◽  
Jet JCS Veldhuijzen van Zanten
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Disease ◽  
Longitudinal Study ◽  
Endothelial Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cross Sectional

scholarly journals Thyroid function and cardiovascular disease risk factors in euthyroid adults: a cross-sectional and longitudinal study

2016 ◽  
Vol 85 (6) ◽  
pp. 932-941 ◽  
Author(s):  
Jane J. Lee ◽  
Alison Pedley ◽  
Ellen Marqusee ◽  
Patrice Sutherland ◽  
Udo Hoffmann ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Longitudinal Study ◽  
Thyroid Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cardiovascular Disease Risk Factors ◽  
Cross Sectional

scholarly journals The Central Role of Acute Phase Proteins in Rheumatoid Arthritis: Involvement in Disease Autoimmunity, Inflammatory Responses, and the Heightened Risk of Cardiovascular Disease

2020 ◽  
Vol 46 (04) ◽  
pp. 465-483 ◽  
Author(s):  
Johannes A. Bezuidenhout ◽  
Etheresia Pretorius
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Disease ◽  
Acute Phase ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Rapid Progression ◽  
Phase Reaction ◽  
Infectious Agents ◽  
Arginine Residues

AbstractRheumatoid arthritis (RA) is an autoimmune disease of complex etiopathogenic origin and traditionally characterized by chronic synovitis and articular erosions. Furthermore, there is strong evidence that infectious agents, including those that become dormant within the host, play a major role in much of the etiology of RA and its hallmark of inflammation. A combination of genetic predisposition, environmental exposure, and presence of infectious agents may therefore lead to a loss of immune tolerance to citrullinated proteins, which present as self-antigens to the human immune system. This results in generation of highly RA-specific autoantibodies, known as anti-citrullinated protein antibodies (ACPAs). Protein citrullination occurs via posttranslational deamination of arginine residues by peptidylarginine deiminase enzymes, which have confirmed sources of both endogenous and infectious origins. A recognized plasma protein target of citrullination and RA autoantibody generation is fibrin and its soluble precursor fibrinogen, both key components of hemostasis and acute phase reaction. Increased titers of ACPAs that accompany rapid progression to clinical RA disease have been shown to drive a variety of proinflammatory processes, and therefore results in aberrant fibrin clot formation and increased cardiovascular risk. However, the full extent to which hemostasis is affected in RA remains controversial, owing to the differential impact that citrullinated fibrin(ogen) and concurrent systemic inflammation may have on resulting hemostatic outcome. This review highlights key events in initiation of autoimmune-driven inflammatory events, including the role of bacterial infectious agents, which subsequently result in clinical RA disease and associated secondary cardiovascular disease risk, with specific focus on plasma proteins that are heavily involved throughout the immunopathological progression process.

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