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Inflammation and lipid profile in rheumatoid arthritis: bridging an apparent paradox
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  1. Miguel A González-Gay1,
  2. Carlos González-Juanatey2
  1. 1Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IFIMAV, Santander, Cantabria, Spain
  2. 2Division of Cardiology, Hospital Universitario Lucus Augusti, Lugo, Spain
  1. Correspondence to Dr Miguel A González-Gay, Rheumatology Division, Hospital Universitario Marqués de Valdecilla, IFIMAV, Avenida de Valdecilla, s/n, Santander, Cantabria 39008, Spain; miguelaggay{at}hotmail.com

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Several pieces of evidence indicate that rheumatoid arthritis (RA) is a proatherogenic disease associated with increased cardiovascular (CV) mortality.1 ,2 Besides genetic and traditional CV risk factors,3 ,4 chronic inflammation has emerged as a pivotal component implicated in the development of this process. A chronic inflammatory burden, determined by the mean values of C-reactive protein (CRP) over the extended follow-up of patients with RA, was associated with subclinical atherosclerosis and increased risk of CV events.5 ,6 In keeping with these observations, in a large retrospective cohort study, CV disease-related mortality was increased in RA patients with elevated measures of inflammation markers.7 These findings are in accordance with data from the general population that showed that CRP could be an independent predictor of CV disease with CRP values ≥3 mg/L defining high CV-risk individuals.8 With respect to this, levels of the proinflammatory cytokine interleukin-6, the main inducer of CRP, also predict outcome following hospitalisation for unstable angina.9

Despite some similarities, there are also some differences between patients with chronic inflammatory diseases and the general population. While the risk to develop atherosclerosis increases progressively with increasing low-density lipoprotein (LDL) cholesterol levels and declines with increasing levels of high-density lipoprotein (HDL) cholesterol in healthy individuals,10 the presence of a proinflammatory state leads to a decrease of total cholesterol, HDL cholesterol and LDL cholesterol in patients with RA.11

Paradoxically, anti-inflammatory therapies increase total cholesterol, HDL cholesterol and LDL cholesterol to variable degrees in patients with RA.11 ,12 This lipid increase is not associated with a rise in the number of CV events in these patients. On the contrary, probably due to the anti-inflammatory effect, conventional disease-modifying antirheumatic drugs, such as methotrexate, and different biological agents have demonstrated a reduction of the CV …

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