The paradigm by which an increase in the inflammatory burden in RA is associated with the lowering of lipid levels has also been noted in other chronic.

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Presentation transcript:

The paradigm by which an increase in the inflammatory burden in RA is associated with the lowering of lipid levels has also been noted in other chronic inflammatory conditions, after MI, after surgery and in cancer treatment [21, 29, 64–70]. In RA, a reduction of inflammation through treatment with traditional and/or biologic DMARDs is reflected in elevations in lipid levels [71]. Data, although limited, suggest the extent to which lipid levels change may be different between RA therapies; however, further studies are required to fully ascertain the relationship between suppression of inflammation, lipid elevations and future cardiovascular risk [71, 102]. MI, myocardial infarction. From: Cardiovascular risk in rheumatoid arthritis: recent advances in the understanding of the pivotal role of inflammation, risk predictors and the impact of treatment Rheumatology (Oxford). 2014;53(12):2143-2154. doi:10.1093/rheumatology/keu224 Rheumatology (Oxford) | © The Author 2014. Published by Oxford University Press on behalf of the British Society for RheumatologyThis is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Systemic inflammation associated with RA may confer both quantitative and qualitative changes to HDL cholesterol underlying the loss of some anti-inflammatory and atheroprotective properties. Known changes to subparticle composition induced by inflammation are summarized in this figure [74, 76–83, 86–88]. apoA1: apolipoprotein A1; apoJ: apolipoprotein J; CETP: cholesteryl ester transfer protein; HDL: high-density lipoprotein; LCAT: lecithin cholesterol acyltransferae; LDL: low-density lipoprotein; PAF-AH: platelet-activating factor acetylhydrolase; PON-1: paraoxonase 1; SAA: serum amyloid A; sPLA<sub>2</sub>: secretory non-pancreatic phospholipase A<sub>2</sub>. From: Cardiovascular risk in rheumatoid arthritis: recent advances in the understanding of the pivotal role of inflammation, risk predictors and the impact of treatment Rheumatology (Oxford). 2014;53(12):2143-2154. doi:10.1093/rheumatology/keu224 Rheumatology (Oxford) | © The Author 2014. Published by Oxford University Press on behalf of the British Society for RheumatologyThis is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

The heightened inflammatory state in RA is linked with accelerated atherosclerosis, with systemic inflammation exacerbating adverse changes in both established and novel cardiovascular (CV) risk factors [16–19]. Additionally, the use of some anti-inflammatory medication is also associated with increasing CV risk [6]. Treat-to-target strategies with traditional and/or biologic DMARDs can be highly effective to rapidly reduce inflammation and achieve tight control of disease activity [146]. Lipid profiles can then be monitored and, if appropriate, treated with lipid-lowering drugs according to national guidelines [147–149]. From: Cardiovascular risk in rheumatoid arthritis: recent advances in the understanding of the pivotal role of inflammation, risk predictors and the impact of treatment Rheumatology (Oxford). 2014;53(12):2143-2154. doi:10.1093/rheumatology/keu224 Rheumatology (Oxford) | © The Author 2014. Published by Oxford University Press on behalf of the British Society for RheumatologyThis is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com