EDITORIAL
Dyslipidaemia, statins and rheumatoid arthritis
1 Department of Internal Medicine, VU University Medical Centre, Amsterdam, The Netherlands
2 Department of Rheumatology, VU University Medical Centre, Amsterdam, The Netherlands
3 VU University Medical Centre, Jan van Breemen Institute, Amsterdam, The Netherlands
Correspondence to:
Dr Michael T Nurmohamed, Departments of Internal Medicine and Rheumatology, VU University Medical Centre, PO Box 7057, Amsterdam, The Netherlands; mt.nurmohamed@vumc.nl
Accepted 11 January 2009
| The first 150 words of the full text of this article appear below. |
Cardiovascular morbidity and mortality are enhanced in rheumatoid arthritis (RA) and there is increasing evidence that this is due to the inflammatory process as well as to an increased prevalence of traditional cardiovascular risk factors, such as dyslipidaemia.1–3
Several investigators have indeed demonstrated dyslipidaemia, defined as higher total cholesterol and/or triglycerides and/or lower high-density lipoprotein (HDL) cholesterol levels in comparison to control subjects, in RA and this appears to be the consequence of systemic release of inflammatory cytokines such as tumour necrosis factor (TNF)
, interleukin (IL)1 and IL6, leading to a proatherogenic state with insulin resistance, endothelial cell activation and hypercoagulation as other consequences.
The dyslipidaemia in RA is dependent on disease activity, ie, a higher disease activity is associated with lower total cholesterol levels and even more depressed HDL cholesterol levels, leading to a higher (ie, unfavourable) atherogenic index.4
Moreover, it appears that dyslipidaemia is already present in
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