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Choy E & Sattar N.

Ann Rheum Dis 2009; 68:460–469.

RA patients have a greater risk of cardiovascular disease (CVD) than the general population and traditional risk factors only partially explain this excess. The high-grade chronic inflammation in RA can directly and indirectly accelerate CVD. However, a paradox exists in that biologics that have been shown to reduce this inflammatory burden are also associated with an increase in lipid levels that in the general population is associated with increased CVD risk.

This review discusses the relationships between CVD risk, inflammation and lipid levels in patients with RA, summarises recent evidence for increased lipid levels in patients treated with biologics and outlines possible underlying mechanisms.

Following a systematic review of the effect of anti-TNFs and tocilizumab on lipid profiles in patients with RA, the authors comment that studies do not support the notion that biologic-induced lipid elevations lead to enhanced CVD risk. In contrast, the potent reduction in RA disease activity is likely to account for both the changes in observed lipid profile and the reduction in CVD risk.

These findings were also true for tocilizumab, which was consistently associated with increased lipid levels in the context of decreasing levels of inflammatory markers; however, no increase in cardiovascular events was reported.

The evidence discussed in this review demonstrates that biologics increase lipid levels; however, the change in lipid profiles is broadly predictable and coincides with reduced inflammation. This supports the hypothesis that inflammation is a more important CVD risk factor than lipid profiles.

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