The evidence that several variables, including inflammation, autoimmunity and traditional cardiovascular (CV) risk factors, closely interact to enhance atherosclerotic risk burden in rheumatoid arthritis (RA) has been well established over the past decade [1]. However, the actual contribution of each parameter is still to be clarified. In this context, among the traditional CV risk factors, the impact of dyslipidaemia on the CV risk of RA patients is the most controversial. Indeed, disease-related inflammatory mechanisms accounting for the “lipid paradox” may be associated with altered lipid profile that make the lipid profile assessment unreliable in RA patients, particularly during the active stages of the disease [2,3].
