Background The causal mechanisms of the elevated cardiovascular (CV) risk in RA have not been totally clarified. In fact, usual standard tests to assess lipid metabolism are not usually different between patients and general population.

Objectives Our objective was to perform a more in depth study of this latter issue using novel and more specific markers. We show here preliminary results

Methods RA patients and matched healthy controls were cross-sectionally evaluated including inflammatory markers (ESR, hsCRP, Pentraxina 3 and SAA), disease activity, by joints counts and DAS28, disability, by MHAQ questionnaire (only for RA patients) and specifically a comprehensive lipid and lipoprotein assessment which in addition of conventional tests included the following determinations: Lipoprotein, and apolipoprotein A1 (ApoA1) and B (ApoB) levels (total and lipoprotein specific), levels of paroxonase 1 (PON1), HDL, LDL, VLDL and total cholesterol, triglycerides and phospholipids levels as well as number of molecules of these lipids (mc, mt and mf respectively) in each lipoprotein, total mass (M) and number of particles (np) of the afore mentioned lipoproteins, and levels of PCSK9 receptor. Standard statistical tests were used for comparing patients and controls.

Results One-hundred twenty-seven RA patients (mean age±: 59.9±12.2 years; 81% women and 63% seropositive) and 29 healthy controls (56.14±9.8; p=NS; 81% women) were evaluated. As expected, patients showed significant higher acute phase reactants levels. Standard lipid determinations including total and HDL, LDL and VLDL cholesterol, triglycerides and others as lipoproteins, phospholipids or Apo-B were comparable in both subsets. However, RA patients presented several risk markers as lower levels of Apo-A1 HDL (p=0.032) and higher of mc LDL and VLDL (p=0.023 and 0.002 respectively), mt LDL and VLDL (p=0.042 and =0.001) and np VLDL (p=0.007). Unexpectedly, paroxonase levels were higher among RA patients (p=0.0001)

Conclusions RA patients present diverse alterations of lipid and lipoprotein metabolism, which may confer them a CV risk profile. The higher levels of paroxonase are against this idea; the reason of this finding might be due to the competitive action for HDL of the inflammatory molecules, such as SAA, which could render functionally inactive the most part of this enzyme.

Disclosure of Interest None Declared