Background RA patients portend a greater risk of cardio-vascular complications than general population. Although most probably diverse mechanisms are implicated, quantity and quality changes in the lipoproteins appear to have an important role. Anti-TNF therapy has shown important benefits in controlling the inflammatory prcess but conflicting results have been reported regarding to its effects on lipid profile.
Objectives To study the effect of anti-TNF agents on the lipid and lipoprotein profile of RA patients using a comprehensive study protocol including novel and more specific parameters for this pourpue.
Methods RA patients in stable treatment with anti-TNF therapy at least during the last six months and a matched (by age, gender and rheumatoid factor status) with stable doses of standard DMARDs (most of them using methotrexate) were clinically evaluated using DAS28, as activity marker and MHAQ to assess disability. In addition, a complete standard lipid profile, a comprehensive lipoprotein assessment was carried out including: 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 before mentioned lipoproteins, levels of PCSK9 receptor. Results of both subsets of patients were performed with standard statistical tests.
Results Sixty-seven RA patients on anti-TNF and 63 matched RA patients on DMARD, mean age (58.7±12.3 and 61±12.1 years), gender distribution (81% females in both cases), disease duration (140±165 and 143±276 months) and RF status (64% in both cases) were comparable. Patients on DMARD were more active (DAS28 4.42±1.35 vs 3.57± 1.27 and hsCRP 9.4±15.2 vs 3.8±5.8 mg/l respectively. Main findings in the lipoprotein analysis are shown in table 1:
Conclusions RA patients treated with anti-TNF, regardless that they show lower levels of clinical activity, they have an improvement in their atherogenic risk profile showing higher levels of ApoA1 and therefore greater antioxidant capacity as well as lower levels of total mass and number of particles of VLDL which are atherogenic risk factors.
Disclosure of Interest None Declared