Anti-TNF Therapy Induces Positive Changes In The Lipoprotein Profile Of RA Patientes. Results Of a Prospective Study

Jaime Calvo-Alén¹, Carmela Baamonde², Ignacio Villa¹, Víctor Martínez-Taboada³, Mario Agudo⁴ and Juan Gómez-Gerique⁵, ¹Rheumatology, Hospital Universitario Sierrallana, Torrelavega, Spain, ²Biochemistry, Hospital Universitario Sierrallana, Torrelavega, Spain, ³Rheumatology, Hospital Universitario Marqués de Valdecilla, Santander, Spain, ⁴Rheumatology, Hospital Universitario Marqués de Valdecilla. IFIMAV, Santander, Spain, ⁵Biochemistry, Hospital Universitario Marqués de Valdecilla. IDIVAL. Santander. Spain, Santander, Spain

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: anti-TNF therapy, Atherosclerosis, Cardiovascular disease, lipids and rheumatoid arthritis, treatment

Session Information

Title: Rheumatoid Arthritis Treatment - Small Molecules, Biologics and Gene Therapy I

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Anti-TNF therapy induces elevations in total cholesterol levels although does not seem to modify the atherogenic index. Otherwise, it appears to have a cardiovascular protective effect. We have tried to study in depth the effect of this therapy in the lipidic metabolism through a comprehensive analysis of the lipid and lipoprotein induced modifications.

Methods:

RA patients naive to any type of biologic therapy starting anti-TNF therapy, were evaluated at two points (first, just before the first dose of the anti-TNF agent and second, at six months of stable anti-TNF therapy) according to a pre-established protocol including the following assessments of lipidic metabolism: 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. Inflammatory markers (ESR, hsCRP, Pentraxina 3 and SAA) and disease activity by joints counts and DAS28 index were also performed. Standard statistical tests were used for comparing both assessments.

Results:

Nineteen RA (mean age±SD: 60.7±13.2 years; disease duration±SD: 124.3±296.8 months; 68% women; 47% seropositive and mean±SD DAS28 at first evaluation: 5.5±1.2) patients were evaluated. As expected patients showed a decrease in disease activity (4.6±1.4; p=0.08)). Regarding to the lipidic determinations, although the total cholesterol increased (191 mg/dl ±25 vs 208 mg/dl ±24; p=0.07) without modifying the atherogenic index, anti-TNF induced several biochemical and structural lipoprotein changes with a final positive balance including the following: increase levels of total and HDL ApoA1 (p=0.05 and 0.04), decrease of LDL ApoB (p=0.08) with increase of ApoB VLDL (p=0.08) increase of MHDL (p=0.003) and HDL triglyceride (p=0.035) and protein (p=0.0003) content, decrease in np LDL (p=0.08) and increase of np VLDL which are less atherogenic.

Conclusion:

Anti-TNF therapy induces global positive lipoprotein balance with increases of ApoA1 levels and a metabolic shift towards HDL and VLDL molecules instead of LDL. Future studies with larger samples and times of follow up will help us to better define this modifications.

Disclosure:

J. Calvo-Alén,
None;

C. Baamonde,
None;

I. Villa,
None;

V. Martínez-Taboada,
None;

M. Agudo,
None;

J. Gómez-Gerique,
None.

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