| Objective To compare the modifications in lipid profiles, vascular endothelial function, cardiovascular system among patients with RA receiving anti-TNF-a agents plus disease modifying anti-rheumatic drugs (DMARDs) versus DMARDs, to investigate the characteristics of lipid profiles in RA patients with active phase and inactive phase, explore the relationship between dyslipidemia, inflammation, endothelial cell dysfunction and cardiovascular risk in RA patients, then provide a theoretical basis for early clinical intervention for the dyslipidemia and cardiovascular complications in patients with RA.Methods The study was included two sections.①100 newly diagnosed RA patients were involved in the first part,50 of them were in active stage and 50 were in nonactive stage. Levels of low-density lipoprotein (LDL), total cholesterol(TC), lipoprotein a (Lpa), triglycerides(TG), apolipoprotein B (Apo-B), high-density lipoprotein cholesterol(HDL), apolipoprotein Al (Apo-Al), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), antibodies against cyclic citrullinated peptide (ACCP)were assayed in the 100 patients, as well as the disease activity score-28(DAS28), atherogenic index of plasma (AIP) was calculated by the results of triglyceride (TG) and high-density lipoprotein (HDL).②100 newly diagnosed RA patients were randomly divided into biological agents treatment group and non-biological agents treatment group, each group included 50 patients. Levels of the above lipid profiles were assessed at baseline and at 12 and 24 weeks, carotid intima-media thickness (CIMT)were studied at 24 weeks. Statistical analyses are performed with SPSS software version 19.0.Results ①Results of the first part can be drawn as follows:compared to the patients with nonactive RA, levels of Lpa, AIP were higher and Apo-Al was lower in patients with active RA, ESR, CRP, DAS28 and Lpa, AIP were positively correlated respectively, ACCP and AIP were positively correlated(all P<0.05). ②Results of the second part can be drawn as follows:baseline values for lipid levels were similar in both groups. Pearson correlation test was carried out and found that CIMT and ESR, CRP, AIP were positively correlated, HDL, Apo-Al were negatively correlated at baseline; At 12 weeks and 24 weeks, CRP, ESR, DAS28 in both two groups were significantly decreased compared with the baseline data respectively; At 12 weeks and 24 weeks in the biological agents treatment group, the levels of HDL, Apo-Al were increased and levels of Lpa, AIP were decreased when compared to the baseline,and at 24 weeks, CIMT was decreased compared to the baseline; At 24 weeks in the non-biological agents treatment group, the levels of HDL was increased, levels of LDL, Lpa, CIMT, AIP were all decreased compared to the baseline. At 12 weeks in the biological agents treatment group, the levels of AIP, Lpa were lower than non-biological agents group, levels of TC, HDL, Apo-Al were higher than non^biological agents group, and at 24 weeks in the biological agents treatment group, the levels of Apo-B, Lpa were lower than non-biological agents group, level of LDL, Apo-Al were higher than non-biological agents group(all P<0.05).Conclusions Compared to the patients with nonactive RA, the patients with active RA had apparent lipids disorders that showed lower Apo-Al and higher Lpa, AIP, which is closely related to the atherosclerosis; Inflammatory status may affect the lipid profiles and the endothelial function and is associated with the atherosclerosis, with the increase of inflammatory activity, the cardiovascular risk also increased. ②HDL, Apo-Al, AIP index can be used as a predictor of endothelial cell dysfunction and has prompted significance for atherosclerosis, ACCP will be of great importance in predicting cardiovascular risk. ③TNF-α antagonist can elevate the protective lipids such as HDL, Apo-Al and weaken nonprotective lipids such as Apo-B, Lpa rapidly, so it has better effect on improving lipid profile compared to the DMARDs. Traditional DMARDs can also improve the lipids especially in terms of LDL cholesterol, but the overall effect is not as good as TNF-a antagonist.④Both TNF-a antagonist and DMARDs can improve the endothelial function and reduce the risk of atherosclerosis in patients with RA. ⑤By reducing the inflammation, improving lipids and vascular endothelial function in RA patients, TNF-a antagonist can reduce the cardiovascular complications in RA, and the protective effect of TNF-a antagonist on cardiovascular complications in RA, and the protective effect of TNF-a antagonist on cardiovascular risk is superior to traditional DMARDs, but the medication’s effect lasts shorter lengths of time, therefore further studies and large samples are needed in the future. |
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