Author(s): Vis M, Nurmohamed MT, Wolbink G, Voskuyl AE, de Koning M, , Vis M, Nurmohamed MT, Wolbink G, Voskuyl AE, de Koning M,
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Abstract OBJECTIVE: Cardiovascular morbidity and mortality appear to be enhanced in rheumatoid arthritis (RA), which might be due to an increased prevalence of cardiovascular risk factors such as dyslipidemia. It was recently shown that effective disease modifying antirheumatic drug treatment had a favorable influence on the lipid profile in patients with active RA. As infliximab markedly reduces disease activity in RA, we investigated the effects of infliximab on the lipid profile. METHODS: Infliximab was administered at baseline and at 2 and 6 weeks in patients with active RA. Total cholesterol and HDL-cholesterol concentrations were measured and their ratio, the atherogenic index (an important cardiovascular risk factor indicator), was assessed. RESULTS: Sixty-nine patients were enrolled. The Disease Activity Index score (DAS-28) was 5.9 (SD +/- 1.4) at baseline and decreased to 4.6 (+/- 1.4) after 2 weeks and further to 4.1 (+/- 1.5) after 6 weeks. Total cholesterol level was 5.2 mmol/l at baseline and increased to 5.7 mmol/l (p < 0.001) at 2 weeks, and was 5.6 mmol/l (p < 0.001 vs baseline) at Week 6. For HDL-cholesterol these values were 1.5, 1.6 (p < 0.001), and 1.6 mmol/l (p < 0.001 vs baseline), respectively. Changes in disease activity were significantly inversely associated with changes in total cholesterol and HDL-cholesterol levels. The atherogenic index, however, remained constant. Corticosteroid use at baseline was associated with significantly higher total cholesterol and HDL-cholesterol levels and a lower (more favorable) atherogenic index at baseline. CONCLUSION: Infliximab treatment was associated with a significant increase of both total cholesterol and HDL-cholesterol levels, which correlated with decreasing disease activity. However, this was not accompanied by a favorable effect on the atherogenic index. The favorable effect of infliximab on cardiovascular comorbidity might not be mediated by effects on lipid metabolism, but longterm investigations are needed to confirm this.
This article was published in J Rheumatol
and referenced in Cardiovascular Therapy: Open Access