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. 2012 Sep;64(9):1282-91.
doi: 10.1002/acr.21693.

Dyslipidemia and changes in lipid profiles associated with rheumatoid arthritis and initiation of anti-tumor necrosis factor therapy

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Dyslipidemia and changes in lipid profiles associated with rheumatoid arthritis and initiation of anti-tumor necrosis factor therapy

Jeffrey R Curtis et al. Arthritis Care Res (Hoboken). 2012 Sep.

Abstract

Objective: To investigate the frequency of lipid testing in clinical practice and to explore the relationship between rheumatoid arthritis (RA), dyslipidemia, and other cardiovascular (CV) risk factors with RA treatment.

Methods: Patients in this retrospective database study were ages ≥18 years and had ≥2 physician diagnoses for RA or osteoarthritis (OA; comparator group) between March 2004 and March 2008. Outcomes of interest included the percentage of RA and OA patients receiving lipid tests, lipid profiles (total cholesterol, low-density lipoprotein [LDL] cholesterol, and high-density lipoprotein [HDL] cholesterol) of RA versus OA patients, and lipid profiles of RA patients before and after initiation with a tumor necrosis factor (TNF) inhibitor. We used multivariable regression to control potential confounders between the cohorts.

Results: Over a median ≥2-year followup, fewer RA patients than OA patients had ≥1 lipid test (62.0% [95% confidence interval (95% CI) 61.5-62.5] versus 69.8% [95% CI 69.5-70.1]). Mean total cholesterol and LDL cholesterol were each 4 mg/dl lower in the RA cohort (P < 0.0001); HDL cholesterol was similar between the cohorts. Across the RA cohort, 25.2% of patients had suboptimal LDL cholesterol levels (≥130 mg/dl). Among RA patients not receiving lipid-lowering therapy who initiated TNF inhibitor therapy (n = 96), mean total cholesterol and LDL cholesterol increased by 5.4 and 4.0 mg/dl, respectively.

Conclusion: Patients with RA were less likely to be tested for hyperlipidemia and had more favorable lipid profiles than patients with OA. TNF inhibitor therapy modestly increased all lipid parameters. Additional studies are needed to determine the effect of traditional CV risk factors and inflammation and the impact of biologic agents on CV outcomes in RA patients.

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Figures

Figure 1
Figure 1. Proportions of RA and OA Patients in Various Lipid Categories Based On ATP-III Classifications
RA and OA cohorts were adjusted using multivariable regression based on factors listed in Table 1. Error bars indicate the 95% confidence interval of the mean.
Figure 2
Figure 2. Changes in Lipid Levels after TNFi Initiation in Patients with RA
Includes patients who underwent lipid testing within 90 days before and after TNFi initiation. Not all patients underwent the complete set of lipid tests (e.g., patients might have undergone only TC testing but not HDL or LDL testing). A linear regression model was used to control for the factors listed in Table 1. *p ≤ 0.0001; †p ≤ 0.01 for the null hypothesis that there was no change in lipid values after TNFi initiation

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