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


  • Jeffrey R. Curtis,

    Corresponding author
    1. University of Alabama, Birmingham
    • UAB Center for Education and Research on Thera- peutics, University of Alabama at Birmingham, FOT 805D, 510 20th Street South, Birmingham, AL 35294
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    • Dr. Curtis has received consultant fees, speaking fees, and/or honoraria (less than $10,000 each) from UCB, Centocor, Pfizer, BMS, and Abbott, and (more than $10,000 each) from Roche/Genentech, Consortium of Rheumatology Researchers of North America, Amgen, and Crescendo.

  • Ani John,

    1. Genentech, South San Francisco, California
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  • Onur Baser

    1. University of Michigan and STATinMED Research, Ann Arbor
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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.


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.


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.


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.