Mechanisms
CETP activity and mass are lower in rheumatoid arthritis patients taking glucocorticoids (J Rheumatol 2013)
Original title: Cholesteryl ester transfer protein in patients with rheumatoid arthritis
This study measured plasma CETP concentration and activity in 101 rheumatoid arthritis (RA) patients and 115 matched controls to examine the relationship of CETP with dyslipidemia and cardiovascular mortality risk. RA patients overall showed lower CETP activity (beta = -10.82, 95% CI, -19.56 to 2.07 pmol/3h; p = 0.02) and lower CETP mass (beta = -0.85, 95% CI, -1.64 to 0.05 ug/mL; p = 0.03) than controls, an effect confined to patients taking glucocorticoids (activity: beta = -8.98, p = 0.00; mass: beta = -0.77, p = 0.03), with RA patients not on glucocorticoids showing no difference from controls. Both current and average 3-month prednisone intake correlated inversely with CETP activity and mass (p = 0.00 and p = 0.01, respectively), and lower CETP activity predicted higher total mortality at higher SCORE cardiovascular risk (beta = -4.7, p = 0.04). The authors conclude CETP is downregulated by glucocorticoid use in RA and that low CETP activity is associated with increased cardiovascular risk in these patients.
Original abstract
Objective: To investigate how cholesteryl ester transfer protein (CETP), one of the enzymes involved in the reverse cholesterol transfer, is expressed in patients with rheumatoid arthritis (RA) and its potential relationship with both dyslipidemia and the risk of cardiovascular mortality observed in these patients.
Methods: Plasma CETP concentrations and CETP activity were measured in 101 patients with RA and 115 sex- and age-matched controls. A multivariable analysis adjusted for standard cardiovascular risk factors, including high-density lipoprotein cholesterol, was performed to evaluate the influence of CETP on dyslipidemia and cardiovascular mortality risk, as assessed by the Systematic Coronary Risk Evaluation (SCORE) risk function.
Results: Patients with RA showed lower CETP activity [beta coefficient = -10.82 (95% CI -19.56 to 2.07) pmol/3 h; p = 0.02] and an inferior CETP mass [β = -0.85 (95% CI -1.64 to 0.05) μg/ml; p = 0.03] versus controls. Divided into those taking and those not taking glucocorticoids, patients taking glucocorticoids revealed lower CETP activity and mass [β = -8.98 (95% CI -14.55 to 3.41) pmol/3 h; p = 0.00, for CETP activity; and β = -0.77 (95% CI -1.46 to 0.08) μg/ml; p = 0.03, for CETP mass]. Patients with RA not taking glucocorticoids showed no differences versus controls in either CETP activity or mass. Both current prednisone intake [β = -16.14 (95% CI -24.87 to 7.41) pmol/3 h; p = 0.00] and average daily prednisone intake during the last 3 months [β = -0.36 (95% CI -0.54 to 0.18) μg/ml; p = 0.01] were strongly and inversely correlated with CETP activity and mass, respectively. CETP activity showed an inverse trend compared to SCORE risk, demonstrating that lower levels were effective predictors of total mortality when a higher SCORE risk was found [β = -4.7 (95% CI -9.3 to 0.02) pmol/3 h; p = 0.04] in patients with RA.
Conclusion: CETP is downregulated in patients with RA who are taking glucocorticoids. Low CETP activity is associated with an increased level of cardiovascular risk in patients with RA.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.