This research evaluates the effects of a cholesterol-lowering medication, atorvastatin, on both arthritis activity and the ability of high-density lipoprotein cholesterol (HDL-C, sometimes referred to as "good cholesterol") to prevent changes in low-density lipoprotein cholesterol (LDL-C, sometimes referred to as "bad cholesterol"), which lead to atherosclerosis, or "hardening of the arteries." We hypothesize that atorvastatin may improve both joint inflammation and the anti-inflammatory properties of HDL cholesterol.
Heart attacks are the leading cause of death in patients with rheumatoid arthritis (RA). Cardiovascular events occur more frequently than would be expected in patients with RA and traditional heart risk factors do not explain this increased risk. Further research is needed to pursue ways of reducing heart disease mortality and improving outcome in patients with RA. There is reason to believe that a class of cholesterol-lowering medications called statins, beneficial in cardiovascular disease prevention, may be able to reduce the irritation of the joints ("inflammation") associated with RA. Statins have been shown to reduce manifestations of inflammation in the blood of patients at increased risk for heart disease, and in the process reduce the risk of heart attack, stroke, and sudden death. Some similarities in the nature of both RA and heart disease may suggest potential benefits of statin therapy in both conditions. In addition to inflammation, another factor which may contribute to coronary heart disease (CHD) risk in RA patients is dysfunctional high-density lipoprotein cholesterol (HDL-C, sometimes referred to as "good cholesterol"). Normally, HDL-C acts to counter a type of damage called "oxidation" within LDL-C which is a critical step in the development and progression of heart disease. Data from patients with RA and system lupus erythematosus (SLE) suggests that patients with active rheumatic diseases such as RA and SLE may have increased amounts of dysfunctional HDL-C, and therefore they may be at increased risk of heart disease. A blood test developed by Dr. Navab and colleagues at UCLA rapidly assesses this HDL-C function. This study will investigate both the level of HDL-C antioxidant function in patients with active RA as well as whether abnormal HDL function can be improved by statin use in this population. This research also evaluates the effects of atorvastatin on arthritis activity. We hypothesize that atorvastatin may improve both joint inflammation and the anti-inflammatory properties of HDL cholesterol.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
QUADRUPLE
Enrollment
20
HDL anti-inflammatory properties at 0 and 12 weeks
Time frame: at 0 and 12 weeks
Highly sensitive C-reactive protein (hs-CRP) at 0 and 12 weeks
Time frame: at 0 and 12 weeks
Disease activity score using a 28 joint count (DAS28) at 0,3,6,12, and 18 weeks
Time frame: at 0,3,6,12, and 18 weeks
Patient and physician global assessments on visual analogue pain scale (VAS; 0-100) at 0,3,6,12, and 18 weeks
Time frame: at 0,3,6,12, and 18 weeks
Swollen and tender joint counts at 0,3,6,12,and 18 weeks
Time frame: at 0,3,6,12, and 18 weeks
Patient pain assessment on VAS (0-100)at 0,3,6,12, and 18 weeks
Time frame: at 0,3,6,12, and 18 weeks
Erythrocyte sedimentation rate(Westergren) at 0,3,6,12, and 18 weeks
Time frame: at 0,3,6,12, and 18 weeks
Cholesterol levels at 0,3,6,12, and 18 weeks
Time frame: at 0,3,6,12, and 18 weeks
Health assessment questionnaire disability index (HAQ-DI) at 0,3,6,12, and 18 weeks
Time frame: at 0,3,6,12, and 18 weeks
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.