Effects of Atorvastatin on Disease Activity and HDL Cholesterol Function in Patients With Rheumatoid Arthritis
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|ClinicalTrials.gov Identifier: NCT00356473|
Recruitment Status : Completed
First Posted : July 26, 2006
Last Update Posted : June 22, 2012
|Condition or disease||Intervention/treatment||Phase|
|Rheumatoid Arthritis||Drug: Atorvastatin||Phase 4|
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 (Clinical Trial)|
|Actual Enrollment :||20 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)|
|Official Title:||Effects of Atorvastatin on Disease Activity and HDL Cholesterol Anti-inflammatory Properties in Patients With Rheumatoid Arthritis|
|Study Start Date :||March 2003|
|Actual Primary Completion Date :||September 2005|
|Actual Study Completion Date :||September 2005|
Placebo Comparator: Placebo
- 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 ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00356473
|Principal Investigator:||Benjamin J Ansell, MD||UCLA David Geffen School of Medicine|