Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


Hyperuricemia Is a Predictor of Subclinical CVD in SLE Patients but Not Controls.

Enama2,  Joseph L., Gilkeson1,  Robert, Scalzi2,  Lisabeth

Case Western Reserve University
Penn State Univ Hershey, Hershey, PA

Purpose:

Both systemic lupus erythematosus (SLE) and hyperuricemia are non-traditional risk factors for atherosclerotic cardiovascular disease (CVD). We compared the associations of serum uric acid levels (UA) and subclinical CVD, while adjusting for traditional CVD risk factors, between patients with SLE and controls.

Methods:

222 patients (140 with SLE, 82 controls), all without clinical CVD, were recruited from rheumatology clinics at two academic medical centers. Demographic information and fasting blood samples were collected from each patient. Coronary artery calcium scores (CAC) were calculated in each patient. Subclinical CVD (lCAC) was defined by [log (CAC +1)]. Associations of uric acid with traditional predictors of CVD were examined in univariate analyses. Traditional and non-traditional CVD risk factors—including dyslipidemia, body mass index (BMI), hypertension (HTN), high sensitivity C-reactive protein, smoking history, diabetes (DM), race, age, and UA—were examined as independent predictors of subclinical CVD. Variables were analyzed using either Chi-square or Student's t-test, dependent on whether they were ordinal versus continuous measures respectively. Final linear regression models were calculated for SLE and controls, including all significant covariates (p < 0.1) for the analyses.

Results:

Mean serum UA levels did not significantly differ between SLE and control patients. (6.0 mg/dL versus 6.4 mg/dL, p = 0.9). UA was significantly associated with advanced age (p = 0.01), hypertension (p < 0.01), and BMI (p < 0.01) in SLE patients. Significant covariates for lCAC in the control group included dyslipidemia (p = 0.05), HTN (p = 0.01), DM (p = 0.037), age (p < 0.01), and UA (p < 0.01). Significant covariates for lCAC in SLE patients included smoking history (p = 0.01), age (p < 0.01), and UA (p < 0.01). The linear regression model in controls demonstrated that only age was a significant predictor for lCAC (p = 0.01). UA was found to be a significant predictor for lCAC in SLE patients, when controlling for age and smoking (p = 0.03). SLE patients with UA in the upper tertile (uric acid >= 4.7 mg/dL) had a significantly higher lCAC (p = 0.04).

Conclusions:

In patients with SLE, the presence of hyperuricemia in patients may predict CVD, independent of other traditional CVD risk factors. Larger studies are needed to determine if uric acid-lowering interventions may lower the risk of CVD in SLE.

To cite this abstract, please use the following information:
Enama, Joseph L., Gilkeson, Robert, Scalzi, Lisabeth; Hyperuricemia Is a Predictor of Subclinical CVD in SLE Patients but Not Controls. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1861
DOI: 10.1002/art.29626

Abstract Supplement

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