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.


Preliminary Results: Baseline Nutritional Vitamin D Level Does Not Predict Progression of Subclinical Atherosclerosis in Women with SLE.

Lertratanakul2,  Apinya, Wu2,  Peggy, Dyer2,  Alan R., Langman1,  Craig, Pearce2,  William, Sutton-Tyrrell4,  Kim, Kondos3,  George

Childrens Memorial Hospital, Chicago, IL
Northwestern University, Chicago, IL
University of Illinois, Chicago, IL
University of Pittsburgh, Pittsburgh, PA

Background:

CV events and subclinical atherosclerosis are increased in women with SLE. Low levels of 25(OH)D have been associated with disease activity and cardiovascular (CV) risk factors in SLE. CV events and subclinical atherosclerosis are increased in women with SLE.

Objective:

Determine if baseline 25(OH)D level predicts progression of subclinical atherosclerosis in women with SLE.

Methods:

Demographic, traditional CV risk factors, disease activity (SLEDAI) and severity (ACR/SLICC-DI), medications and imaging to assess subclinical atherosclerosis by carotid B-mode ultrasound to measure carotid plaque index (PI), intima-media thickness (IMT) and electron beam or multidimensional computed tomography to measure coronary artery calcification (CAC), and aortic calcification (AC) were measured at baseline and 3 yrs later in the Study of Lupus Vascular and Bone Long-Term Endpoints (SOLVABLE). Abnormal PI, CAC, and AC were defined as PI>=1, CAC>10 and AC>100. Progression at 3y was defined as abnormal and an increase in PI, CAC>10 and AC>100 with an increase of >10% in CAC and AC. Hypertension (HTN) was defined as SBP>=140 or DBP>=90 or on treatment. Regression models investigated the relationship between PI, CAC, AC, and IMT and traditional CV risk factors, SLEDAI and ACR/SLICC-DI as well as baseline 25(OH)D (adjusted for age, race, & season) and progression of each imaging marker.

Results:

In 118 women, mean±SD age, disease duration, SLEDAI, ACR/SLICC-DI, and 25(OH)D levels at baseline were 44.3±9.6 yrs, 12.6±8.8, 3.6±3.2, 1.7±1.7 and 28.2±11.6 ng/mL, respectively. Preliminary imaging data at baseline and 3y followup were available on 118 women for IMT and PI, 91 with CAC, and 56 with AC. The frequency at baseline (#, %) of abnormal PI, CAC, and AC was 45 (38%), 21(23%), and 16 (29%), respectively. The frequency of progression at 3y followup (#, %) of PI, CAC, and AC was 34 (29%), 23 (25%), and 24 (61%), respectively. 13, 5, and 9 patients progressed from normal to abnormal at 3y followup visit for PI, CAC, and AC, respectively. The mean (SD) for IMT at baseline and 3y followup was 0.61 (0.12) and 0.64 (0.15), respectively. IMT change was associated with triglycerides (p=0.035, b=0.019,95% CI 0.001–0.037). PI, AC, and CAC progression were associated with HTN (p=0.045,OR=3.96,95% CI 1.14–18.41), (p=0.038,OR=2.91,95% CI 1.09–8.30), (p=0.017,OR=3.59,95% CI 1.32–10.98), respectively. AC and CAC progression were associated with ACR/SLICC-DI (p=0.003, OR=1.61,95% CI 1.20–2.26), (p=0.002, OR=1.63,95% CI 1.22–2.25). CAC progression was also associated with fibrinogen (p=0.039,OR=1.64,95% CI 1.03–2.70).

Vitamin D and Progression of PI, CAC, AC, and IMT

Imaging Type Adjusted vitamin D model 
 bOR95% CIp
PI 0.730.33,1.480.40
CAC 0.950.51,1.740.88
AC 1.180.62,2.260.62
IMT-0.02 -0.04,0.0020.08

Conclusion:

These preliminary results suggest that baseline 25(OH)D levels did not predict progression of PI, CAC, AC, or IMT over 3 yrs in women with SLE. However, traditional CV risk factors and SLE-related markers may be important in predicting progression of vascular bed abnormalities.

To cite this abstract, please use the following information:
Lertratanakul, Apinya, Wu, Peggy, Dyer, Alan R., Langman, Craig, Pearce, William, Sutton-Tyrrell, Kim, et al; Preliminary Results: Baseline Nutritional Vitamin D Level Does Not Predict Progression of Subclinical Atherosclerosis in Women with SLE. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1168
DOI: 10.1002/art.28934

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