Vitamin D deficiency does not predict progression of coronary artery calcium, carotid intima-media thickness or high-sensitivity C-reactive protein in systemic lupus erythematosus.

Abstract

Vitamin D deficiency is common in SLE. Cardioprotective effects of vitamin D have been postulated due to modulation of inflammatory cytokines. However, the effects of vitamin D supplementation on inflammatory cytokines in trials have been inconsistent. We determined whether levels of vitamin D at baseline were associated with subclinical measures of atherosclerosis, or with changes in subclinical measures over 2 years. Of the 200 patients enrolled in the Lupus Atherosclerosis Prevention Study, complete baseline and follow-up data [including coronary artery calcium (CAC), carotid intima-media thickness (IMT), 25-hydroxy vitamin D [25(OH)D] and high-sensitivity CRP (hsCRP) levels] were available for 154 patients. Assessments were repeated 2 years later. 25(OH)D values ranged from 4 to 79 ng/ml. Among African American patients, 25(OH)D values ranged from 4 to 55 ng/ml. With low 25(OH)D (vitamin D <21 ng/ml), a higher proportion had a CAC score >100 (11%) compared with those with vitamin D insufficiency (21-32 ng/ml) (10%) and normal (≥32 ng/ml) 25(OH)D (3%), which was not statistically significant. 25(OH)D was neither associated with nor did it predict progression of CAC or carotid IMT over 2 years. The mean hsCRP decreased over 2 years. 25(OH)D was not associated with any measure of subclinical atherosclerosis. 25(OH)D deficiency was associated with higher hsCRP at baseline, but did not predict a change in hsCRP over 2 years.