Objective We investigated whether an increase in vitamin D levels in patients with systemic lupus erythematosus was associated with improvement in disease activity. Methods 1006 SLE patients were followed over 128 weeks. SLE patients with low levels of 25-hydroxy Vitamin D (<40 ng/mL) were supplemented with 50,000 units Vitamin D2 weekly, with Ca/D3 200 units twice daily. Longitudinal regression models were used to estimate the association between levels of vitamin D and various measures of disease activity. Results The SLE patients were 91% female, mean age 49.6, 54% Caucasian, 37% African-American and 8% other ethnicity. For those with low 25-hydroxy Vitamin D (<40 ng/mL), a 20 unit increase in 25-hydroxy Vitamin D was associated with a decrease in mean SELENA-SLEDAI by 0.22 (CI: −0.41, −0.02) (p= 0.032). This corresponded with a 21% decrease in the odds of having a SELENA-SLEDAI higher than 4 (CI: 1%, 37%). Mean urine protein-to-creatinine ratio decreased 2% (CI: −0.03, −0.01) (p=0.009), corresponding to a 15% decrease in the odds of having a ratio of 0.5 or greater (CI: 2%, 27%). Conclusion We found that a 20 ng/mL increase in vitamin D was associated with a 21% decrease in the odds of having a high activity score and a 15% decrease in the odds of having clinically important proteinuria. Though these associations were statistically significant, the clinical importance is relatively modest. There was no evidence of additional benefit beyond a level of 40 ng/mL.
Accelerated atherosclerosis remains a major cause of death in late systemic lupus erythematosus (SLE). Omega-3 has been reported to have benefit for endothelial dysfunction, one of the earliest stages of atherosclerosis, and to reduce disease activity in SLE. We performed a randomized, double-blind placebo-controlled trial to examine the effect of Omega-3 on endothelial function, disease activity, inflammatory markers and lipids in SLE. SLE patients (n = 85, mean age 47, 55 % Caucasian, 38 % African-American, 94 % female) were randomly assigned to 3 g of Omega-3 (Lovaza, GSK) versus placebo for 12 weeks. Endothelial function was measured at baseline and at 12 weeks using flow-mediated dilation, calculated using high-resolution B-mode ultrasound of the brachial artery diameter in response to vasoactive stimuli (hyperemia). Disease activity was measured using the physician global assessment and SELENA-SLEDAI score. Inflammatory markers (sICAM-1, sVCAM-1, IL-6) and fasting lipid profile were done at baseline and 12-week follow-up. There was no difference between the treatment groups with respect to changes in flow-mediated dilation parameters or disease activity. An average increase in LDL cholesterol of 3.11 mg/dL (±21.99) was found with Omega-3 versus a decrease of 1.87 mg/dL (±18.29) with placebo (p = 0.0266). In this trial, Omega-3 did not improve endothelial function, disease activity, nor reduce inflammatory markers in SLE. Longer trials might be required if there are delayed clinical effects. There was evidence that Omega-3 may increase LDL cholesterol, but not the LDL/HDL ratio.
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