pstrongAim /strongTo analyze the effect of vitamin D administration on serum 25(OH)D levels and biomarkers of metabolic syndrome and atherosclerosis (homeostatic model assessment of insulin resistance HOMA-IR, adiponectin, homocysteine, and high sensitivity C-reactive protein hs-CRP) in epilepsy patients receiving enzymatic antiseizure medications (ASMs)./p pstrongMethods /strongThis double-blind, randomized, placebo-controlled trial randomized 40 adult epilepsy patients treated with enzymatic ASMs to receive vitamin D3 (2,000 IU/day) or placebo for 12 weeks. The primary outcome was the change in serum 25-hydroxyvitamin D (25OHD) levels. Secondary outcomes included changes in HOMA-IR, adiponectin, homocysteine, and hs-CRP. Data were analyzed using a per-protocol approach./p pstrongResults /strongThirty-four patients completed the study. Vitamin D supplementation yielded a significantly greater increase in serum 25(OH)D (10.67 plusmn; 8.16 vs. ndash;1.29 plusmn; 3.96 ng/mL; p lt; 0.001) and adiponectin (1.38 plusmn; 3.05 vs. 0.34 plusmn; 1.89 micro;g/mL; p = 0.045), as well as a significantly greater reduction in hs-CRP (ndash;6.74 plusmn; 14.65 vs. 1.81 plusmn; 7.75 mg/L; p = 0.041) compared with placebo. Conversely, no significant differences were observed between groups regarding the changes in HOMA-IR (ndash;0.24 plusmn; 3.71 vs. ndash;0.14 plusmn; 3.38; p = 0.940) or homocysteine (7.90 plusmn; 1.79 vs. 8.15 plusmn; 2.70 micro;mol/L; p = 0.290)./p pstrongConclusion /strongVitamin D supplementation (2,000 IU/day) effectively restores 25(OH)D levels and improves adiponectin and hs-CRP in epilepsy patients on enzymatic ASMs, suggesting a potential benefit for cardiovascular risk reduction. However, vitamin D alone did not prevent the rise in homocysteine, likely due to the concurrent cessation of B-vitamin supplementation./p
Handayani et al. (Fri,) studied this question.