Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trial
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Open Access
- 1 April 2006
- journal article
- research article
- Published by Elsevier in The American Journal of Clinical Nutrition
- Vol. 83 (4) , 754-759
- https://doi.org/10.1093/ajcn/83.4.754
Abstract
Background:Elevated circulating concentrations of proinflammatory cytokines may contribute to the pathogenesis of congestive heart failure (CHF). In vitro studies suggest that vitamin D suppresses proinflammatory cytokines and increases antiinflammatory cytokines. Objective:We evaluated the effect of vitamin D supplementation on the survival rate and different biochemical variables in patients with CHF. Design:One hundred twenty-three patients randomly received either 50 μg vitamin D3/d plus 500 mg Ca/d [D(+) group] or placebo plus 500 mg Ca/d [D(–) group] for 9 mo. Biochemical variables were assessed at baseline and after 9 mo. The survival rate was calculated for a follow-up period of 15 mo. Results:Ninety-three patients completed the study. Significant treatment effects were observed on logarithmic-transformed serum concentrations of 25-hydroxyvitamin D (P = 0.001), parathyroid hormone (P = 0.007), tumor necrosis factor α (P = 0.006), and interleukin 10 (P = 0.042). 25-Hydroxyvitamin D increased by 26.8 ng/mL in the D(+) group but increased only by 3.6 ng/mL in the D(–) group. Compared with baseline, parathyroid hormone was significantly lower and the antiinflammatory cytokine interleukin 10 was significantly higher in the D(+) group after 9 mo. The proinflammatory cytokine tumor necrosis factor α increased in the D(–) group but remained constant in the D(+) group. The survival rate did not differ significantly between the study groups during the follow-up period. Conclusions:Vitamin D3 reduces the inflammatory milieu in CHF patients and might serve as a new antiinflammatory agent for the future treatment of the disease. Our data provide evidence for the involvement of an impaired vitamin D–parathyroid hormone axis in the progression of CHF.Keywords
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