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Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind,
Stefanie S Schleithoff1, Armin Zittermann, Gero Tenderich
1Institute of Nutrition and Food Science, University of Bonn, Bonn, Germany.
Insights
Vitamin D supplementation in congestive heart failure (CHF) patients reduced inflammation markers like tumor necrosis factor alpha. However, it did not significantly impact survival rates over 15 months.
Area of Science:
- Cardiology
- Endocrinology
- Immunology
Background:
- Elevated proinflammatory cytokines are implicated in congestive heart failure (CHF) pathogenesis.
- In vitro studies suggest vitamin D modulates cytokine production, suppressing proinflammatory and increasing anti-inflammatory types.
Purpose of the Study:
- To investigate the impact of vitamin D supplementation on survival and biochemical markers in CHF patients.
Main Methods:
- A 9-month randomized trial involving 123 CHF patients, assigning them to vitamin D3 plus calcium or placebo plus calcium.
- Biochemical variables were measured at baseline and 9 months; survival was tracked for 15 months.
Main Results:
- Vitamin D supplementation significantly increased 25-hydroxyvitamin D levels and interleukin 10, while decreasing parathyroid hormone.
- Proinflammatory tumor necrosis factor alpha remained stable in the vitamin D group but increased in the placebo group.
- No significant difference in survival rates was observed between the groups over the 15-month follow-up.
Conclusions:
- Vitamin D3 demonstrates potential as an anti-inflammatory agent for CHF, modulating the inflammatory environment.
- The findings suggest a role for the vitamin D-parathyroid hormone axis in CHF progression.
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 mug vitamin D(3)/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 alpha (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 alpha 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 D(3) 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.
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