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Licensed Unlicensed Requires Authentication Published by De Gruyter July 13, 2012

Vitamin D deficiency parallels inflammation and immune activation, the Ludwigshafen Risk and Cardiovascular Health (LURIC) study

  • Christian Murr , Stefan Pilz , Tanja B. Grammer , Marcus E. Kleber , Andreas Meinitzer , Bernhard O. Boehm , Winfried März and Dietmar Fuchs EMAIL logo

Abstract

Background: Low vitamin D concentrations are detected in patients suffering from various clinical conditions which are characterized also by inflammation and immune activation. We investigated whether vitamin D levels in patients with coronary artery disease (CAD) are related to markers of immune activation.

Methods: Serum concentrations of 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] and the immune activation markers neopterin and high sensitivity C-reactive protein (hsCRP) were measured in 2015 patients derived from the LUdwigshafen RIsk and Cardiovascular Health (LURIC) study, a cohort study among patients referred for coronary angiography.

Results: Serum concentrations of 25(OH)D and 1,25(OH)2D did not differ between patients with CAD [mean±SD: 25(OH)D: 17.4±9.4 μg/L; 1,25(OH)2D: 34.4±13.3 ng/L] and controls [25(OH)D: 18.4±11.7 μg/L; 1,25(OH)2D: 35.3±12.7 ng/L; Welch’s t-test: p=n.s.] but CAD patients had higher neopterin (8.6±7.4 nmol/L) and hsCRP (9.6±19.6 mg/L) concentrations compared to controls (neopterin: 7.5±4.8 nmol/L; p=0.0004; hsCRP: 5.4±10.0 mg/L; p<0.0001). There was an inverse correlation between serum 25(OH)D or 1,25(OH)2D concentrations and serum neopterin [Spearman’s rank correlation: 25(OH)D: rs=–0.183; 1,25(OH)2D: rs=–0.230] and hsCRP [25(OH)D: rs=–0.142; 1,25(OH)2D: rs=–0.130; all p<0.0001] concentrations.

Conclusions: Our results indicate increased inflammatory processes in patients with low vitamin D status. Further studies should clarify the underlying mechanisms for the observed associations of vitamin D status and inflammatory parameters.


Corresponding author: Dietmar Fuchs, Division of Biological Chemistry, Biocenter, Innsbruck Medical University, Innrain 80, 6020 Innsbruck, Austria Phone: +43 512 9003 70350, Fax: +43 512 9003 73330

The authors extend their appreciation to the participants of the LURIC study as without their collaboration this article would not have been written. We also thank Mrs. Maria Pfurtscheller, Innsbruck, for excellent technical assistance and the members of the LURIC study team either temporarily or permanently involved in patient recruitment and sample and data handling, the laboratory staff at the Ludwigshafen General Hospital, and at the Universities of Freiburg, Ulm and Graz. LURIC has received funding trough the 6th Framework Program (integrated project Bloodomics, grant LSHM-CT-2004-503485) and the 7th Framework Program (integrated project Atheroremo, Grant Agreement number 201668) of the European Union.

Conflict of interest statement

Authors’ conflict of interest disclosure: The authors stated that there are no conflicts of interest regarding the publication of this article. Research funding played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

Research funding: None declared.

Employment or leadership: None declared.

Honorarium: None declared.

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Received: 2012-03-14
Accepted: 2012-06-14
Published Online: 2012-07-13
Published in Print: 2012-12-01

©2012 by Walter de Gruyter Berlin Boston

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