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Thorax. 2015 Jul;70(7):617-24. doi: 10.1136/thoraxjnl-2014-206680. Epub 2015 Apr 22.

Vitamin D deficiency contributes directly to the acute respiratory distress syndrome (ARDS).

Author information

1
Centre for Translational Inflammation and Fibrosis Research, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK.
2
School of Cancer Sciences, University of Birmingham, Birmingham, UK.
3
Centre for Endocrinology, Diabetes and Metabolism, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK.
4
Norwich Medical School, University of East Anglia, Norwich, UK.
5
Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
6
Department of Medicine, Concord Medical School, University of Sydney, Sydney, New South Wales, Australia.
7
Institute of Immunity and Transplantation, University College London, London, UK.
8
Blizard Institute, Queen Mary University of London, London, UK.
9
Warwick Clinical Trials Unit, Warwick Medical School, University of Warwick, Coventry, UK.

Abstract

RATIONALE:

Vitamin D deficiency has been implicated as a pathogenic factor in sepsis and intensive therapy unit mortality but has not been assessed as a risk factor for acute respiratory distress syndrome (ARDS). Causality of these associations has never been demonstrated.

OBJECTIVES:

To determine if ARDS is associated with vitamin D deficiency in a clinical setting and to determine if vitamin D deficiency in experimental models of ARDS influences its severity.

METHODS:

Human, murine and in vitro primary alveolar epithelial cell work were included in this study.

FINDINGS:

Vitamin D deficiency (plasma 25(OH)D levels <50 nmol/L) was ubiquitous in patients with ARDS and present in the vast majority of patients at risk of developing ARDS following oesophagectomy. In a murine model of intratracheal lipopolysaccharide challenge, dietary-induced vitamin D deficiency resulted in exaggerated alveolar inflammation, epithelial damage and hypoxia. In vitro, vitamin D has trophic effects on primary human alveolar epithelial cells affecting >600 genes. In a clinical setting, pharmacological repletion of vitamin D prior to oesophagectomy reduced the observed changes of in vivo measurements of alveolar capillary damage seen in deficient patients.

CONCLUSIONS:

Vitamin D deficiency is common in people who develop ARDS. This deficiency of vitamin D appears to contribute to the development of the condition, and approaches to correct vitamin D deficiency in patients at risk of ARDS should be developed.

TRIAL REGISTRATION:

UKCRN ID 11994.

KEYWORDS:

ARDS; Innate Immunity

PMID:
25903964
PMCID:
PMC4484044
DOI:
10.1136/thoraxjnl-2014-206680
[Indexed for MEDLINE]
Free PMC Article

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