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Vitamin D deficiency contributes directly to the acute respiratory distress syndrome (ARDS)
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(2015) Vitamin D deficiency contributes directly to the acute respiratory distress syndrome (ARDS). Thorax, 70 (7). pp. 617-624. doi:10.1136/thoraxjnl-2014-206680 ISSN 0040-6376.
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Official URL: http://dx.doi.org/10.1136/thoraxjnl-2014-206680
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
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