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

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.

SUBMITTER: Dancer RC 

PROVIDER: S-EPMC4484044 | biostudies-literature | 2015 Jul

REPOSITORIES: biostudies-literature