Association of selenium status with endothelial activation during acute systemic inflammation in children

Evidence that selenium has a role in endothelial function comes mainly from experimental research, but few clinical studies have examined the pathophysiology of selenium in endothelial activation. We aimed to investigate whether there are associations between selenium status and the magnitude of endothelial activation and the severity of multiple organ dysfunction during the acute phase of systemic inflammatory response syndrome (SIRS) in children.

A prospective cohort study was carried out in 109 children with SIRS admitted to a pediatric ICU (PICU). Erythrocyte and plasma selenium were measured on admission and selenoprotein P and soluble plasma forms of the intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), sP-selectin, and endoCAM on days 1, 2 and 3 of hospitalization. Generalized estimating equations models were adjusted for clinical severity parameters, C-reactive protein, procalcitonin, and serum lactate. The effect of selenium status on organ dysfunction was defined by the Pediatric Logistic Organic Dysfunction (PELOD-2) during the PICU stay.

Erythrocyte selenium was associated with sP-selectin and endoCAM, but not with ICAM-1 and VCAM-2. An increase of 10 μg/L in erythrocyte selenium resulted in increases of 43.2 ng/mL (p = 0.001) in sP-selectin and of 0.04 ng/mL (p < 0.001) in endoCAM. Erythrocyte selenium was also associated with a decrease in PELOD-2 (p = 0.015). Plasma selenium was not related to any of the outcomes.

Erythrocyte selenium is associated with endothelial activation in the early phase of the systemic inflammatory response in children, and has a protective effect on multiple organ dysfunction during their PICU stay. Registered at: www.clinicaltrials.gov (NCT00708799).