Abstract
Selenium (Se) is an important micronutrient affecting multiple physiologic functions. Low Se levels observed in a general population are mainly caused by its limited availability in the diet.
Se, incorporated in seleno-enzymes, plays a key role in protection against oxidative stress, a principle phenomenon in inflammatory response and sepsis. Se levels decrease early in inflammation.
This decrease is probably caused by destruction of the enzymes as well as redistribution of Se, and its consumption. Se and seleno-enzyme levels correlate well with biomarkers and severity of sepsis.
This observation sparked a hypothesis that Se supplementation would restore Se levels, improving the morbidity and mortality in sepsis. Standard-dose supplementation did not normalize Se levels.
In contrast, high-dose supplementation in systemic inflammation and sepsis restored Se levels and improved some biomarkers of sepsis in several small-scale early studies. Similar benefits were observed in both experimental and clinical studies in cerebral insults.
However, despite a well-established pathophysiological role of Se in reducing oxidative stress in systemic inflammation, recent large clinical studies did not fully confirm a substantial benefit of high-dose Se supplementation in sepsis. Well-designed prospective studies are needed to establish the role of Se in therapy of critically ill patients.