The decrease in serum selenium observed during critical illness is believed to result from redistribution of the micronutrient to high priority organs (Angstwurm & Gaertner 2006). The selenium distribution (Hill et al. 2003; Renko et al. 2008) and negative acute phase functions (Dreher et al. 1997) of SelP support a potential role for this protein in selenium changes observed during critical illness. Recently, a newly developed immunoassay was used to show a decrease in SelP in the serum of septic patients (Hollenbach et al. 2008). The exact mechanism responsible for this decreased protein expression is not known; however, the authors propose that it is due to proinflammatory cytokines that are induced as a result of the acute phase reaction occurring during sepsis, since several cytokines can repress SEPP1 expression (Dreher et al. 1997; Mostert et al. 2001). The evidence presented here also supports a potential role for the GR in regulating SEPP1 expression. Glucocorticoid responsiveness of SEPP1 could be of significance in critically ill patients, as these patients tend to have increased levels of free plasma cortisol levels (Hamrahian et
