Our findings may have also been influenced by pooling trials where GLN was provided only enteral or through both the enteral and parenteral routes. This may appear as a confounding element in the analysis because of the different metabolic pathways and utilization of GLN. In fact, when given enterally GLN should be mainly active on the gut mucosal layer being the preferential substrate for the enterocytes and intestinal immune cells. Subsequently, the intestinal barrier function, which plays a critical role in critically ills, may control permeability and protect against the occurrence of systemic infections by decreasing bacterial translocation. When given intravenously, GLN should protect tissues against oxidative stress, toxic agents, or pathologic insults by increasing gluthation production and enhancing heat shock protein expression. On the other hand, many of the potential protective mechanisms of GLN given enterally or parenterally are overlapping and quite similar.76 For these reasons, we decided that there was a strong rational in pooling both routes.