Direct effects of modest hyperglycaemia on susceptibility to infection in the critically ill patient

In their recent study, Otto and colleagues suggested that the adverse effects of hyperglycaemia on immune function may be mediated by hyperosmotic stress [1]. In granulocytes both oxidative burst and phagocytosis were suppressed by hyperosmolar stress with mannitol, but no significant effect was observed on cytokine release from peripheral blood mononuclear cells [1]. The concentration of glucose (and mannitol) used in these experiments (500 mg/dl or 27.8 mmol/l), however, is rarely encountered in critically ill patients – and then only transiently. One may question how relevant this mechanism is, when it appears that modest levels of hyperglycaemia (11.1 mmol/l) have deleterious effects in this population [2].