Physiological changes during sepsis generate a hypermetabolic state and an increase in the production of adenosine triphosphate (ATP) through the electron transport chain in mitochondria. Hydrogen peroxide (H 2O 2) and oxidative stress have been suggested to be possible instigators of both the systemic inflammatory response and the increased vascular permeability associated with sepsis and septic shock through their effects on vascular endothelial cells. Sepsis is one of the most common causes of death in the intensive care unit despite advances in care. In this cohort, increased H 2O 2 in urine is thus associated with mortality in patients with sepsis and septic shock as well as in patients with burn injury. Likewise, urine concentrations of H 2O 2 were higher in non-survivors as compared to survivors ( p < 0.001) at day 28 in all diagnostic groups, as well as in patients with severe infections and burn injury ( p < 0.001 for both). those without AKI, in all diagnostic groups displayed higher concentrations of urine H 2O 2 ( p < 0.001).
Patients with acute kidney injury (AKI), vs. The mean concentrations of H 2O 2 were found to be lower in patients with severe infections compared to burn injury patients and healthy subjects. We measured H 2O 2 concentrations in the urine of 82 patients with severe infections, such as sepsis, septic shock, and infections not fulfilling sepsis-3 criteria, in patients with major burn injury with associated systemic inflammation, and healthy subjects. Hydrogen peroxide (H 2O 2) and oxidative stress have been suggested as possible instigators of both the systemic inflammatory response and the increased vascular permeability associated with sepsis and septic shock.
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