The effect of Na-selenite treatment on the oxidative stress-antioxidants balance of multiple organ failure.

PURPOSE: Our study tested the hypothesis that sodium (Na)-selenite expression treatment can reduce oxidative stress and increase plasma antioxidants, whereas modulating white blood cell antigen expression in severe sepsis. Selenite is a well known cofactor of glutathione peroxidases and other antioxidant enzymes; therefore, one may expect an antioxidant effect of treatment. MATERIALS: We randomized 40 severe septic patients into treatment and control groups. Treatment group (n = 21) received 1000-µg/2 hours Na-selenite load, followed by a 1000-µg/die medication. Oxidative stress markers, including malondialdehyde, maximal free radical production, and plasma antioxidants: free sulfhydryl groups, glutathione levels, and superoxide dismutase and catalase enzyme activity were measured. RESULTS: According to our results, the treatment regime successfully restored serum selenium levels. Treatment group developed a significant malondialdehyde increase by the fifth study day, whereas reactive oxygen species production decreased significantly. Reduced glutathione and plasma sulfhydryl groups showed no significant difference. Treatment group showed deteriorated expression of CD11a and slight increase of CD49d expression on monocytes throughout our study. CONCLUSIONS: Although our Na-selenite treatment regime successfully restored the selenium deficiency of severe septic patients, antioxidant and white blood cell antigen expression modulating effect of the therapy was not observed in our patient group.

Microparticles and acute renal dysfunction in septic patients.

PURPOSE: The role of microparticles (MPs) in the pathogenesis of sepsis is not completely elucidated. We aimed to assess changes in the number of MPs during severe sepsis to follow the effect of sepsis-related organ failures, particularly renal impairment, an independent mortality factor of sepsis. MATERIALS AND METHODS: Thirty-seven severe septic patients and 20 controls were enrolled. Patient status as well as organ failure-related laboratory markers was followed up to 5 consecutive days. Microparticles (annexin V+ events in MP size gate) of platelet (CD41, CD42a, and PAC1), monocyte (CD14), and myeloid cell line (CD13) origin were measured using flow cytometry. RESULTS: Significantly increased total MP and CD41-, CD42a-, and PAC1-positive particle numbers were found in septic patients compared with controls. Actual number of organ dysfunctions on sample collection showed no correlation with MP numbers. Septic patients with renal dysfunction showed an increase in total MP, CD41(+), and CD13(+) particle numbers on admission. Amounts of platelet-derived CD42a(+) particles from patients with sepsis-related renal injury correlated negatively with actual blood urea nitrogen and creatinine concentrations. CONCLUSION: The increased numbers of platelet-derived MPs in severe septic patients emphasize the possible contribution of the hemostasis system in the development of sepsis-related renal impairments.