Parenteral selenium supplementation in critically ill patients--effects on antioxidant metabolism.

Decreased plasma selenium (Se) levels are common in critically ill patients. Oxidative stress is regarded as one possible cause of the Se deficiency. We investigated in 20 critically ill patients with decreased plasma selenium concentrations the antioxidant metabolism during parenteral selenium supplementation (week 1: 2 x 500 micrograms; week 2:1 x 500 micrograms, week 3:3 x 100 micrograms sodium selenite). As marker of oxidative stress we measured the plasma malondialdehyde levels on days 0, 1, 3, 7, 14, and 21. The content of reduced and oxidized glutathione as well as the leucocyte activity marker elastase were estimated on the same days. Initial plasma Se levels were considerably decreased (0.44 +/- 0.1 mumol/l, mean +/- SEM). After one day of supplementation Se concentrations were in the reference range. Plasma malondialdehyde levels and the ratio of oxidized and reduced glutathione were initially elevated and decreased beginning on day 3 of supplementation. The mean elastase level was 113 +/- 10 micrograms/l on day 0. On day 3 elastase values decreased significantly (85 +/- 13 micrograms/l, p < 0.05; day 21, 19 +/- 7 micrograms/l, p < 0.001). Antioxidant metabolism showed significant changes beginning after 72 hours of therapy. This latency may be explained with the induction of the enzyme glutathione peroxidase. The lowered plasma Se concentrations measured in the critically ill patients and the significant effects on antioxidant metabolism during supplementation emphasized the importance of selenium administration in these patients.

[Effect of selenium administration on various laboratory parameters of patients at risk for sepsis syndrome]. / Einfluss einer Selensubstitution auf verschiedene Laborparameter bei sepsisgefährdeten Patienten.

BACKGROUND: Low selenium plasma levels were often measured in ICU patients with polytrauma, major surgery or various severe diseases. Activation of selenium-dependent functions of the antioxidant metabolism and the immune system is suggested to be causally. METHODS: In a prospective randomized clinical trial including 24 critically ill patients we investigated the plasma levels of selenium, malondialdehyde, glutathione, elastase, fT3, fT4, TSH, IL-2R, IL-6 and IL-8 with and without parenteral selenium supplementation for 3 weeks (study design: week 1: twice 500 micrograms daily, week 2: once 500 micrograms, week 3: three times 100 micrograms sodium selenite). RESULTS: Following 24 hours of supplementation selenium plasma levels were normalized. Malondialdehyde level decreased in the therapy group significantly beginning at day 3. In the control group we observed increased malondialdehyde values, a disturbed glutathione metabolism and an elevated elastase activity. fT3-values were diminished at day 0 in all patients. In the therapy group we measured a gradual fT3 restoration. In the control group a reactive TSH increase was observed. Selenium supplementation did not lead to an excessive stimulation of IL-2R, IL-6 or IL-8. CONCLUSIONS: 1. Rapid normalization of selenium plasma levels can be achieved with the applied selenium dosage. 2. Parameters of radical metabolism are significantly reduced following selenium administration. 3. T3 synthesis correlates closely with the selenium levels. 4. Excessive stimulation of the immune system does not appear in the applied dosage.