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Levels of oxidized low-density lipoproteins are increased in patients with severe sepsis

Abstract Background It was hypothesized that the inflammatory response of patients with severe sepsis may result in changes of plasma levels of oxidized low-density lipoproteins (ox-LDLs) and that drotrecogin α (activated) (DAA) (Xigris, Eli Lilly and Company [Indiana 46285, USA]) may influence ox-L...

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Published in:Journal of critical care 2008-12, Vol.23 (4), p.537-541
Main Authors: Behnes, Michael, MS, Brueckmann, Martina, MD, Liebe, Volker, MD, Liebetrau, Claudia, Lang, Siegfried, PhD, Putensen, Christian, MD, Borggrefe, Martin, MD, Hoffmann, Ursula, MD
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Language:English
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Summary:Abstract Background It was hypothesized that the inflammatory response of patients with severe sepsis may result in changes of plasma levels of oxidized low-density lipoproteins (ox-LDLs) and that drotrecogin α (activated) (DAA) (Xigris, Eli Lilly and Company [Indiana 46285, USA]) may influence ox-LDL levels. Materials and Methods The ox-LDL levels were measured in severe septic patients on day 1, 4, and 7 of severe sepsis. Patients were treated either with or without DAA. Results The ox-LDL levels increased significantly ( P < .05) from day 1 to day 7 (day 1, mean ± SEM, 25.4 ± 1.8 U/L; day 4, mean ± SEM, 34.3 ± 2.1 U/L; day 7, mean ± SEM, 38.3 ± 2.1 U/L) in all patients (n = 68). The ox-LDL levels increased significantly from day 1 to day 7 both in patients treated with (n = 31) and without DAA (n = 37) ( P < .001) (DAA-group: day 1, mean ± SEM, 24.4 ± 2.8 U/L; day 4, mean ± SEM, 35.5 ± 2.9 U/L; day 7, mean ± SEM, 40.7 ± 3.2 U/L) (control group: day 1, mean ± SEM, 26.3 ± 2.8 U/L; day 4, mean ± SEM, 33.2 ± 2.9 U/L; day 7, mean ± SEM, 36.4 ± 2.9 U/L). No significant differences of ox-LDL levels were observed between both groups at any point of time ( P > .05). Conclusions The ox-LDL concentrations increase significantly during the first week of severe sepsis and are not affected by administration of drotrecogin α (activated) (Xigris).
ISSN:0883-9441
1557-8615
DOI:10.1016/j.jcrc.2008.09.002