• Stefan Barlage, Carsten Gnewuch, Gerhard Liebisch, Zsuzsanna Wolf, Franz-Xaver Audebert, Thomas Glück, Dieter Fröhlich, Bernhard K Krämer, Gregor Rothe, and Gerd Schmitz.
• Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, 93042, Regensburg, Germany.
• Intensive Care Med. 2009 Nov 1;35(11):1877-85.

ObjectiveLipoproteins modulate vascular cell function in inflammation. In this study, we analyzed whether plasma concentrations of lipoproteins and apolipoproteins in human sepsis are related to patient survival and the activation of blood monocytes and platelets.DesignObservational study.SettingMedical and surgical intensive care units (ICU) of a university hospital.Patients151 consecutive patients after sepsis criteria had been met for the first time.InterventionsNone.MeasurementsPlasma lipoproteins, apolipoproteins, platelet CD62P-expression, monocyte HLA-DR-expression, SAPS II-scores (Simplified Acute Physiology Score) and 30-day-mortality were recorded.ResultsTotal cholesterol, high-density-lipoprotein (HDL) and low-density-lipoprotein (LDL) cholesterol, apolipoprotein (apo)-AI and apo-B were all found to be significantly lower in non-survivors than in survivors. In contrast to other (apo)lipoproteins, apo-AI and HDL cholesterol further decreased in non-survivors during the ICU stay. Logistic regression analysis revealed apo-AI to be an independent predictor of 30-day-mortality. A significant inverse correlation was found for apo-AI/HDL-cholesterol and platelet activation. Later in the course of the disease, HLA-DR expression on monocytes correlated positively to apo-AI and apo-CI concentrations and inversely to the apo-E concentration.ConclusionLow apo-AI is independently related to 30-day mortality in human sepsis and the decrease in apo-AI/HDL cholesterol correlates to increased platelet activation. Moreover, changes in apolipoproteins supposed to modulate lipopolysaccharide effects, such as apo-CI and apo-E, correlate to monocyte activation.

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