Changes in HDL-associated apolipoproteins relate to mortality in human sepsis and correlate to monocyte and platelet activation.
OBJECTIVE
Lipoproteins 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.


METHODS
Observational study.


METHODS
Medical and surgical intensive care units (ICU) of a university hospital.


METHODS
151 consecutive patients after sepsis criteria had been met for the first time.


METHODS
None.


METHODS
Plasma lipoproteins, apolipoproteins, platelet CD62P-expression, monocyte HLA-DR-expression, SAPS II-scores (Simplified Acute Physiology Score) and 30-day-mortality were recorded.


RESULTS
Total 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.


CONCLUSIONS
Low 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.
Barlage
Stefan
S
Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, 93042, Regensburg, Germany.
Gnewuch
Carsten
C
Liebisch
Gerhard
G
Wolf
Zsuzsanna
Z
Audebert
Franz-Xaver
FX
Glück
Thomas
T
Fröhlich
Dieter
D
Krämer
Bernhard K
BK
Rothe
Gregor
G
Schmitz
Gerd
G
D018806:APACHE; D000328:Adult; D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood / Q000172:deficiency; D001053:Apolipoproteins / Q000172:deficiency / Q000276:immunology; D001055:Apolipoproteins B / Q000097:blood / Q000172:deficiency; D002784:Cholesterol / Q000097:blood / Q000172:deficiency; D008076:Cholesterol, HDL / Q000097:blood / Q000172:deficiency; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D005858:Germany / Q000453:epidemiology; D006684:HLA-DR Antigens / Q000097:blood; D006801:Humans; D007009:Hypolipoproteinemias / Q000097:blood / Q000150:complications / Q000276:immunology; D008075:Lipoproteins, HDL / Q000172:deficiency / Q000276:immunology; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000276:immunology*; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D012372:ROC Curve; D018805:Sepsis / Q000097:blood / Q000276:immunology / Q000401:mortality; D018709:Statistics, Nonparametric; D015996:Survival Rate
D016632:Apolipoprotein A-I; D001053:Apolipoproteins; D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006684:HLA-DR Antigens; D008075:Lipoproteins, HDL; D019007:P-Selectin; D002784:Cholesterol