title: Changes in HDL-associated apolipoproteins relate to mortality in human sepsis and correlate to monocyte and platelet activation.
abstract: 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.
authors: Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, 93042, Regensburg, Germany.
authors: Stefan
authors: S
authors: Barlage
authors: Carsten
authors: C
authors: Gnewuch
authors: Gerhard
authors: G
authors: Liebisch
authors: Zsuzsanna
authors: Z
authors: Wolf
authors: Franz-Xaver
authors: FX
authors: Audebert
authors: Thomas
authors: T
authors: Glück
authors: Dieter
authors: D
authors: Fröhlich
authors: Bernhard K
authors: BK
authors: Krämer
authors: Gregor
authors: G
authors: Rothe
authors: Gerd
authors: G
authors: Schmitz
mesh_terms: 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
chemical_list: 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