title: Platelet function in sepsis.
abstract: BACKGROUND
  Coagulation abnormalities and thrombocytopenia are common in severe sepsis, but sepsis-related alterations in platelet function are ill-defined.
  
  
  OBJECTIVE
  The purpose of this study was to elucidate the effect of sepsis on platelet aggregation, adhesiveness, and growth factor release.
  
  
  METHODS
  Agonist-induced platelet aggregation was measured in platelet-rich plasma separated from blood samples collected from 47 critically ill patients with sepsis of recent onset. Expression of platelet adhesion molecules was measured by flow cytometry and the release of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) was measured by ELISA in the supernatant of platelet aggregation.
  
  
  RESULTS
  Septic patients had consistently decreased platelet aggregation compared with controls, regardless of the platelet count, thrombin generation, or overt disseminated intravascular coagulation (DIC) status. The severity of sepsis correlated to the platelet aggregation defect. Adhesion molecules, receptor expression (CD42a, CD42b, CD36, CD29, PAR-1), and alpha-granule secretion detected by P-selectin expression remained unchanged but the release of growth factors was differentially regulated with increased VEGF and unchanged PDGF after agonist activation even in uncomplicated sepsis.
  
  
  CONCLUSIONS
  Sepsis decreases circulating platelets' hemostatic function, maintains adhesion molecule expression and secretion capability, and modulates growth factor production. These results suggest that sepsis alters the hemostatic function of the platelets and increases VEGF release in a thrombin-independent manner.
authors.affiliation: Departments of Intensive Care Medicine and Hematology, Erasme Hospital, Free University of Brussels, Brussels, Belgium.
authors.forename: A
authors.initials: A
authors.lastname: Yaguchi
authors.forename: F L M
authors.initials: FL
authors.lastname: Lobo
authors.forename: J-L
authors.initials: JL
authors.lastname: Vincent
authors.forename: O
authors.initials: O
authors.lastname: Pradier
mesh_terms: D000368:Aged; D001791:Blood Platelet Disorders / Q000175:diagnosis; D001792:Blood Platelets / Q000378:metabolism / Q000382:microbiology / Q000502:physiology*; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006133:Growth Substances / Q000097:blood; D006801:Humans; D008297:Male; D008875:Middle Aged; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D010982:Platelet-Derived Growth Factor / Q000096:biosynthesis / Q000378:metabolism; D018805:Sepsis / Q000097:blood*; D013917:Thrombin / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000097:blood / Q000378:metabolism
chemical_list: D006133:Growth Substances; D010982:Platelet-Derived Growth Factor; D042461:Vascular Endothelial Growth Factor A; D013917:Thrombin