We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Persisting high levels of plasma pentraxin 3 over the first days after severe sepsis and septic shock onset are associated with mortality.
- Authors
Mauri, Tommaso; Bellani, Giacomo; Patroniti, Nicolo'; Coppadoro, Andrea; Peri, Giuseppe; Cuccovillo, Ivan; Cugno, Massimo; Iapichino, Gaetano; Gattinoni, Luciano; Pesenti, Antonio; Mantovani, Alberto
- Abstract
Pentraxin 3 (PTX3) is an inflammatory mediator produced by neutrophils, macrophages, myeloid dendritic and endothelial cells. During sepsis a massive inflammatory activation and coagulation/fibrinolysis dysfunction occur. PTX3, as a mediator of inflammation, may represent an early marker of severity and outcome in sepsis. This study is based on a prospective trial regarding the impact of glycemic control on coagulation in sepsis. Ninety patients admitted to three general intensive care units were enrolled when severe sepsis or septic shock was diagnosed. At enrollment, we recorded sepsis signs, disease severity, coagulation activation [prothrombin fragments 1 + 2 (F1+2)] and fibrinolysis inhibition [plasminogen activator inhibitor-1 (PAI-1)]. We measured plasma PTX3 levels at enrollment, everyday until day 7, then at days 9, 11, 13, 18, 23 and 28. Mortality was recorded at day 90. Although not different on day 1, PTX3 remained significantly higher in non-survivors than in survivors over the first 5 days ( p = 0.002 by general linear model). On day 1, PTX3 levels were higher in septic shock than in severely septic patients ( p = 0.029). Day 1 PTX3 was significantly correlated with platelet count ( p < 0.001), SAPS II score ( p = 0.006) and SOFA score ( p < 0.001). Day 1 PTX3 was correlated with F1+2 concentration and with PAI-1 activity and concentration ( p < 0.05 for all). Persisting high levels of circulating PTX3 over the first days from sepsis onset may be associated with mortality. PTX3 correlates with severity of sepsis and with sepsis-associated coagulation/fibrinolysis dysfunction.
- Subjects
BLOOD plasma; BLOOD; INFLAMMATION; PATHOLOGY; FIBRINOLYSIS; BLOOD coagulation
- Publication
Intensive Care Medicine, 2010, Vol 36, Issue 4, p621
- ISSN
0342-4642
- Publication type
Article
- DOI
10.1007/s00134-010-1752-5