%0 Journal Article
%T Elevated plasma levels of heparin-binding protein in intensive care unit patients with severe sepsis and septic shock
%A Adam Linder
%A Per £¿kesson
%A Malin Inghammar
%A Carl-Johan Treutiger
%A Anna Linn¨¦r
%A Jonas Sund¨¦n-Cullberg
%J Critical Care
%D 2012
%I BioMed Central
%R 10.1186/cc11353
%X A prospective study was conducted of two patient cohorts treated in the ICU at Karolinska University Hospital Huddinge in Sweden. A total of 179 patients was included, of whom 151 had sepsis (126 with septic shock and 25 patients with severe sepsis) and 28 a non-septic critical condition. Blood samples were collected at five time points during six days after admission.HBP levels were significantly higher in the sepsis group as compared to the control group. At admission to the ICU, a plasma HBP concentration of ¡İ15 ng/mL and/or a HBP (ng/mL)/white blood cell count (109/L) ratio of >2 was found in 87.2% and 50.0% of critically ill patients with sepsis and non-septic illness, respectively. A lactate level of >2.5 mmol/L was detected in 64.9% and 56.0% of the same patient groups. Both in the sepsis group (n = 151) and in the whole group (n = 179), plasma HBP concentrations at admission and in the last measured sample within the 144 hour study period were significantly higher among 28-day non-survivors as compared to survivors and in the sepsis group, an elevated HBP-level at baseline was associated with an increased case-fatality rate at 28 days.Plasma HBP levels were significantly higher in patients with severe sepsis or septic shock compared to patients with a non-septic illness in the ICU. HBP was associated with severity of disease and an elevated HBP at admission was associated with an increased risk of death. HBP that rises over time may identify patients with a deteriorating prognosis. Thus, repeated HBP measurement in the ICU may help monitor treatment and predict outcome in patients with severe infections.Sepsis is defined as the systemic inflammatory response to infection. In its more severe forms it causes tissue hypoperfusion, hypoxia, lactic acidosis, and organ dysfunction [1,2]. Despite increasing awareness of the diagnosis, faster administration of antibiotics and intravenous fluids, better technological support of organ function and other recent advance
%U http://ccforum.com/content/16/3/R90