title: Procalcitonin is persistently increased among children with poor outcome from bacterial sepsis.
abstract: OBJECTIVE
  To examine the relationships between procalcitonin, bacterial infection, sepsis-induced multiple organ failure, and mortality rate in children.
  
  
  METHODS
  Cohort study.
  
  
  METHODS
  A multidisciplinary, tertiary-care pediatric intensive care unit.
  
  
  METHODS
  Seventy-eight children meeting criteria for sepsis or septic shock and 12 critically ill children without sepsis.
  
  
  METHODS
  Venous or arterial blood sampling.
  
  
  RESULTS
  Demographic, epidemiologic, and outcome data were recorded. Plasma from children with sepsis were collected on days 1 and 3, and procalcitonin concentrations were measured by immunoluminometric assay. Organ failure index scores were determined, and multiple organ failure was defined as organ failure index > or = 3. Persistent multiple organ failure was defined by presence of multiple organ failure on day 3. Procalcitonin concentrations (median [25th percentile-75th percentile]) were increased among children with sepsis on day 1 (2.4 ng/mL [0.2-24.2], p < .01) but not on day 3 (0.8 ng/mL [0.1-8.1], p = nonsignificant) vs. controls (0.2 ng/mL [0.1-0.5]). This increase in procalcitonin concentration was particularly robust among children with bacterial sepsis on day 1 (7.1 ng/mL [0.9-44.8], p < .001) and on day 3 (2.9 ng/mL [0.1-32.4], p < .05). Procalcitonin concentrations were not increased among children with fungal, viral, or culture-negative sepsis vs. controls. Procalcitonin concentrations were persistently increased over time among patients with bacterial sepsis who had persistent multiple organ failure (p < .05) and who died (p < .01) but not among patients with nonbacterial sepsis.
  
  
  CONCLUSIONS
  Procalcitonin is persistently increased among children with poor outcome from bacterial sepsis. Further study is needed to better delineate this differential procalcitonin response to bacterial vs. nonbacterial sepsis and to characterize any mechanistic role that procalcitonin might play in the development of bacterial sepsis-induced multiple organ failure and mortality.
authors.affiliation: Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
authors.forename: Yong Y
authors.initials: YY
authors.lastname: Han
authors.forename: Lesley A
authors.initials: LA
authors.lastname: Doughty
authors.forename: Danny
authors.initials: D
authors.lastname: Kofos
authors.forename: Howell
authors.initials: H
authors.lastname: Sasser
authors.forename: Joseph A
authors.initials: JA
authors.lastname: Carcillo
mesh_terms: D000293:Adolescent; D000704:Analysis of Variance; D002116:Calcitonin / Q000097:blood*; D015740:Calcitonin Gene-Related Peptide; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007223:Infant; D015278:Intensive Care Units, Pediatric; D008297:Male; D009102:Multiple Organ Failure / Q000097:blood* / Q000382:microbiology; D011498:Protein Precursors / Q000097:blood*; D018805:Sepsis / Q000097:blood* / Q000382:microbiology; D012772:Shock, Septic / Q000097:blood* / Q000382:microbiology
chemical_list: C000606589:CALCA protein, human; D011498:Protein Precursors; D002116:Calcitonin; D015740:Calcitonin Gene-Related Peptide