title: Biomarkers of hypercoagulability and inflammation in childhood-onset arterial ischemic stroke.
abstract: OBJECTIVE
  To test the hypothesis that acute elevations of biomarkers of hypercoagulability and inflammation are common in children with arterial ischemic stroke (AIS), particularly among etiologic subtypes that carry an increased risk of recurrent stroke.
  
  
  METHODS
  In this prospective/retrospective institutional-based cohort study of acute childhood-onset AIS (n = 50) conducted between 2005 and 2009, D-dimer, factor VIII (FVIII) activity, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were serially evaluated at the time of clinical blood sampling. Patients were classified by stroke subtype as cardioembolic, moyamoya, non-moyamoya arteriopathy, or other.
  
  
  RESULTS
  Both D-dimer and CRP were frequently elevated in acute childhood-onset AIS and exhibited a decreasing trend with time. Acute D-dimer levels were significantly higher in cardioembolic AIS compared with noncardioembolic AIS (median, 2.04 microg/mL [range 0.54-4.54 microg/mL] vs 0.32 microg/mL [0.22-3.18 microg/mL]; P = .002). At an optimal threshold of > or = 0.50 microg/mL, the sensitivity and specificity of D-dimer for cardioembolic subtype were 78% and 79%, respectively.
  
  
  CONCLUSIONS
  Our findings identify D-dimer and CRP as candidate biomarkers for etiology and prognosis in childhood-onset AIS. Further studies should investigate the role of these and other biomarkers of hypercoagulability and inflammation in childhood-onset AIS.
authors.affiliation: Department of Pediatrics, Section of Child Neurology, Mountain States Regional Hemophilia and Thrombosis Center, University of Colorado Denver and The Children's Hospital, Aurora, CO 80045-0507, USA. timothy.bernard@ucdenver.edu
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Bernard
authors.forename: Laura Z
authors.initials: LZ
authors.lastname: Fenton
authors.forename: Susan D
authors.initials: SD
authors.lastname: Apkon
authors.forename: Richard
authors.initials: R
authors.lastname: Boada
authors.forename: Greta N
authors.initials: GN
authors.lastname: Wilkening
authors.forename: C Corbett
authors.initials: CC
authors.lastname: Wilkinson
authors.forename: Jennifer B
authors.initials: JB
authors.lastname: Soep
authors.forename: Shelley D
authors.initials: SD
authors.lastname: Miyamoto
authors.forename: Mark
authors.initials: M
authors.lastname: Tripputi
authors.forename: Jennifer
authors.initials: J
authors.lastname: Armstrong-Wells
authors.forename: Timothy A
authors.initials: TA
authors.lastname: Benke
authors.forename: Marilyn J
authors.initials: MJ
authors.lastname: Manco-Johnson
authors.forename: Neil A
authors.initials: NA
authors.lastname: Goldenberg
mesh_terms: D000293:Adolescent; D017668:Age of Onset; D015415:Biomarkers / Q000097:blood*; D002545:Brain Ischemia / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D002097:C-Reactive Protein / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D003120:Colorado / Q000453:epidemiology; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005500:Follow-Up Studies; D006801:Humans; D015994:Incidence; D007249:Inflammation / Q000097:blood* / Q000150:complications; D008297:Male; D011379:Prognosis; D011446:Prospective Studies; D012189:Retrospective Studies; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood* / Q000150:complications; D013997:Time Factors
chemical_list: D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D005169:Factor VIII; D002097:C-Reactive Protein