title: Symptomatic ischemic stroke in full-term neonates : role of acquired and genetic prothrombotic risk factors.
abstract: OBJECTIVE
  The present multicenter case-control study was prospectively designed to assess the extent to which single and combined clotting factor abnormalities influence the onset of symptomatic ischemic stroke in full-term neonates.
  
  
  METHODS
  Lipoprotein (Lp)(a); the factor V (FV) G1691A mutation; the prothrombin (PT) G20210A variant; the methylenetetrahydrofolate reductase (MTHFR) T677T genotype; antithrombin; protein C; protein S; and anticardiolipin antibodies (ACAs) were investigated in 91 consecutively recruited neonatal stroke patients and 182 age- and sex-matched healthy controls.
  
  
  RESULTS
  Sixty-two of 91 stroke patients (68.1%) had at least 1 prothrombotic risk factor compared with 44 control subjects (24.2%) (odds ratio [OR]/95% confidence interval [CI], 6.70/3.84 to 11.67). An increased Lp(a) level (>30 mg/dL) was found in 20 patients and 10 controls (OR/95% CI, 4.84/2. 16 to 10.86); FV G1691A was present in 17 patients and 10 controls (OR/95% CI, 3.95/1.72 to 9.0); the PT G20210A variant was detected in 4 patients and 4 controls (OR/95% CI, 2.04/0.49 to 8.3); the MTHFR TT677 genotype was found in 15 patients and 20 controls (OR/95% CI, 1.59/0.77 to 3.29); and protein C type I deficiency was found in 6 neonates. Neither antithrombin deficiency nor protein S deficiency was found in the neonatal patients studied. Acquired IgG ACAs were found in 3 cases. Additional triggering factors, ie, asphyxia, septicemia, maternal diabetes, and perinatally acquired renal venous thrombosis, were reported in 54.0% of patients.
  
  
  CONCLUSIONS
  Besides acquired triggering factors, the data presented here suggest that genetic prothrombotic risk factors play a role in symptomatic neonatal stroke.
authors.affiliation: Department of Paediatrics, University of Magdeburg, Magdeburg, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Günther
authors.forename: R
authors.initials: R
authors.lastname: Junker
authors.forename: R
authors.initials: R
authors.lastname: Sträter
authors.forename: R
authors.initials: R
authors.lastname: Schobess
authors.forename: K
authors.initials: K
authors.lastname: Kurnik
authors.forename: C
authors.initials: C
authors.lastname: Heller
authors.forename: A
authors.initials: A
authors.lastname: Kosch
authors.forename: U
authors.initials: U
authors.lastname: Nowak-Göttl
mesh_terms: D001049:Apnea / Q000150:complications; D001778:Blood Coagulation Disorders / Q000097:blood / Q000175:diagnosis / Q000235:genetics*; D002545:Brain Ischemia / Q000097:blood / Q000175:diagnosis / Q000235:genetics*; D016022:Case-Control Studies; D002561:Cerebrovascular Disorders / Q000097:blood / Q000175:diagnosis / Q000235:genetics; D005165:Factor V / Q000235:genetics / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005820:Genetic Testing; D006801:Humans; D007231:Infant, Newborn; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D009123:Muscle Hypotonia / Q000150:complications; D016017:Odds Ratio; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000097:blood / Q000235:genetics; D011446:Prospective Studies; D020151:Protein C Deficiency / Q000097:blood / Q000175:diagnosis / Q000235:genetics; D011516:Prothrombin / Q000235:genetics* / Q000378:metabolism; D012307:Risk Factors; D012640:Seizures / Q000150:complications; D020521:Stroke / Q000097:blood / Q000175:diagnosis / Q000235:genetics*; D013927:Thrombosis / Q000097:blood / Q000175:diagnosis / Q000235:genetics
chemical_list: D017270:Lipoprotein(a); D005165:Factor V; D011516:Prothrombin; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2)