title: The plasminogen activator inhibitor (PAI)-1 promoter 4G/4G genotype is not associated with ischemic stroke in a population of German children. Childhood Stroke Study Group.
abstract: OBJECTIVE
  To investigate the relationship between an insertion/deletion (4G/5G) polymorphism of the plasminogen activator inhibitor (PAI)-1 gene and childhood patients with a past history of ischemic stroke.
  
  
  METHODS
  The PAI-1 4G/4G genotype and the coinheritance with lipoprotein (Lp) (a) levels, the factor V (FV) G1691A mutation, the prothrombin (PT) G20210A variant, and the methylene-tetrahydrofolate reductase (MTHFR) T677T genotype were studied in 198 Caucasian children with stroke and 951 controls (same age, sex and ethnical distribution). In a randomly selected subgroup of patients/controls (n=60) PAI-I activities have been investigated.
  
  
  RESULTS
  The distribution of the 4G/5G genotypes was no different in childhood stroke patients and controls, with a 4G allele frequency of 55.8% in patients compared with 53.8% in control subjects (P=0.49). The 4G/4G genotype compared with the remaining genotypes was present in 43 cases and 167 (17.6% vs. 21.7%; OR/CI: 1.30/0.89-1.98; P=0.3). PAI-1 activity was significantly elevated (P < 0.001) in the patient group.
  
  
  CONCLUSIONS
  Data presented here suggest that the 4G/4G genotype is not a major risk factor in the aetiology of childhood ischemic stroke.
authors.affiliation: Paediatric Haematology and Oncology, University Hospital Münster, Germany. leagottl@uni-muenster.de
authors.forename: U
authors.initials: U
authors.lastname: Nowak-Göttl
authors.forename: R
authors.initials: R
authors.lastname: Sträter
authors.forename: A
authors.initials: A
authors.lastname: Kosch
authors.forename: A
authors.initials: A
authors.lastname: von Eckardstein
authors.forename: R
authors.initials: R
authors.lastname: Schobess
authors.forename: P
authors.initials: P
authors.lastname: Luigs
authors.forename: P
authors.initials: P
authors.lastname: Nabel
authors.forename: H
authors.initials: H
authors.lastname: Vielhaber
authors.forename: K
authors.initials: K
authors.lastname: Kurnik
authors.forename: R
authors.initials: R
authors.lastname: Junker
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D020016:Activated Protein C Resistance / Q000453:epidemiology / Q000235:genetics; D000293:Adolescent; D017668:Age of Onset; D002545:Brain Ischemia / Q000453:epidemiology / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D005165:Factor V / Q000032:analysis; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D005858:Germany / Q000453:epidemiology; D006801:Humans; D007223:Infant; D017270:Lipoprotein(a) / Q000032:analysis; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D016254:Mutagenesis, Insertional; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000235:genetics; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D017354:Point Mutation; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics*; D011446:Prospective Studies; D011516:Prothrombin / Q000235:genetics; D012307:Risk Factors; D017384:Sequence Deletion; D019851:Thrombophilia / Q000150:complications / Q000235:genetics*; D044465:White People / Q000235:genetics
chemical_list: D020413:3' Untranslated Regions; D017270:Lipoprotein(a); D017395:Plasminogen Activator Inhibitor 1; C095381:factor V Leiden; D005165:Factor V; D011516:Prothrombin; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2)