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Pediatr Res. 2011 Dec;70(6):642-6. doi: 10.1203/PDR.0b013e31823240dd.

Candidate genes and risk for CP: a population-based study.

Author information

1
Department of Neurology, University of California, San Francisco, California 94143, USA. wuy@neuropeds.ucsf.edu

Abstract

Studies suggest that genetic polymorphisms may increase an individual's susceptibility to CP. Most findings have yet to be corroborated in an independent cohort. This case-control study is nested within all 334,333 infants ≥36 wk gestation born at Kaiser Permanente Medical Care Program, 1991-2002. We included only non-Hispanic whites who had a neonatal blood sample available. Case patients (n = 138) were identified from medical records to have spastic or dyskinetic CP. Controls (n = 165) were randomly selected from the population. We genotyped polymorphisms previously associated with CP: inducible NOS (iNOS)-231, apolipoprotein E (apoE) ε2 and ε4 alleles, TNF-α-308, IL-8 -251, lymphotoxin 60, endothelial NOS -922, endothelial protein C receptor 219, mannose-binding lectin 54 and 52, factor V Leiden, methyltetrahydrofolate reductase 1298 and 667, prothrombin 20210, and platelet activator inhibitor 11053. Similar to previous reports, the iNOS-231 T allele (25.7 versus 18.9%, p = 0.04) and the apoE ε4 allele (19.3 versus 13.2%, p = 0.04) were more common in patients with CP than in controls. However, there was no statistically significant association between any genetic polymorphism and CP after correction for multiple comparisons.

PMID:
21857382
PMCID:
PMC3210921
DOI:
10.1203/PDR.0b013e31823240dd
[Indexed for MEDLINE]
Free PMC Article

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