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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.

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Department of Neurology, University of California, San Francisco, California 94143, USA.


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.

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