Replication of genetic associations in the inflammation, complement, and coagulation pathways with intraventricular hemorrhage in LBW preterm neonates

Kelli K Ryckman; John M Dagle; Keegan Kelsey; Allison M Momany; Jeffrey C Murray

doi:10.1203/PDR.0b013e31821ceb63

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Replication of genetic associations in the inflammation, complement, and coagulation pathways with intraventricular hemorrhage in LBW preterm neonates

Journal article

Open access

Peer reviewed

Replication of genetic associations in the inflammation, complement, and coagulation pathways with intraventricular hemorrhage in LBW preterm neonates

Kelli K Ryckman, John M Dagle, Keegan Kelsey, Allison M Momany and Jeffrey C Murray

Pediatric research, Vol.70(1), pp.90-95

07/2011

DOI: 10.1203/PDR.0b013e31821ceb63

PMCID: PMC3117229

PMID: 21659962

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Abstract

Intraventricular hemorrhage (IVH) is a significant morbidity seen in very LBW infants. Genes related to the inflammation, infection, complement, or coagulation pathways have been implicated as risk factors for IVH. We examined 10 candidate genes for associations with IVH in 271 preterm infants (64 with IVH grades I-IV and 207 without IVH) weighing <1500 g. The heterozygous genotype OR = 8.1, CI = 2.5-26.0, p = 4 × 10(-4)) and the A allele (OR = 7.3, CI = 2.4-22.5, p = 1 × 10(-4)) of the coagulation factor V (FV) Leiden mutation (rs6025) were associated with an increased risk of developing IVH grade I or II but not grade III or IV after correction for multiple testing with Bonferroni. Lack of association in the severe grades of IVH may be a result of lack of power to detect an effect given the small sample size (n = 8). However, this result is consistent with previous research that demonstrates that the heterozygous genotype of the FV mutation is associated with increased risk for the development of IVH but a decreased risk for the progression or extension to more severe grades of IVH.

Humans

Male

Inflammation - blood

Intracranial Hemorrhages - genetics

Intracranial Hemorrhages - blood

Inflammation Mediators - metabolism

Complement System Proteins - genetics

Female

Integrin beta3 - genetics

Odds Ratio

Cytokines - genetics

Infant, Newborn

Severity of Illness Index

Infant, Low Birth Weight

Genetic Predisposition to Disease

Reproducibility of Results

Genetic Association Studies

Risk Assessment

Gene Frequency

Risk Factors

Logistic Models

Inflammation - immunology

Gestational Age

Linkage Disequilibrium

Iowa

Phenotype

Estrogen Receptor alpha - genetics

Infant, Premature

Intracranial Hemorrhages - immunology

Inflammation - genetics

Blood Coagulation - genetics

Heterozygote

Factor V - genetics

Polymorphism, Single Nucleotide

Details

Title: Subtitle: Replication of genetic associations in the inflammation, complement, and coagulation pathways with intraventricular hemorrhage in LBW preterm neonates
Creators: Kelli K Ryckman - Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA
John M Dagle
Keegan Kelsey
Allison M Momany
Jeffrey C Murray
Resource Type: Journal article
Publication Details: Pediatric research, Vol.70(1), pp.90-95
DOI: 10.1203/PDR.0b013e31821ceb63
PMID: 21659962
PMCID: PMC3117229
NLM abbreviation: Pediatr Res
ISSN: 1530-0447
eISSN: 1530-0447
Publisher: United States
Grant note: 5T32 HL 007638-24 / NHLBI NIH HHS R01 HD052953-01 / NICHD NIH HHS R01 HD052953 / NICHD NIH HHS K99 HD065786-01 / NICHD NIH HHS R01 HD-52953 / NICHD NIH HHS T32 HL007638-24 / NHLBI NIH HHS T32 HL007638 / NHLBI NIH HHS K99 HD065786 / NICHD NIH HHS R01 HD057192 / NICHD NIH HHS R01 HD-57192 / NICHD NIH HHS R01 HD057192-01A2 / NICHD NIH HHS
Language: English
Date published: 07/2011
Academic Unit: Anatomy and Cell Biology; International Programs; Stead Family Department of Pediatrics; Epidemiology; Iowa Neuroscience Institute; Pediatric Dentistry; Craniofacial Anomalies Research Center; Nursing; Public Policy Center (Archive); Biochemistry and Molecular Biology; Dental Research; Neonatology
Record Identifier: 9983995054602771

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