Placental and Cord Blood Markers Associated With Premature Birth and Disorders of Premature Birth in Newborn Infants
The purpose of this study is to determine if changes in specific gene products in the placenta or cord/infant blood affect a baby's birth weight, increase the risk of premature birth, or increase the risk of developing diseases of prematurity. We would also like to characterize whether placental epigenetic changes or placental markers of environmental exposures are associated with premature birth.
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||Study of Environmental Toxicants and Inflammatory Markers in Prematurity and Diseases of Prematurity|
- Comparisons of placental gene expression and cord blood immune markers [ Time Frame: through hospital discharge ] [ Designated as safety issue: No ]Placental gene expression and cord-blood immune markers/function will be compared between 50 term infants and 150 preterm infants. Further, among preterm infants it will be determined whether certain patterns of gene expression and immune marker distribution are associated with specific diseases/condition and growth outcomes. Similarly, epigenetic changes in the immune genes and markers of environmental exposure will be compared between preterm infants and term infants. Associations between environment exposures and epigenetic changes and diseases of prematurity will also be determined.
Biospecimen Retention: Samples With DNA
whole blood, placenta
|Study Start Date:||June 2009|
|Estimated Study Completion Date:||December 2014|
|Estimated Primary Completion Date:||December 2014 (Final data collection date for primary outcome measure)|
Infants born at greater than 37 weeks gestation
Infants born at less than 37 weeks gestation
Prematurity, diseases of prematurity and growth-disorders of newborn infants contribute significantly to morbidity and mortality seen in newborn infants [1,2,3]. One out of eight newborn infants in the USA is born premature (gestational age less than 37 completed weeks). In 2004, of the 27,860 infants dying within the first year of life, greater than 16,000 were born premature . Moreover, premature infants who survive the neonatal period are at increased risk of cerebral palsy, developmental delays, growth impairment and long-term respiratory disability [3-5]. Additionally, fetal growth restriction and fetal growth excess results in infants being delivered as small for gestational age infants or large for gestational age infants, respectively. Infants born with such growth-disorders are at increased risk of perinatal morbidity and mortality and as adults are at significant risk of obesity, type II diabetes and heart disease [6,7].
While the etiology of preterm birth and growth-disorders can be ascribed to maternal conditions, chromosomal defects or specific maternal environmental exposures in some newborn infants, for a majority the etiology remains unknown [8,9]. There is increasing evidence pointing to the role of genetic susceptibility factors in the causation of prematurity and growth-disorders of the newborn infant [8, 10-12]. Further, epigenetic changes in growth regulating or inflammatory genes in the placenta can program the fetus for premature birth, growth-disorders and other diseases in the postnatal period.
The overall objective of this application is four-fold.
- To determine whether altered placental or fetal expression of imprinted genes is associated with disorders of growth, prematurity or other postnatal diseases in newborn infants.
- To determine whether altered placental expression of genes that regulate the innate immune response is associated with premature birth or other postnatal diseases in newborn infants.
- To determine whether placental markers of environmental exposure (such as Polycyclic Aromatic Hydrocarbons or PAH) or epigenetic changes in placental inflammatory genes or growth genes are associated with prematurity or postnatal diseases in newborn infants.
- To determine whether cord blood immune responses and markers of immune-cell function are different between preterm and term infants and are associated with postnatal diseases in preterm infants.
|Contact: Venkatesh Sampath, MBBSfirstname.lastname@example.org|
|Contact: Kathleen Meskin, BSNemail@example.com|
|United States, Wisconsin|
|Froedtert Memorial Lutheran Hospital||Recruiting|
|Wauwatosa, Wisconsin, United States, 53226|
|Principal Investigator:||Venkatesh Sampath, MBBS||Medical College of Wisconsin|