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Placental and Cord Blood Markers Associated With Premature Birth and Disorders of Premature Birth in Newborn Infants

Medical College of Wisconsin logo

Medical College of Wisconsin

Status

Completed

Conditions

Premature Birth

Study type

Observational

Funder types

Other

Identifiers

NCT01439048
CHW 09/102, GC 900

Details and patient eligibility

About

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.

Full description

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 [2]. 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.

  1. 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.
  2. 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.
  3. 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.
  4. 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.

Enrollment

82 patients

Sex

All

Ages

1 minute to 3 months old

Volunteers

Accepts Healthy Volunteers

Inclusion criteria

  • all infants born alive

Exclusion criteria

  • infants who are born with no signs of life

Trial design

82 participants in 2 patient groups

Term infants
Description:
Infants born at greater than 37 weeks gestation
Preterm Infants
Description:
Infants born at less than 37 weeks gestation

Trial contacts and locations

1

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Data sourced from clinicaltrials.gov

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