Premature BirthNCT01439048
Placental and Cord Blood Markers Associated With Premature Birth and Disorders of Premature Birth in Newborn Infants
An observational study of Premature Birth, run by Medical College of Wisconsin at 1 site in United States.
Trial summary
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. Read more about this study
- Who is it for?
- Ages 1 minute to 3 monthsHealthy volunteers can take part
- Conditions the study is for
- Premature Birth
- How many people
- 82 participants
- Where
- 1 siteUnited States
- Study dates
- Jun 2009to Aug 2015
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 1 minute to 3 months
- All sexes
- Healthy volunteers accepted
- Child
Study population: Infants who are born both premature (less than 37 weeks gestation) and full term infants (greater than 37 weeks gestation).
Who may be able to join
- all infants born alive
Who cannot join
- infants who are born with no signs of life
Trial locations and contacts
1 site in 1 country.
United States1 site
Froedtert Memorial Lutheran Hospital
Wauwatosa, Wisconsin, 53226
About this study
Official title: Study of Environmental Toxicants and Inflammatory Markers in Prematurity and Diseases of Prematurity
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.
Read the detailed 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.
- 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.
- Conditions
- Premature Birth
- Keywords
- Placenta, Cord Blood, PAH, Environmental Markers, Toll-Like Receptors
- Medical subject headings
- Premature Birth
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Term infants | Infants born at greater than 37 weeks gestation | |
| Preterm Infants | Infants born at less than 37 weeks gestation |
What is being measured
The primary outcome is the main question the study is designed to answer.
Comparisons of placental gene expression and cord blood immune markers
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.
Measured: through hospital discharge
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted22 Sep 2011 (estimated)
- Study startJun 2009
- Primary completionAug 2015
- Study completionAug 2015
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (12)Papers the sponsor has linked to this study.
- Other trials for Premature BirthStudies of the same condition, open and under way.
- More trials run by Medical College of WisconsinThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Prospective
- Enrolment
- 82 participants (actual)
Sponsor and investigators
- Lead sponsor
- Medical College of Wisconsin
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Venkatesh Sampath, Medical College of Wisconsin
- Investigators
- Venkatesh Sampath, MBBS, Principal investigator, Medical College of Wisconsin
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01439048
- Sponsor's protocol ID
- CHW 09/102, GC 900
- Status last verified
- Aug 2015
- First submitted
- 21 Sep 2011
- Last updated
- 28 Aug 2015
- Results posted
- No
- Data monitoring committee
- No
Publications
Guyer B, Martin JA, MacDorman MF, Anderson RN, Strobino DM. Annual summary of vital statistics--1996. Pediatrics. 1997 Dec;100(6):905-18. doi: 10.1542/peds.100.6.905.
PubMed 9374556Mathews TJ, MacDorman MF. Infant mortality statistics from the 2003 period linked birth/infant death data set. Natl Vital Stat Rep. 2006 May 3;54(16):1-29.
PubMed 16711376Stoll BJ, Hansen N. Infections in VLBW infants: studies from the NICHD Neonatal Research Network. Semin Perinatol. 2003 Aug;27(4):293-301. doi: 10.1016/s0146-0005(03)00046-6.
PubMed 14510320Stoll BJ, Hansen N, Fanaroff AA, Wright LL, Carlo WA, Ehrenkranz RA, Lemons JA, Donovan EF, Stark AR, Tyson JE, Oh W, Bauer CR, Korones SB, Shankaran S, Laptook AR, Stevenson DK, Papile LA, Poole WK. Late-onset sepsis in very low birth weight neonates: the experience of the NICHD Neonatal Research Network. Pediatrics. 2002 Aug;110(2 Pt 1):285-91. doi: 10.1542/peds.110.2.285.
PubMed 12165580Stoll BJ, Hansen NI, Adams-Chapman I, Fanaroff AA, Hintz SR, Vohr B, Higgins RD; National Institute of Child Health and Human Development Neonatal Research Network. Neurodevelopmental and growth impairment among extremely low-birth-weight infants with neonatal infection. JAMA. 2004 Nov 17;292(19):2357-65. doi: 10.1001/jama.292.19.2357.
PubMed 15547163Chakraborty S, Joseph DV, Bankart MJ, Petersen SA, Wailoo MP. Fetal growth restriction: relation to growth and obesity at the age of 9 years. Arch Dis Child Fetal Neonatal Ed. 2007 Nov;92(6):F479-83. doi: 10.1136/adc.2006.109728. Epub 2007 Feb 14.
PubMed 17301112Valsamakis G, Kanaka-Gantenbein C, Malamitsi-Puchner A, Mastorakos G. Causes of intrauterine growth restriction and the postnatal development of the metabolic syndrome. Ann N Y Acad Sci. 2006 Dec;1092:138-47. doi: 10.1196/annals.1365.012.
PubMed 17308140Adams KM, Eschenbach DA. The genetic contribution towards preterm delivery. Semin Fetal Neonatal Med. 2004 Dec;9(6):445-52. doi: 10.1016/j.siny.2004.04.001.
PubMed 15691782Kramer MS. Intrauterine growth and gestational duration determinants. Pediatrics. 1987 Oct;80(4):502-11.
PubMed 3658568Hao K, Wang X, Niu T, Xu X, Li A, Chang W, Wang L, Li G, Laird N, Xu X. A candidate gene association study on preterm delivery: application of high-throughput genotyping technology and advanced statistical methods. Hum Mol Genet. 2004 Apr 1;13(7):683-91. doi: 10.1093/hmg/ddh091. Epub 2004 Feb 19.
PubMed 14976157Clausson B, Lichtenstein P, Cnattingius S. Genetic influence on birthweight and gestational length determined by studies in offspring of twins. BJOG. 2000 Mar;107(3):375-81. doi: 10.1111/j.1471-0528.2000.tb13234.x.
PubMed 10740335Treloar SA, Macones GA, Mitchell LE, Martin NG. Genetic influences on premature parturition in an Australian twin sample. Twin Res. 2000 Jun;3(2):80-2. doi: 10.1375/136905200320565526.
PubMed 10918619
Study at a glance
From the registry record, last updated by the sponsor on 28 Aug 2015. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Study of Environmental Toxicants and Inflammatory Markers in Prematurity and Diseases of Prematurity
- ClinicalTrials.gov ID
- NCT01439048
- Acronym / sponsor ID
- CHW 09/102, GC 900
- Conditions
- Premature Birth
- Keywords
- Placenta, Cord Blood, PAH, Environmental Markers, Toll-Like Receptors
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 82 participants (actual)
- Lead sponsor
- Medical College of WisconsinUniversity, hospital or other
- Study start
- Jun 2009
- Primary completion
- Aug 2015 (actual)
- Study completion
- Aug 2015 (actual)
- First posted
- 22 Sep 2011 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Detailed 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.
- 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.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Term infants | – | –Infants born at greater than 37 weeks gestation |
| Preterm Infants | – | –Infants born at less than 37 weeks gestation |
Who may qualify
- Ages
- 1 minute to 3 months
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child
- Study population
- Infants who are born both premature (less than 37 weeks gestation) and full term infants (greater than 37 weeks gestation).
Key inclusion criteria (1 listed)
- all infants born alive
Key exclusion criteria (1 listed)
- infants who are born with no signs of life
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Comparisons of placental gene expression and cord blood immune markers
Time frame: through hospital discharge
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.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 28 Aug 2015.
- Background: PubMed 9374556Guyer B, Martin JA, MacDorman MF, Anderson RN, Strobino DM. Annual summary of vital statistics--1996. Pediatrics. 1997 Dec;100(6):905-18. doi: 10.1542/peds.100.6.905.
- Background: PubMed 16711376Mathews TJ, MacDorman MF. Infant mortality statistics from the 2003 period linked birth/infant death data set. Natl Vital Stat Rep. 2006 May 3;54(16):1-29.
- Background: PubMed 14510320Stoll BJ, Hansen N. Infections in VLBW infants: studies from the NICHD Neonatal Research Network. Semin Perinatol. 2003 Aug;27(4):293-301. doi: 10.1016/s0146-0005(03)00046-6.
- Background: PubMed 12165580Stoll BJ, Hansen N, Fanaroff AA, Wright LL, Carlo WA, Ehrenkranz RA, Lemons JA, Donovan EF, Stark AR, Tyson JE, Oh W, Bauer CR, Korones SB, Shankaran S, Laptook AR, Stevenson DK, Papile LA, Poole WK. Late-onset sepsis in very low birth weight neonates: the experience of the NICHD Neonatal Research Network. Pediatrics. 2002 Aug;110(2 Pt 1):285-91. doi: 10.1542/peds.110.2.285.
- Background: PubMed 15547163Stoll BJ, Hansen NI, Adams-Chapman I, Fanaroff AA, Hintz SR, Vohr B, Higgins RD; National Institute of Child Health and Human Development Neonatal Research Network. Neurodevelopmental and growth impairment among extremely low-birth-weight infants with neonatal infection. JAMA. 2004 Nov 17;292(19):2357-65. doi: 10.1001/jama.292.19.2357.
- Background: PubMed 17301112Chakraborty S, Joseph DV, Bankart MJ, Petersen SA, Wailoo MP. Fetal growth restriction: relation to growth and obesity at the age of 9 years. Arch Dis Child Fetal Neonatal Ed. 2007 Nov;92(6):F479-83. doi: 10.1136/adc.2006.109728. Epub 2007 Feb 14.
- Background: PubMed 17308140Valsamakis G, Kanaka-Gantenbein C, Malamitsi-Puchner A, Mastorakos G. Causes of intrauterine growth restriction and the postnatal development of the metabolic syndrome. Ann N Y Acad Sci. 2006 Dec;1092:138-47. doi: 10.1196/annals.1365.012.
- Background: PubMed 15691782Adams KM, Eschenbach DA. The genetic contribution towards preterm delivery. Semin Fetal Neonatal Med. 2004 Dec;9(6):445-52. doi: 10.1016/j.siny.2004.04.001.
- Background: PubMed 3658568Kramer MS. Intrauterine growth and gestational duration determinants. Pediatrics. 1987 Oct;80(4):502-11.
- Background: PubMed 14976157Hao K, Wang X, Niu T, Xu X, Li A, Chang W, Wang L, Li G, Laird N, Xu X. A candidate gene association study on preterm delivery: application of high-throughput genotyping technology and advanced statistical methods. Hum Mol Genet. 2004 Apr 1;13(7):683-91. doi: 10.1093/hmg/ddh091. Epub 2004 Feb 19.
- Background: PubMed 10740335Clausson B, Lichtenstein P, Cnattingius S. Genetic influence on birthweight and gestational length determined by studies in offspring of twins. BJOG. 2000 Mar;107(3):375-81. doi: 10.1111/j.1471-0528.2000.tb13234.x.
- Background: PubMed 10918619Treloar SA, Macones GA, Mitchell LE, Martin NG. Genetic influences on premature parturition in an Australian twin sample. Twin Res. 2000 Jun;3(2):80-2. doi: 10.1375/136905200320565526.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Venkatesh Sampath, MBBS principal investigator
Medical College of Wisconsin
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Premature Birth, run by Medical College of Wisconsin at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 28 Aug 2015. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Comparisons of placental gene expression and cord blood immune markers (time frame: through hospital discharge). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01439048, which also lists 12 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 28 Aug 2015.