Ignite Creation Date:
2024-05-05 @ 5:18 PM
Last Modification Date:
2024-10-26 @ 9:30 AM
Study NCT ID:
NCT00425867
Status:
UNKNOWN
Last Update Posted:
2007-01-26
First Post:
2007-01-22
Brief Title:
PAR Family Polymorphisms and Placental Invasion Disorders
Sponsor:
Shaare Zedek Medical Center
Organization:
Shaare Zedek Medical Center
Study Overview
Official Title:
None
Status:
UNKNOWN
Status Verified Date:
2007-01
Last Known Status:
NOT_YET_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The present study will be undertaken to establish whether genetic variations of PAR1 could be involved in the occurrence of any of the placental syndromes of preterm delivery preeclampsia andor small for gestational age babies and recurrent pregnancy loss
Detailed Description:
Polymorphisms of Protease Activated Receptor 1 and adverse pregnancy outcomes Protease Activated Receptor 1 PAR1 the main thrombin receptor on vascular cells Coughlin1999 plays a critical role in orchestrating human placentation based on temporally and spatially constrained PAR1 expression in the normal invasive trophoblasts OBrien et al 2003 and its overexpression in pathological invasive trophoblast Even-Ram et al 2003
Various proteases of the PAR family as well as matrix metalloproteinases have been implicated in ancillary regulation of cancer metastases and tumor-related angiogenesis PAR1 in particular has been proposed to be involved in invasive processes of various cancers Ruf Mueller 2006 Boire et al 2005 Similarly it might be surmised that remodeling of the placenta microenvironment as well as the requisites of trophoblast invasiveness may be PAR1 sensitive Grisaru-Granovsky et al 2005 Therefore one might hypothesize that PAR1 gene variability may be involved in early placentation and that adverse pregnancy outcomes of the placental syndromes may have their origin in PAR1 dysregulation
Study Design This is a prospective case-control pilot study Subject enrolment and data collection will be performed via the Admission Service of the Division for Maternal Fetal Medicine in a large tertiary obstetrics department in Jerusalem Israel Demographic data including maternal characteristics past reproductive history and information about previous complications during pregnancy delivery and the neonatal period will be culled The blood samples will be collected at routine admission after obtaining informed consent by the physician on the floor
Four groups are described patients with spontaneous preterm delivery of a singleton before 35 weeks of gestation patients with a singleton pregnancy complicated by preeclampsia diagnosed according the Working Group Criteria 2000 patients who deliver a small for gestational age SGA singleton defined as a birth weight below the 10th percentile for the gestational age according to the Israeli growth curves Dollberg et al 2005 and for comparison patients who deliver a singleton at term with appropriate size for gestational age Patients who suffer delivery with intrauterine fetal demise andor neonates with malformations will be excluded
Maternal and umbilical cord blood samples in 011moll sodium tri citrate will be paired DNA will be prepared from white blood cells by standard techniques and subsequently stored at -4C for batched analysis The laboratory staff will be blinded as to the clinical status of the samples
Polymorphism analysis will be performed for the following polymorphisms of the PAR1 gene -1426CT 506 insertion of 13 bpIVS-14AT as per standard PCR techniques using appropriate restriction endonucleases Arnaud et l 2000
Various proteases of the PAR family as well as matrix metalloproteinases have been implicated in ancillary regulation of cancer metastases and tumor-related angiogenesis PAR1 in particular has been proposed to be involved in invasive processes of various cancers Ruf Mueller 2006 Boire et al 2005 Similarly it might be surmised that remodeling of the placenta microenvironment as well as the requisites of trophoblast invasiveness may be PAR1 sensitive Grisaru-Granovsky et al 2005 Therefore one might hypothesize that PAR1 gene variability may be involved in early placentation and that adverse pregnancy outcomes of the placental syndromes may have their origin in PAR1 dysregulation
Study Design This is a prospective case-control pilot study Subject enrolment and data collection will be performed via the Admission Service of the Division for Maternal Fetal Medicine in a large tertiary obstetrics department in Jerusalem Israel Demographic data including maternal characteristics past reproductive history and information about previous complications during pregnancy delivery and the neonatal period will be culled The blood samples will be collected at routine admission after obtaining informed consent by the physician on the floor
Four groups are described patients with spontaneous preterm delivery of a singleton before 35 weeks of gestation patients with a singleton pregnancy complicated by preeclampsia diagnosed according the Working Group Criteria 2000 patients who deliver a small for gestational age SGA singleton defined as a birth weight below the 10th percentile for the gestational age according to the Israeli growth curves Dollberg et al 2005 and for comparison patients who deliver a singleton at term with appropriate size for gestational age Patients who suffer delivery with intrauterine fetal demise andor neonates with malformations will be excluded
Maternal and umbilical cord blood samples in 011moll sodium tri citrate will be paired DNA will be prepared from white blood cells by standard techniques and subsequently stored at -4C for batched analysis The laboratory staff will be blinded as to the clinical status of the samples
Polymorphism analysis will be performed for the following polymorphisms of the PAR1 gene -1426CT 506 insertion of 13 bpIVS-14AT as per standard PCR techniques using appropriate restriction endonucleases Arnaud et l 2000
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None