Antenatal Allopurinol in Intrauterine Growth Restriction
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT00346463|
Recruitment Status : Unknown
Verified June 2006 by UMC Utrecht.
Recruitment status was: Not yet recruiting
First Posted : June 30, 2006
Last Update Posted : April 28, 2008
Growth retardation in utero may be caused by uteroplacental vascular insufficiency. When Doppler ultrasound studies of the umbilical artery are abnormal pathological intrauterine growth restriction (IUGR) can be diagnosed. IUGR fetuses have a higher mortality and morbidity, both perinatally and on the longer term. This is probably due to chronic malnourishment and hypoxia due to placental insufficiency. This placental dysfunction causes generation of harmful free oxygen radicals in the fetus. The IUGR fetus has a diminished antioxidative capacity which means these free radicals cannot be buffered sufficiently. This leads to fetal oxidative stress.
Previous studies have shown that allopurinol can inhibit the cascades that lead to generation of free radicals. High dosed allopurinol also scavenges radicals and binds free iron without adverse effects on the fetus or mother.
As IUGR is associated with placental insufficiency and excessive production of free radicals we hypothesize that antenatal allopurinol administration could lead to a decrease in oxidative stress in the mother and fetus and subsequent improvement of the maternal and/or neonatal outcome.
|Condition or disease||Intervention/treatment||Phase|
|Fetal Growth Retardation||Drug: Allopurinol||Not Applicable|
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||50 participants|
|Intervention Model:||Parallel Assignment|
|Official Title:||Does Antenatal Allopurinol Administration Improve Maternal and Neonatal Outcome in Intrauterine Growth Restriction?|
|Study Start Date :||July 2006|
|Estimated Study Completion Date :||July 2013|
- free radical production / oxidative stress
- foetal parameters (Doppler, cardiotocography)
- postponement of birth
- morbidity (including long term neurodevelopmental outcome)
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00346463
|Contact: Manon Benders, MD, PhD||0031 30 email@example.com|
|Contact: Frank van Bel, Prof MD, PhD||0031 30 firstname.lastname@example.org|
|Wilhelmina Children's Hospital / UMC Utrecht|
|Utrecht, Netherlands, 3508 AB|
|Principal Investigator: Manon Benders, MD, PhD|
|Sub-Investigator: Helen Torrance, MD|
|Study Director:||Frank van Bel, Prof MD, PhD||Wilhelmina Children's Hospital / UMC Utrecht|
|Principal Investigator:||Manon Benders, MD, PhD||Wilhelmina Children's Hospital, UMC Utrecht|
|Principal Investigator:||Helen Torrance, MD||Wilhelmina Children's Hospital / UMC Utrecht|