Erythropoietin in Infants With Hypoxic Ischemic Encephalopathy (HIE)
![]() |
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: NCT00945789 |
Recruitment Status
:
Completed
First Posted
: July 24, 2009
Last Update Posted
: September 28, 2009
|
Tracking Information | |||
---|---|---|---|
First Submitted Date ICMJE | July 23, 2009 | ||
First Posted Date ICMJE | July 24, 2009 | ||
Last Update Posted Date | September 28, 2009 | ||
Study Start Date ICMJE | October 2007 | ||
Actual Primary Completion Date | December 2008 (Final data collection date for primary outcome measure) | ||
Current Primary Outcome Measures ICMJE |
|
||
Original Primary Outcome Measures ICMJE | Same as current | ||
Change History | Complete list of historical versions of study NCT00945789 on ClinicalTrials.gov Archive Site | ||
Current Secondary Outcome Measures ICMJE |
Nitric oxide concentrations in the plasma [ Time Frame: 2 weeks ] | ||
Original Secondary Outcome Measures ICMJE | Same as current | ||
Current Other Outcome Measures ICMJE | Not Provided | ||
Original Other Outcome Measures ICMJE | Not Provided | ||
Descriptive Information | |||
Brief Title ICMJE | Erythropoietin in Infants With Hypoxic Ischemic Encephalopathy (HIE) | ||
Official Title ICMJE | Human Recombinant Erythropoietin (HrEPO) in Asphyxia Neonatorum: A Pilot Trial | ||
Brief Summary | In this prospective trial the investigators plan to study the efficacy of erythropoietin as a therapeutic agent in neonates who suffer from brain injury following perinatal asphyxia. | ||
Detailed Description | During HIE free radicals are generated within mitochondria and also as byproducts in the synthesis of prostaglandins.These free radicals ignite a secondary phase of subsequent damage to the brain by attacking membranal fatty acids. Nitric oxide (NO) is involved in the cascade of metabolic events that contributes to HIE. It mediates, in part, the cytotoxic activity of macrophages, induces relaxation of blood vessels, and also acts as a neurotransmitter in the central and peripheral nervous system. Therefore, the therapeutic value of NO synthase inhibitors, among many other agents used to ameliorate the course of HIE, is currently under investigation in experimental animals. Erythropoietin (EPO) is a cytokine originally identified for its role in erythropoiesis and more recently shown to be produced in the central nervous system.Relative insufficiency of endogenous EPO during periods of ischemic stress may trigger neuronal apoptosis, whereas the provision of exogenous EPO has been shown to inhibit this process. The potential immediate protective effects of EPO include decreased NO production, activation of antioxidant enzymes, reduction of glutamate toxicity, inhibition of lipid peroxidation, and reduction of inflammation. Long-term protective effects of EPO include the generation of neuronal anti-apoptotic mechanisms, stimulation of angiogenesis, and modulation of neurogenesis. Preliminary data supports a protective role of exogenous EPO to neuronal cells. The presence of EPO rescues in vitro cultured neurons from NO-induced death. It specifically protects cultured neurons from N-methyl-D-aspartate (NMDA) receptor-mediated glutamate toxicity. Intercerebroventricular injection of EPO offered significant protection of neuronal tissue in animals with focal cerebral ischemia. EPO is able to cross the blood brain barrier, and its concentration in the cerebrospinal fluid in normal rats significantly increases within 30 minutes following intravenous administration. EPO also offered neuronal protection when it was administered systemically to animals suffering from global and focal cerebral ischemia. In adult patients with stroke, the administration of EPO ameliorates the course of the disease. Therefore, EPO has recently received much attention and is speculated to have a role in the protection of HIE infants. However, despite the biological plausibility and the encouraging preliminary data from animals and adult humans, surprisingly EPO has never been tried in newborns with HIE even though it has already been used in neonates for other indications and is known to be safe. |
||
Study Type ICMJE | Interventional | ||
Study Phase | Phase 1 Phase 2 |
||
Study Design ICMJE | Allocation: Non-Randomized Intervention Model: Parallel Assignment Masking: Triple (Participant, Investigator, Outcomes Assessor) Primary Purpose: Treatment |
||
Condition ICMJE | Hypoxic Ischemic Encephalopathy | ||
Intervention ICMJE |
|
||
Study Arms |
|
||
Publications * | Elmahdy H, El-Mashad AR, El-Bahrawy H, El-Gohary T, El-Barbary A, Aly H. Human recombinant erythropoietin in asphyxia neonatorum: pilot trial. Pediatrics. 2010 May;125(5):e1135-42. doi: 10.1542/peds.2009-2268. Epub 2010 Apr 12. | ||
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline. |
|||
Recruitment Information | |||
Recruitment Status ICMJE | Completed | ||
Actual Enrollment ICMJE |
45 | ||
Original Actual Enrollment ICMJE | Same as current | ||
Actual Study Completion Date | June 2009 | ||
Actual Primary Completion Date | December 2008 (Final data collection date for primary outcome measure) | ||
Eligibility Criteria ICMJE | Inclusion Criteria:
Exclusion Criteria:
|
||
Sex/Gender |
|
||
Ages | up to 24 Hours (Child) | ||
Accepts Healthy Volunteers | No | ||
Contacts ICMJE | Contact information is only displayed when the study is recruiting subjects | ||
Listed Location Countries ICMJE | Egypt | ||
Removed Location Countries | |||
Administrative Information | |||
NCT Number ICMJE | NCT00945789 | ||
Other Study ID Numbers ICMJE | 1102007 | ||
Has Data Monitoring Committee | Yes | ||
U.S. FDA-regulated Product | Not Provided | ||
IPD Sharing Statement | Not Provided | ||
Responsible Party | Abdul rahman Al Mashad, MD Associate Professor of Pediatrics, Tanta University Faculty of Medicine | ||
Study Sponsor ICMJE | Tanta University | ||
Collaborators ICMJE | Not Provided | ||
Investigators ICMJE | Not Provided | ||
PRS Account | Tanta University | ||
Verification Date | September 2009 | ||
ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP |