The Role of Angiopoietin, Tie-2, and Vascular Endothelial Growth Factor (VEGF) in Sepsis-Induced Multiple Organ Dysfunction Syndrome (MODS)
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|ClinicalTrials.gov Identifier: NCT00908635|
Recruitment Status : Unknown
Verified May 2009 by Chang Gung Memorial Hospital.
Recruitment status was: Recruiting
First Posted : May 27, 2009
Last Update Posted : May 27, 2009
|Condition or disease|
|Sepsis Multiple Organ Dysfunction Syndrome|
Multiple Organ Dysfunction Syndrome (MODS) frequently leads to death in patients with sepsis. Our previous work has demonstrated that endothelial injury is closely associated with MODS development and mortality in septic patients. The sepsis-induced damage of endothelial cell membrane gives rise to increased capillary permeability. Evidence suggests that increased capillary permeability in patients with sepsis was associated with higher incidence of MODS and death during the ICU stay than those with decreased permeability. Angiopoietin (Ang) system is the key mediator for maintaining capillary permeability. Ang-2 triggers an inflammatory response and inducing permeability by activating the endothelium. In contrast, Ang-1 is anti-inflammatory, can inhibit adhesion molecule expression and attenuate permeability increase in different stimuli. The disrupted angiopoietin system has been reported in patients with sepsis, but the association between angiotension and MODS in septic patients has not been well addressed.
This study is designated to determine serum concentrations of Ang-1, Ang-2, Ang-1/Ang-2 ratio, and Tie-2 in patients with sepsis-induced MODS and to investigate the association among increased permeability, inflammatory mediators,autonomic dysfunction, and these serum mediators in development of organ failure. In addition, the study will incubate endothelial cells with septic patients' serum or tumor necrosis factor (TNF)-alfa, and determine the effects of ang-1 administration and blockade of ang-2 on disruption of endothelial cell structure, permeability increase, and expression of adhesion molecules. The study will also determine the signaling pathways and altered NF-kB dimmer composition that is responsible for the inhibitory effect for ang-1 administration on TNF-alfa-induced intercellular adhesion molecule (ICAM)-1 expression on endothelial surface.
|Study Type :||Observational|
|Estimated Enrollment :||120 participants|
|Official Title:||The Role of Angiopoietin, Angiopoietin Receptor Tie-2, and Vascular Endothelial Growth Factor in Sepsis-Induced Multi-Organ Dysfunction Syndrome|
|Study Start Date :||July 2008|
|Estimated Primary Completion Date :||August 2010|
|Estimated Study Completion Date :||August 2010|
survivors of patients
non-survivors of patients
- mortality [ Time Frame: in hospital mortality ]
- organ failure [ Time Frame: In ICU stay ]
Biospecimen Retention: Samples Without DNA
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): NCT00908635
|Chang Gung Memorial Hospital||Recruiting|
|Taoyuan, Taiwan, 333|
|Contact: Shu-Min Lin, MD 88633281200 ext 8467 firstname.lastname@example.org|
|Principal Investigator: Shu-Min Lin, MD|
|Principal Investigator:||Shu-Min Lin, MD||Chang Gung Memorial Hospital|