Macrophage Migration Inhibitory Factor (MIF)- Cardiac Surgery
It has been repeatedly demonstrated that cardiac surgery with the use of extracorporeal circulation elicits a systemic inflammatory response and provokes ischemia-reperfusion related oxidative stress which could further lead to the development of organ failure in critically ill patients. Perioperative levels of macrophage migration inhibitory factor (MIF) and other inflammatory mediators could be involved in adverse outcomes in cardiac surgery.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Macrophage Migration Inhibitory Factor (MIF) as a Marker of Perioperative Inflammatory Reaction During Heart Surgery|
- Pilot study: correlation between clinical and lab parameters [ Time Frame: two months ] [ Designated as safety issue: Yes ]Possible correlation between several clinical and laboratory parameters will be analyzed. This is a pilot study to generate hints at future items to be studied in controlled trials.
Biospecimen Retention: Samples Without DNA
inflammatory markers (different)
|Study Start Date:||January 2011|
|Primary Completion Date:||December 2012 (Final data collection date for primary outcome measure)|
A single group of 100 consecutive patients will undergo additional blood sampling at different time points
Procedure: Blood sampling
Blood sampling at various time points. Additional 92 mL blood.
The trace element selenium (Se) serves as an essential co-factor for the antioxidant enzymes Thioredoxin - reductase (TRR) and many other antioxidant enzymes, which protect tissues from oxidative stress. In septic patients it has previously been shown that thioredoxin, a TRR regulated Redox Enzyme, has the ability to suppress the synthesis of MIF.
Aim of the present study is therefore to investigate the relation between perioperative selenium decrease and the reduction of TRR activity with a possible release of MIF during the inflammatory response after cardiac surgery.