Iodide Levels in Infants and Children Receiving Extracorporeal Membrane Oxygenation (ECMO).
Iodine & Thyroid in ECMO
What is the goal of the study?
In humans with injury or illness also experience changes in the oxidizing and reducing potentials which are required to sustain the appropriate chemical environment to sustain life. (1) Iodide is an elemental reducing agent (ERA).(2) ERAs include sulfide, selenium and bromide. It is thought that ERAs may help to protect tissue from oxidative damage. (2-4) Changes in oxygen consumption create a corresponding need for corresponding changes in reducing activity. Studies in patients with acute myocardial infarction (AMI) have shown that the reducing power of the red cell cytoplasm is significantly decreased while plasma and heart tissue oxidative injury is increased. (5, 6) Studies have shown that ERAs, including iodide, reduce heart damage in a mouse model of AMI. (2-4) The oxidized forms of iodine (iodate) and selenium (selenite) are chemically reduced in red blood cells (RBCs). (7, 8) The reduced form of these elements leaves the RBCs thus adding to the reducing power of the organism. (2) Iodide is also required for thyroid hormone synthesis. Patients with critical illness often have low levels of circulating triiodothyronine (T3). (2). The precise manifestations of the decreased level remain unclear. Some researchers and clinicians argue that thyroid hormone should be replaced. Others disagree. Researchers at the Fred Hutchinson Cancer Research institution and Harborview Medical Center are currently studying iodide levels in adult trauma patients. Their preliminary results suggest that patients with severe trauma have lower iodide levels and that these lower levels are associated with greater mortality. These studies are ongoing and have not yet been published. The goal of this study is observational. We plant to measure iodide levels in patients who receive extracorporeal membrane oxygenation (ECMO). Because of the importance of iodide in thyroid hormone synthesis these levels will be measured as well. References 1. Radak Z, Zhao Z, Koltai E, Ohno H, Atlay M. Oxygen consumption and usage during physicial exercise: the balance between oxidative stress and ROS-dependent adaptive signaling. Antiox Redox Signal 2013: 18: 1208-1246. 2. Iwata A, Morrison ML, Roth MB. Iodide protects heart tissue from reperfusion injury. PLoS One 2014; 9:e112458 3. Iwata A, Morrison ML, Blackwood JE, et a.l Selenide targets to reperfusing tissue and protects it from injury. Crit Care Med 2015; 43:1361?1367 4. Elrod JW, Calvert JW, Morrison J, et al. Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. Proc Natl Acad Sci U S A 2007; 104:15560?15565 5. Coffman JD, Gregg DE. Oxygen metabolism and oxygen debt repayment after myocardial ischemia. Am J Physiol 1961; 201: 881-887. 6. Senthil S, Veerappan RM, Ramakrishna Rao M, et al. Oxidative stress and antioxidants in patients with cardiogenic shock complicating acute myocardial infarction. Clin Chim Acta 2004; 348:131?137 7. Suzuki KT, Itoh M. Metabolism of selenite labelled with enriched stable isotope in the bloodstream. J Chromatogr B Biomed Sci Appl 1997; 692:15?22 8. Orringer EP, Roer MEAn ascorbate-mediated transmembrane-reducing system of the human erythrocyte. J Clin Invest 1979; 63:53?58 9. Maiden MJ, Torpy DJ. Thyroid hormone in critical illness. Crit Care Clin 2019; 35: 375-388.
Who can participate in the study?
Please contact the study team listed below to learn more.