Location: Children's Nutrition Research CenterTitle: Stanniocalcin in pediatric critical illness) Author
Submitted to: Critical Care Medicine
Publication Type: Abstract only
Publication Acceptance Date: 10/1/2008
Publication Date: 12/1/2008
Citation: Castro, D., Zhang, L., Gordon, W., Castillo, L., Sheikh-Hamad, D. 2008. Stanniocalcin in pediatric critical illness [abstract]. Critical Care Medicine. 36(12):A36(Suppl). Interpretive Summary:
Technical Abstract: Stanniocalcin (STC) is a pleiotropic, homodimeric glycoprotein, originally described as an important regulator of calcium homeostasis in fish. In mammals, STC is expressed in multiple organs, including heart, kidney, neurons, macrophages, thymus, and spleen. It modulates the immune/inflammatory response and is up-regulated in cardiomyocytes and blood vessel walls of patients with heart failure. We hypothesized that given the significant regulatory role of STC on calcium metabolism and the ubiquitous role of calcium on signaling and physiological processes, STC would be up-regulated in vivo, at the whole-body level in critically ill children. We studied 15 critically ill children (infants: N=5, age 5 +/- 3 months, wt 5.3 +/- 1.5kg; children: N=5, age 3 /- 0.9 years, wt 14. =/- 3.5kg; adolescents: N=5, age 15.2 +/- 0.9 years, wt 63.+/- 23kg) admitted to the PICU. Blood samples and demographic and clinical data were obtained. Western blots and specific STC antibodies were used to determine the presence of STC, Beta-actin was used as control. Western blots showed the presence of STC in the plasma of critically ill children, and it was significantly (p<0.05) correlated with acidosis. There was a trend toward correlation with renal failure (p< 0.07), but there was no correlation with severity of disease. From this preliminary data we conclude that STC is found in the plasma of critically ill children and is correlated with acidosis. To our knowledge, this is the first description of STC in vivo in human plasma. The origin and role of STC under conditions of critical illness remains to be determined, but immune/inflammatory and renal cells may contribute to the production of STC in critically ill children.