Selenium and Selenoprotein P Deficiency Correlates With Complications and Adverse Outcome After Major Trauma

Abstract

Background: A declining selenium (Se) status constitutes a characteristic of critical illness and may affect disease course and survival. The dynamics of trauma-induced changes in biomarkers of Se status are poorly characterized, and an association with multiple organ failure (MOF) and mortality can be hypothesized. It was the aim of this study to investigate Se and selenoprotein P (SELENOP) concentrations in major trauma patients during the early posttraumatic period. Patients and Methods: Twenty-four patients after major trauma (ISS ≥16) were included at our level one trauma center. Se supplementation ever during the 90-day observation period was defined as an exclusion criterion. Serum samples were drawn within less than 60 min after trauma, and after 6 h, 12 h, 24 h, 48 h, and 72 h. Serum Se was analyzed by X-ray fluorescence and SELENOP concentrations by ELISA. The data were correlated to clinical parameters, occurrence of MOF defined by MOF and APACHE II score, lung injury defined by Horowitz index and clinical outcome (90-days survival). Results: Serum Se and SELENOP concentrations of the trauma patients were significantly below the average of healthy European subjects (mean ±SD; Se, 41.2±8.1 vs. 84.7±23.3 μg/L, P < 0.001; SePP, 1.5±0.3 vs. 4.3±1.0 mg/L, P < 0.001). A strong deficit was present already at the first time point (Se; 33.6±10.5 μg/L, SELENOP: 1.4±0.5 mg/L). The clinical scores collectively showed an inverse relation between health status and Se biomarkers. Patients who did not survive the 90-day observation period exhibited significantly lower initial post-trauma Se status than the surviving patients (mean±SD; Se, 24.7±7.2 vs. 39.2±8.4 μg/L, P<0.05; SePP, 1.1±0.4 vs. 1.6±0.4 mg/L, P<0.05). Conclusion: Very low Se and SELENOP concentrations occur fast after major trauma and are associated with poor survival odds. These findings support the notion that early Se substitution may constitute a meaningful adjuvant treatment strategy in trauma patients.

Selenium Deficiency is Associated with Mortality Risk from COVID-19

“…Secondly, in disease and upon the growing inflammation, a potentially pre-existing low Se status may decline further. This notion is supported from similar findings in other severe diseases, especially sepsis [14] and polytraumatic injury [15], where low, declining and mortality-relevant Se deficiency has been observed that is unlikely a predisposition. Moreover, the negative acute phase response of hepatic SELENOP biosynthesis [33], together with the suppressive effects of hypoxia [34] or cytokines, e.g.…”

“…Se deficiency is also a risk factor for death from severe disease, as shown e.g. for sepsis [14] or polytraumatic injury [15]. Notably, the cure rate from COVID-19 was recently associated with basal Se status in different areas of China [16].…”

Selenium Deficiency Is Associated with Mortality Risk from COVID-19

“…Secondly, in disease and upon the growing inflammation, a potentially pre-existing low Se status may decline further. This notion is supported from similar findings in other severe diseases, especially sepsis [14] and polytraumatic injury [15], where low, declining, and mortality-relevant Se deficiency has been observed that is unlikely a predisposition. Moreover, the negative acute phase response of hepatic SELENOP biosynthesis [36], together with the suppressive effects of hypoxia [37] or cytokines, e.g., IL-6 [38], argue in favor of this mechanism contributing to the differences.…”

“…Keshan disease is an endemic cardiomyopathy related to Se deficiency, and supplemental Se has proven meaningful for reducing the virus-associated disease incidence [13]. Se deficiency is also a risk factor for death from severe disease, as shown, e.g., in sepsis [14] or polytraumatic injury [15]. Notably, the cure rate from COVID-19 was recently associated with basal Se status in different areas of China [16].…”

The Relevance of Selenium Status in Rheumatoid Arthritis

“…Likewise, the systemic inflammatory response has been associated with a reduction of up to 48% in plasma Se concentration when CRP is >80 mg/L [ 112 , 113 ]. It has been suggested that inflammatory cytokines (IL-1β, TNF-α and IFNγ) repress the expression of SeP and that the metabolism of Se could be disturbed during the acute phase reaction [ 114 ]. The low concentration of Se can deplete circulating antioxidants and thus exacerbate the inflammatory state of the disease through uncontrolled ROS production [ 115 ].…”