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.
Background. It is not predictable which patients will develop a severe inflammatory response after successful cardiopulmonary resuscitation (CPR), also known as “postcardiac arrest syndrome.” This pathology affects only a subgroup of cardiac arrest victims. Whole body ischemia/reperfusion and prolonged shock states after return of spontaneous circulation (ROSC) may both contribute to this devastating condition. The vascular endothelium with its glycocalyx is especially susceptible to initial ischemic damage and may play a detrimental role in the initiation of postischemic inflammatory reactions. It is not known to date if an immediate early damage to the endothelial glycocalyx, detected by on-the-scene blood sampling and measurement of soluble components (hyaluronan and syndecan-1), precedes and predicts multiple organ failure (MOF) and survival after ROSC. Methods. 15 patients after prehospital resuscitation were included in the study. Serum samples were collected on the scene immediately after ROSC and after 6 h, 12 h, 24 h, and 48 h. Hyaluronan and syndecan-1 were measured by ELISA. We associated the development of multiple organ failure and 30-day survival rates with these serum markers of early glycocalyx damage. Results. Immediate serum hyaluronan concentrations show significant differences depending on 30-day survival. Further, the hyaluronan level is significantly higher in patients developing MOF during the initial and intermediate resuscitation period. Also, the syndecan-1 levels are significantly different according to MOF occurrence. Conclusion. Serum markers of glycocalyx shedding taken immediately on the scene after ROSC can predict the occurrence of multiple organ failure and adverse clinical outcome in patients after cardiac arrest.
In December 2019, the new severe acute respiratory syndrome coronavirus 2 (COVID-19) emerged in China and has rapidly spread worldwide affecting the global population in a dramatic manner. 1 Reports from high prevalence regions in different countries
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