6 ng/mL in patients with sepsis [14] are similar to the levels and magnitude of increase sellckchem we found in patients following CA. TRX was also found to be elevated after cardiopulmonary bypass or heart failure, two clinical situations that combine great inflammation and circulatory disturbances [27,28]. Moreover, as has been previously reported for patients with sepsis [14] or meningococcal septic shock [11], we found that TRX levels were significantly higher in non-survivors than in survivors, even if ability to predict ICU death was not robust. In addition, patients dying within 24 hours exhibited the highest levels of TRX, with admission concentration carrying a very good ability to predict early death.Our findings suggest that patients suffer from major oxidative stress and inflammation during post-cardiac arrest syndrome, which cannot be counteracted by increased TRX production.

Others have suggested that prolonged oxidative stress in patients with coronary risk factors wastes the serum antioxidant pool such as vitamin C and that serum TRX is recruited to compensate [29]. That our data show highest levels associated with worse outcome following CA is perhaps suggestive of the severity of oxidative stress associated with the condition. These findings confirm and broaden the data of post-cardiac arrest syndrome pathophysiology, supporting the hypothesis that oxidative stress and inflammatory insults are much more marked in the most severe patients and contribute largely to the high initial mortality. Likewise, when focusing on the cause of CA, cardiac etiologies had lower TRX levels.

This is in line with the overall better prognosis of CA of coronary origin [30].When focusing on disease severity, TRX concentrations were correlated to admission arterial lactate levels, a biological parameter that is constantly associated with unfavorable outcome [31]. We also found a strong association between low-flow duration and TRX levels, whereas this was not observed with the no-flow duration. This illustrates the pathophysiology of the ischemia reperfusion injury, with a major reactive oxygen species production during the reperfusion phase [16,17,32]. This is also consistent with the well-known observation that the severity of the post-cardiac arrest syndrome is much more driven by the low-flow duration [33].

Finally, the absence of correlation with SAPS II, by contrast with association with SOFA score, could be explained by the fact that SOFA score describes strictly organ failures [34]. Conversely, SAPS II score takes into account not only medical condition, but also underlying comorbidities [35].Perhaps, surprisingly, we observed that TRX levels decreased within of Dacomitinib short range of time. As inflammatory and pro-oxidant states are known to persist after CA, this finding might suggest that TRX half-life is relatively short, or that release is minimized after the initial insult, or that other serum antioxidants have been replenished.