Abstract
BackgroundAlarmins, including high-mobility group box 1 (HMGB-1), can be released from damaged tissues and activated cells as inflammatory mediators. We aimed to evaluate HMGB-1 and mitochondrial DNA dynamics and estimate the prognostic value for neurological outcome in patients with post-cardiac arrest syndrome after out-of-hospital cardiac arrest.MethodsWe evaluated the dynamics of HMGB-1, mitochondrial DNA, and other variables in patients with return of spontaneous circulation after out-of-hospital cardiac arrest. Patients were divided into two groups according to the cerebral performance category at 30 days: the favourable outcome group (cerebral performance categories 1 and 2) and unfavourable group (≥3).ResultsTwenty-one patients were included, and 11 demonstrated favourable outcomes. HMGB-1 levels and mitochondrial DNA on day 1 were significantly higher than on days 2, 3, 5, and 7. Plasma levels of HMGB-1 on day 1 correlated with prognostic parameters (estimated interval to return of spontaneous circulation, lactate, and NH3), tissue damage, systemic inflammation, and disease severity. HMGB-1 on day 1 in the unfavourable group was significantly higher than in the favourable group (median [interquartile range] 15.5 [6.65–18.7], 39.4 [17–69.5], P = 0.009). These findings were not observed regarding mitochondrial DNA. Regarding HMGB-1 prediction accuracy for a good neurological outcome, the area under the receiver operating characteristic curve was 0.864 (95 % confidence interval 0.702, 1.000).ConclusionsHMGB-1 may be involved in acute-phase post-cardiac arrest syndrome pathophysiology, and an increase in plasma levels may be associated with a poor neurological outcome. The study was registered with the University Hospital Medical Information Network Clinical Trials Registry ID: UMIN000006714.Electronic supplementary materialThe online version of this article (doi:10.1186/s40560-016-0161-4) contains supplementary material, which is available to authorized users.
Highlights
Alarmins, including high-mobility group box 1 (HMGB-1), can be released from damaged tissues and activated cells as inflammatory mediators
In 2008, post-cardiac arrest syndrome (PCAS) was proposed as a new term that incorporates all pathophysiological processes occurring after a return of spontaneous circulation after cardiac arrest [1]
In systemic inflammatory response syndrome (SIRS) associated with PCAS, it has been suggested that alarmins may cause a noninfectious systemic inflammatory response [2, 6]
Summary
Alarmins, including high-mobility group box 1 (HMGB-1), can be released from damaged tissues and activated cells as inflammatory mediators. We aimed to evaluate HMGB-1 and mitochondrial DNA dynamics and estimate the prognostic value for neurological outcome in patients with post-cardiac arrest syndrome after out-of-hospital cardiac arrest. There are four elements to PCAS: (1) hypoxic brain injury, (2) myocardial dysfunction, (3) systemic ischemia/reperfusion response, Omura et al Journal of Intensive Care (2016) 4:37 internal and endogenous molecules are released from damaged tissues and promote immunity, coagulation, and inflammatory responses [4]. These molecules are called “alarmins” [5]. The purpose of this study was to evaluate HMGB-1 and mtDNA dynamics, the relationship between HMGB-1, mtDNA, and severity of conditions and estimate the prognostic values of these molecules in patients with post-cardiac arrest syndrome after out-of-hospital cardiac arrest
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
