However, this does not sufficiently explain how systemic I/R affects neurological outcome on the basis of the limited data available. Previous pilot studies showed that elevated serum HMGB1 is related to poor neurological outcome in PCAS. Inflammatory cytokines play an important role in systemic I/R and are promoted by high-mobility group box 1 protein (HMGB1). The inflammatory response in patients with post-cardiac arrest syndrome (PCAS) causes systemic ischemia/reperfusion injury (I/R), which may lead to multiple organ dysfunction and mortality, and is described as “sepsis-like syndrome”. It is expected that research on HMGB1 focused on systemic I/R will help prevent aggravating neurological outcomes. This result suggests that systemic I/R may contribute to secondary brain aggravation. Serum HMGB1 for first 24 h after cardiac arrest was significantly correlated with SOFA score, NSE, and IL-6. The early phase of HMGB1 (0–24 h), all phases of IL-6, and the delayed phase of NSE (24–168 h) manifested poor neurological outcome.
ResultsĪ total of 128 patients were enrolled in this study. Serum HMGB1, NSE, and IL-6 were evaluated for variability, correlation with each biomarker, or the Sequential Organ Function Assessment (SOFA) score and CPC at return of spontaneous circulation at 0, 24, 48, and 168 h.
Subjects were observed for 90 days, and neurological outcome was classified according to the Glasgow-Pittsburgh Cerebral Performance Categories Scale (CPC). This study was designed as a single-institution prospective observational study.
The purpose of this study was to demonstrate the pathophysiology of systemic I/R for secondary brain damage using the biomarkers high-mobility group box 1 (HMGB1), neuron-specific enolase (NSE), and interleukin-6 (IL-6). The inflammatory response in PCAS causes systemic I/R. Ischemia/reperfusion injury (I/R) is an important pathophysiology of post-cardiac arrest syndrome (PCAS) against multiple organ dysfunction and mortality.
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