부산대학교 도서관

Introduction: Inflammatory response and metabolic derangements may accelerate neurodegeneration after cardiac surgery. Insulin, insulin growth factor (IGF), and insulin-like growth factor binding protein acid labile subunit (IGFALS) are the centerpieces of glucose metabolism, the critical factor determining long-term recovery from cardiac surgery and neurodegeneration progression[1]. IGFALS is a regulatory element of IGF that increases their half-life and vascular localizationHypothesis: We investigate the dynamics of IGFALS up to 3 months after cardiac surgery. We hypothesize that post-cardiac surgery IGFALS serum level abnormalities are related to changes in neuroinflammatory (BDNF, CXCL13) and neurodegeneration marker (tau).Methods: Patients (n=25) scheduled for non-emergent heart surgery were included, except for patients with pre-existing immunological aberrancies. Blood was collected before surgery(tbaseline), 24 hours later(t24h) after the first sample, 7 days(t7d), and 3 months(t3m) after tbaseline. Variables regarding the surgery were collected from medical records. IGFALS levels were measured via ELISA, while neurodegeneration and neuroinflammation markers via multiplex technology.Results: Demographic variables had limited effects on IGFALS. The serum levels of IGFALS varied significantly (H[4;221]=9.146; 0.0274) (Figure 1). The serum levels were significantly lower at t7d but recovered at t3m. During the acute inflammatory response at t24h IGFALS, serum levels remained unaltered. BDNF at 3m correlated with IGFALS at t7d (r=0.38;p=0.012) and t3m (r=0.39;p=0.018). CXCL13 demonstrated similar interactions. Tau level did not correlate with IGFALS dynamics.Conclusions: The data demonstrated a significant long-term decline in IGFALS level after cardiac surgery. The correlations suggest a potential link between IGFALS and some neuroinflammatory markers. 1. Westwood, A.J Neurology, 2014.82(18): p. 1613-9.