Circulating Leukocyte as an Inflammatory Biomarker: Association with Fibrinogen and Neuronal Damage in Acute Ischemic Stroke

BACKGROUND AND PURPOSE: Leukocytes and fibrinogen are inflammatory markers involved in circulating and central inflammatory response after ischemic stroke. However, the interaction between circulating leukocytes and serum fibrinogen and neuronal injury in acute ischemic stroke (AIS) patients is still unclear. The present study aimed to investigate the association between circulating leukocyte and serum fibrinogen and neuronal injury respectively in AIS. METHODS: A cross-section study with 431 hospitalized AIS patients from department of neurology was performed. Circulating leukocytes and fibrinogen were measured, and neuron-specific enolase (NSE) was detected to evaluate central neuronal damage. A propensity score matching method was used to minimize the effects of confounding factors. The relationship between leukocytes and NSE and fibrinogen was analyzed by linear curve fitting analysis and multiple logistic regression models respectively. RESULTS: The mean levels of NSE, leukocyte, and fibrinogen were significantly higher in the matched AIS group (n=89) than those of in the healthy control group (n=89) (all p<0.05). Both serum NSE and fibrinogen were increased with the increasing of leukocyte in AIS patients (both p<0.05). Smoothed plots suggested that there are linear relationships between leukocyte and NSE and fibrinogen respectively. Multiple logistic regression analysis showed the OR (95%) for the relationship between leukocyte and high NSE were 1.13 (1.01–1.26, p=0.031) and 1.13 (1.00–1.28, p=0.048), and between leukocyte and high fibrinogen were 1.40 (1.22–1.61, p<0.001) and 1.35 (1.15–1.58, p<0.001) in all AIS patients before and after adjusting for potential confounders. CONCLUSION: Our study suggests that elevated circulating leukocyte was associated with high fibrinogen and neuronal injury in AIS. Therefore, there may be potential targets among circulating leukocyte, fibrinogen and NSE that should be intervened to reduce inflammatory reaction after ischemic stroke.