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  • Additionally in the presented study both the NSE

    2019-07-15

    Additionally, in the presented study both the NSE values and MFI levels of the CD45−CD34 + CXCR7+ (S)-Mephenytoin correlated positively with the inflammatory parameter – CRP. CXCR7 expression has been found to be enhanced during pathological processes such as inflammation and neoplasms (Janssens et al., 2017; Ngamsri et al., 2017; Sanchez-Martin et al., 2013). In these processes, CXCR7 expression is augmented on peripheral endothelial cells and immune cells, but is diminished on leukocytes after they infiltrate the tissues (Sanchez-Martin et al., 2013). One of the hypothetic mechanisms explaining the negative correlation between the NSE values and the levels of the CXCR7+ stem/progenitor cells could be a higher rate of infiltration of these cells into the more injured and thus more inflammatory-active tissue. We have also found negative correlations between NSE values and percentage levels of the CD45−CD34 + and the CD45−CD34 + CXCR4+ cells. However, such correlations have not been found for MFI values of these cells. In our recent study, correlations for MFI values of the CD45−CD34 + CXCR4+ cells followed the correlations of the CD45−CD34 + CXCR7+ cells only in terms of arterial stiffness. Patients with higher arterial stiffness had significantly higher levels of the CD45−CD34 + CXCR4+ and the CD45−CD34 + CXCR7+ cells on day 1. Furthermore, only levels of the CD45−CD34 + CXC4+ cells seemed to be influenced by co-existing diabetes and obesity, while CD45−CD34 + CXCR7+ cells by hypertension (Gójska-Grymajło et al., 2018). It remains to be elucidated whether this could be a trait of different and separate patterns of activation of the CXCR4+ and CXCR7+ progenitor/stem cells in the acute phase of ischemic stroke or whether it is combined with a specific influence of preexisting co-morbidities (see discussion - Gójska-Grymajło et al., 2018). These results are partially consistent with other studies, where NSE serum concentrations were observed to rise during several consequent sampling days, with peak values on day 2–3 (Brea et al., 2009; Missler et al., 1997). There were some studies that prove very early NSE peak (up to 18 h) followed by a decrease and then with another rise within first 4–5 days (Wunderlich et al., 2006, 1999). In another study the researchers distinguished 5 patterns of NSE release: no significant change, a continuous increase, a continuous decrease, one peak and two peaks (Kim et al., 2014). The discrepancies between the results may have methodological reasons (Anand and Stead, 2005), but can also indicate complex pathophysiological processes underlying NSE release after focal ischemia (Herrmann and Ehrenreich, 2003). High NSE serum concentrations early after stroke onset may correspond to the induced cytoplasmatic loss of NSE in neurons. A second increase in NSE values is attributed to secondary mechanisms of neuronal damage due to edema, hemorrhagic transformation or increase in intracranial pressure (Herrmann and Ehrenreich, 2003; Kim et al., 2014). Regardless of the underlying mechanisms many studies concordantly confirm a continuous or secondary increase in NSE concentrations in stroke patients with a deterioration of the neurological status (Alatas et al., 2015; Brea et al., 2009; Schaarschmidt et al., 1994; Sienkiewicz-Jarosz et al., 2009; Wunderlich et al., 2006). Additionally, a 2-peak pattern was also observed more frequently in patients with atrial fibrillation and cardioembolic stroke (Kim et al., 2014). Our study seems to confirm this pattern of association, since patients with chronic atrial fibrillation had higher NSE values on day 1 and 6–7. It would be interesting to learn whether NSE, most probably in composition with other biomarkers, could help to distinguish between different stroke etiologies (Ng et al., 2017).
    Conclusions In this study NSE values indicated some activity of the CD45−CD34 + CXCR7+, CD45−CD34 + and CD45−CD34 + CXCR4+ stem/progenitor cells in the first 7 days after ischemic stroke. Additionally, this study supports the thesis that NSE might be a valuable prognostic marker in acute ischemic stroke.