CDP-choline treatment increases circulating endothelial progenitor cells in acute ischemic stroke
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Published on: September 22, 2020
Tomás Sobrino1, Raquel Rodríguez-González, Miguel Blanco
1Clinical Neuroscience Research Laboratory, Department of Neurology, Hospital Clínico Universitario, IDIS, University of Santiago de Compostela, Spain.
Objectives:
The increase in circulating endothelial progenitor cells (EPCs) is associated with a better outcome in patients with acute ischemic stroke. CDP-choline (citicoline) increases brain plasticity after experimental stroke. Therefore, we study if citicoline treatment could increase the EPC concentration after ischemic stroke.
Methods:
Forty-eight patients with a first-ever non-lacunar ischemic stroke were consecutively included in the study within 12 hours of symptoms onset. Patients received treatment (n = 26) or non-treatment (n = 22) with oral citicoline (2000 mg/day) from acute phase of ischemic stroke and for 6 weeks. EPC colonies were quantified as early outgrowth colony forming unit-endothelial cell (CFU-EC) at admission (before citicoline treatment) and day 7. We defined the EPC increment during the first week as the difference in the numbers of CFU-EC between day 7 and admission.
Results:
CFU-ECs were similar at baseline between patients treated and non-treated with citicoline (7.7±6.1 versus 9.1±7.3 CFU-EC, P = 0.819). However, patients treated with citicoline and recombinant tissue-plasminogen activator (rt-PA) showed a higher EPC increment compared to patients treated only with citicoline or non-treated (35.4±15.9 versus 8.4 ± 8.1 versus 0.9 ± 10.2 CFU-EC, P < 0.0001). In a logistic model, citicoline treatment [odds ratio (OR), 17.6; confidence interval (CI) 95%, 2.3-137.5, P = 0.006] and co-treatment with citicoline and rt-PA (OR, 108.5; CI 95%, 2.9-1094.2, P = 0.001) were independently associated with an EPC increment⩾4 CFU-EC.
Conclusion:
The administration of citicoline and the co-administration of citicoline and rt-PA increase EPC concentration in acute ischemic stroke.
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