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Background: Migraine has been considered a vascular risk factor especially in young women. Factors predisposing to endothelial damage in migraine are still being debated. The insufficiency of circulating endothelial precursor circulating cells (EPCs) suggested a link between migraine and cardiovascular risk. This research aimed to study a subtype of EPCs, those expressing e-selectin, to assess endothelial activation and, therefore, endothelial dysfunction in migraine. Methods: Consecutive headache patients (n=99) and 35 adjusted controls were recruited. Total EPCs, defined as CD34+/KDR+ cells, and EPC colony-forming units (CFUs) were assayed. We identified as "early" EPCs those CD62E- EPCs, and "late" EPCs, CD62E+, a surrogate marker for endothelial damage. Plasmatic calcitonin-gene related protein (CGRP) and vascular-endothelial growth factor (VEGF) were analyzed. Results: We did not find differences in the total number of CFUs among clinical groups. Means of total CD34+/KDR+ and "early" EPCs were not significant among clinical groups. Nevertheless, the mean of "late" EPCs was lower (log10-transformed mean=1.715; SD=0.393) in the control group than in the migraine patients (log10-transformed mean=2.167;SD=0.685), even after adjustment by VEGF plasma level and other confounding factors. Linear regression analyses disclosed significant predictors for "late" EPCs for controls vs migraine (β=0.452 SE±0.13; p=0.001).We did not observe differences between migraine with or without aura. Conclusion: We observed higher number of activated EPCs in migraine patients than in controls. CD62E+ EPCs might be considered a marker for vascular damage in migraine patients. [ABSTRACT FROM AUTHOR]

A response from the authors of the article "Analysis of endothelial precursor cells in chronic migraine: a case-control study" in the 2013 issue is presented.