Abstract
Dear Sir,
We are grateful to Rodriguez-Osorio et al. for their interest in our article. The authors compared and commented on methodological issues from their article (1) and ours. (2) It is well known that endothelial-precursor circulating cells (EPCs) are under the influence of a lot of stimuli, which might modify their number and function depending on the moment of analysis, medication or even the last bout of vascular event (in this case, migraine). We used different methodology and sampling. In this regard, even when subjects were recruited if fitting chronic or episodic migraine criteria – and we permitted other confounding factors, such as analgesics – results did not differ much from Rodriguez-Osorio et al. (1) because both investigations concluded that migraine is associated with endothelial impairment. Rodriguez-Osorio et al. (1) used a very selected sample, which is of interest for avoiding confounding factors. Some sampling differences might be responsible for differences observed at least in some results. Age is an important factor for vascular events and for number of EPCs and colony-forming units (CFUs); both, CFUs and EPCs decrease with age. Our sample was approximately 5 years younger than that of Rodriguez-Osorio et al. (1), in which controls were 6 years younger than migraine patients, although this difference was not significant, mainly because they analysed a low number of subjects. In addition, they included almost exclusively females, while we included one third of males in each clinical group. With Rodriguez-Osorio et al. (1), subjects having any common vascular risk factor were excluded; but we included some subjects having dyslipemia, smoking or hypertension in both groups, controls and cases.
This is also true when explaining differences in results concerning calcitonin-gene related peptide (CGRP) determination. Nevertheless, with Oterino et al. (2), levels of plasmatic CGRP in controls were lower, although differences were not significant, than in migraine patients. CGRP has recently been found to be a good marker for chronic migraine, but its interpretation is not trouble free (3).
In spite of differences such as age, common vascular factors and methodology in EPC determination, both investigations concluded that migraine induces endothelial damage. We emphasize that we observed endothelial dysfunction in a younger migraine sample, which is more comparable to that attended every day in headache-dedicated clinics.