Abstract

The relationship of migraine with cardiovascular diseases has been clarified by many studies, and currently, migraine is suggested to be a systematic vasculopathy. Inflammation, thrombosis and impaired vascular reactivity are the underlying pathophysiological mechanisms of the vasculopathy. In the present study, we aimed to investigate the relationship between prolactin levels and subclinical atherosclerosis risk factors such as soluble CD40 ligand (sCD40L) and high-sensitivity CRP (hsCRP) in migraine patients during interictal period. Fifty female migraine patients and age-matched 25 female control cases were enrolled in the study. Migraine diagnosis was settled according to the ICHD-II diagnostic criteria. A questionnaire was completed about the existence of vascular risk factors. Serum samples were used to measure sCD40L, hsCRP and prolactin levels. No difference was found between the prolactin levels of the migraine patients and the controls. The sCD40L levels were significantly higher in migraine patients (p < 0.001). High-sensitivity CRP levels showed no difference between the groups. There was no correlation between prolactin, sCD40L, and hs-CRP levels in migraine patients. We consider that the migraine patients are prone to subclinical atherosclerosis, but this tendency is independent of prolactin levels.

Highlights

  • Migraine is a kind of headache which is caused by the alterations in trigeminovascular system, but the pathophysiological mechanisms have not still been fully delineated

  • We aimed to investigate the relationship between prolactin levels and subclinical atherosclerosis risk factors such as soluble CD40 ligand and high-sensitivity C-reactive protein (CRP) in migraine patients during interictal period

  • No difference was found between the prolactin levels of the migraine patients and the controls

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Summary

Introduction

Migraine is a kind of headache which is caused by the alterations in trigeminovascular system, but the pathophysiological mechanisms have not still been fully delineated. It is known that the vascular alterations are not limited to cranial vessels, and migraine is suggested to be a systemic vasculopathy [1]. The vasculopathy of migraine is thought to reflect the endothelial dysfunction and impaired vascular reactivity. The demonstration of similar C-reactive protein (CRP) levels in migraineurs and healthy control subjects in recent studies [5, 6], it had been found high in previous studies [7,8,9], necessitates new investigations and data about this issue. The increasing number of studies in the past decade showed that the risk of cardiovascular disease is increased in migraine [10,11,12,13].

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