Abstract
BackgroundThe main objective of this study was to investigate the angiotensin converting enzyme (ACE) genotype as a possible risk factor for migraine (both with and without aura) compared to controls. We also wanted to examine whether a clinical response to an ACE inhibitor, lisinopril, or an angiotensin II receptor blocker, candesartan, in migraine prophylaxis was related to ACE genotype.Methods347 migraine patients aged 18–68 (155 migraine without aura (MoA), 187 migraine with aura (MwA) and 5 missing aura subgroup data) and 403 healthy non-migrainous controls > 40 years of age were included in the study. A polymerase chain reaction (PCR) was performed on the genomic DNA samples to obtain the ACE insertion (I)/deletion(D) polymorphisms.ResultsNo significant differences between migraine patients and controls were found with regard to ACE genotype and allele distributions. Furthermore, there was no significant difference between the controls and the MwA or MoA subgroups.ConclusionIn our sample there is no association between ACE genotype or allele frequency and migraine. In addition, ACE genotype in our experience did not predict the clinical response to lisinopril or candesartan used as migraine prophylactics.
Highlights
The main objective of this study was to investigate the angiotensin converting enzyme (ACE) genotype as a possible risk factor for migraine compared to controls
There was no significant difference between the controls and the migraine with aura (MwA) or migraine without aura (MoA) subgroups, nor between responders and non-responders to lisinopril and candesartan, and no difference was detected when stratifying by sex
Within the migraine group differences in genotype could not explain the presence of aura (n = 342, missing data = 5, p = 0.64), of coexisting tension-type headache among migraineurs (n = 343, missing data = 4, p = 1.0), differences in age of debut (n = 342, missing = 5, p = 0.69) or frequency of migraine (n = 342, missing = 5, p = 0.52) or in headache frequency as recorded in the placebo period in the candesartan study (n = 56, missing = 3, p = 0.77)
Summary
The main objective of this study was to investigate the angiotensin converting enzyme (ACE) genotype as a possible risk factor for migraine (both with and without aura) compared to controls. Two small open studies reported an improvement of the headache in migraine patients using an angiotensin-converting enzyme (ACE) inhibitor [1,2]. Placebo controlled studies conducted by our research group have evidence for efficacy of an ACE inhibitor (lisinopril) and an ARB (candesartan) in migraine prophylaxis [4,5]. This and other evidence points in the direction of involvement of the renin-angiotensin system (RAS) in migraine pathophysi-. For migraine an Italian (Paterna) [8], an Australian (Lea) [9], and a Japanese (Kowa) [10] study has demonstrated different results regarding whether an association between the ACE polymorphisms and this condition exists (Table 1)
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