Angiotensin-converting enzyme gene insertion/deletion polymorphism in migraine patients
1 Department of Neurosciences, Norwegian University of Science and Technology, Trondheim, Norway
2 Department of Neurology and Clinical Neurophysiology, University Hospital of Trondheim, Trondheim, Norway
3 AstraZeneca, R&D Genetics, Mereside, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK
BMC Neurology 2008, 8:4 doi:10.1186/1471-2377-8-4Published: 26 March 2008
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. 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.
347 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.
No 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.
In 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.