Angiotensin-converting enzyme gene insertion/deletion polymorphism in migraine patients

Erling Tronvik¹^,2 , Lars J Stovner¹^,2 , Gunnar Bovim² , Linda R White¹^,2 , Amanda J Gladwin³ , Kathryn Owen³ and Harald Schrader¹^,2

¹Department of Neurosciences, Norwegian University of Science and Technology, Trondheim, Norway

²Department of Neurology and Clinical Neurophysiology, University Hospital of Trondheim, Trondheim, Norway

³AstraZeneca, R&D Genetics, Mereside, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK

author email corresponding author email

BMC Neurology 2008, 8:4doi:10.1186/1471-2377-8-4


Published:	26 March 2008

Abstract

Background

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.

Methods

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.

Results

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.

Conclusion

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.