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dc.contributor.authorTronvik, Erling
dc.contributor.authorStovner, Lars Jacob
dc.contributor.authorBovim, Gunnar
dc.contributor.authorWhite, Linda
dc.contributor.authorGladwind, AJ
dc.contributor.authorOwen, k
dc.contributor.authorSchrader, Harald
dc.date.accessioned2015-09-25T11:34:40Z
dc.date.accessioned2015-10-07T14:20:05Z
dc.date.available2015-09-25T11:34:40Z
dc.date.available2015-10-07T14:20:05Z
dc.date.issued2008
dc.identifier.citationBMC Neurology 2008, 26(8)nb_NO
dc.identifier.issn1471-2377
dc.identifier.urihttp://hdl.handle.net/11250/2353224
dc.description.abstractBackground: 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.nb_NO
dc.language.isoengnb_NO
dc.publisherBioMed Centralnb_NO
dc.titleAngiotensin-converting enzyme gene insertion/deletion polymorphism in migraine patientsnb_NO
dc.typeJournal articlenb_NO
dc.typePeer revieweden_GB
dc.date.updated2015-09-25T11:34:40Z
dc.source.volume26nb_NO
dc.source.journalBMC Neurologynb_NO
dc.source.issue8nb_NO
dc.identifier.doi10.1186/1471-2377-8-4
dc.identifier.cristin363201
dc.description.localcode© 2008 Tronvik et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.nb_NO


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