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Vol. 43, No. 3, 2000
Issue release date: April 2000
Eur Neurol 2000;43:133–136

Angiotensin-Converting Enzyme Gene Deletion Polymorphism Determines an Increase in Frequency of Migraine Attacks in Patients Suffering from Migraine without Aura

Paterna S. · Di Pasquale P. · D’Angelo A. · Seidita G. · Tuttolomondo A. · Cardinale A. · Maniscalchi T. · Follone G. · Giubilato A. · Tarantello M. · Licata G.
aDepartment of Internal Medicine and bInstitute of Molecular Biology, University of Palermo, and cDivision of Cardiology ‘Paolo Borsellino’, G.F. Ingrassia Hospital, Palermo, Italy

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Many authors have reported an association between the angiotensin-converting enzyme (ACE)-D allele and coronary heart disease and other cardiovascular diseases. The mechanism underlying the positive associations between the ACE-D alleles and diseases are not yet clear. Previous reports showed an association between migraine without aura and ACE-D allele polymorphism. The study is aimed to evaluate if the DD genotype could also be associated with the frequency and duration of migraine without aura. In 302 patients suffering from migraine without aura (at least for 1 year), with no history of cardiovascular diseases and major risk factors for ischemic events, the genotypes of the ACE gene, plasma ACE activity, and the frequency (weekly) and duration of migraine attacks were evaluated. No drugs were given before (4 weeks) and during the study. The same evaluations were performed in 201 subjects without migraine. The molecular biologist and the physician evaluating the patient data were blinded to the clinical history and ACE-DD gene determination. Genotypes were determined by polymerase chain reaction amplification. Plasma ACE activity was performed by the HPLC method. The groups were similar for sex, age and smoking habit (migraines: 302 patients (200 F/102 M), mean age 37.8 ± 8.2 years; control: 201 subjects (127 F/74 M), mean age 37.5 ± 9.3 years). Patients with migraine without aura showed higher incidence of the ACE-DD gene (48.34%) than control subjects (37.32%), p < 0.05. The frequency of migraine (average attacks per week) was higher in patients with DD (2.11 ± 1.9) than in patients with ID (1.54 ± 1.44), p < 0.05. No difference in duration of migraine attacks (hours per week) was observed. Plasma ACE activity was increased in patients with the ACE-DD gene. Our data suggest that ACE-DD gene polymorphism could have an important role in determining migraine attacks and the frequency of these attacks. Further data are needed through further studies, especially on the biomolecular level.

Copyright © 2000 S. Karger AG, Basel

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  1. Cambien F, Poirer O, Lecerf L, Evans A, Cambou JP, Arvailer D, Luc G, Barn L, Ricard S, Tiret L, Amouyer P, Soubrier F: Deletion polymorphis in the gene for angiotensin – Converting enzyme is a potent risk factor for myocardial infarction. Nature 1992;359:641–644.
  2. Lindpainter K, Pfeffer MA, Kreutz R, Stampfer MJ, Godstein F, La Motte F, Buring G, Hennekens CH: A prospective evaluation of an angiotensin-converting-enzyme gene polymorphism and the risk of ischemic heart disease. N Engl J Med 1995;332:706–711.
  3. Mattu RK, Needham EW, Galton DJ, Frangos E, Clark AJ, Caulfield M: A DNA variant at the angiotensin-converting-enzyme gene locus associates with coronary artery disease in the Carphilly Heart Study. Circulation 1995;91:270–274.
  4. Ludwig E, Cornell PS, Anderson JL, Marshall HW, Laoulel JM, Ward RH: Angiotensin-converting enzyme gene polymorphism is associated with myocardial infarction but not with development of coronary stenosis. Circulation 1995;91:2120–2124.
  5. Nakai K, Itoh C, Miura Y, Hotta K, Musha T, Itoh T, Miyakawa T, Iwasaku R, Hiramori K: Deletion polymorphism of the angiotensin I-converting enzyme gene associated with serum ACE-concentration and increased risk for CAD in the Japanese. Circulation 1994;90:2199–2201.
  6. Markus HS, Barley S, Lunt R, Bland J, Jeffrey S, Carter N, Brown M: Angiotensin converting enzyme gene polymorphism: A new risk factor for lacunar stroke but not carotid atheroma. Stroke 1996;126:1329–1333.
  7. Margaglione M, Celentano E, Grandone E, et al: Deletion polymorphism in the angiotensin converting enzyme gene in patients with a history of ischemic stroke. Arterioscler Thromb Vasc Biol 1996;16:304–309.
  8. Paterna S, Di Pasquale P, Cottone C, Seidita G, Cardinale A, Parrinello G, Ferrari G, Licata G: Migraine without aura and ACE-gene deletion polymorphism: Is there a correlation? Preliminary findings. Cardiovasc Drug Ther 1997;11:603–604.
  9. Costerousse O, Allegrini J, Lopez M, Albenc-Gelas F: Angiotensin I converting enzyme in human circulating mononuclear cells: Genetic polymorphism of expression in T lymphocytes. Biochem J 1993;290:33–40.
  10. Cambien F, Costerousse O, Tiret L, Poirier O, Lecerf L, Gonzales MF, Evans A, Arveiler D, Cambou JP, Luc G, Rakotovao R, Ducimetiere P, Soubrier F, Albenc-Gelas F: Plasma level and gene polymorphism of angiotensin-converting enzyme in relation to myocardial infarcton. Circulation 1994;90:669–676.
  11. Rigat B, Hubert C, Alhenc-Gelas F, Cambien F, Corvol P, Soubrier F: An insertion-deletion polymorphism in the antiogensin I converting enzyme gene accounting for half the variance of serum enzyme levels. J Clin Invest 1990;86:1343–1346.
  12. Tiert L, Rigat B, Visvikis S, Breda C, Corvol P, Cambien F, Soubrier F: Evidence from combined segregation and linkage analysis, that a variant of the angiotensin I converting enzyme gene controls plasma ACE levels. Am J Hum Genet 1992;51:197–205.
  13. Paterna S, Di Pasquale P, Martino S, Arrostuto A, Cascio Ingurgio N, Parrinello G, Gullotti D, Licata G: Captopril versus placebo nella profilassi dell’emicrania senza aura. Clin Ter 1992;141:475–481.

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