Hostname: page-component-78c5997874-g7gxr Total loading time: 0 Render date: 2024-11-10T10:03:34.119Z Has data issue: false hasContentIssue false

Methylenetetrahydrofolate reductase C677T gene mutation as risk factor for sudden sensorineural hearing loss: association with plasma homocysteine, folate and cholesterol concentrations

Published online by Cambridge University Press:  24 May 2010

E J Lee*
Affiliation:
Department of Otolaryngology-Head and Neck Surgery, Chonbuk National University School of Medicine, Jeon-ju, South Korea
Y J Cho
Affiliation:
Department of Otolaryngology-Head and Neck Surgery, Chonbuk National University School of Medicine, Jeon-ju, South Korea
Y J Yoon
Affiliation:
Department of Otolaryngology-Head and Neck Surgery, Chonbuk National University School of Medicine, Jeon-ju, South Korea
*
Address for correspondence: Dr Eun Jung Lee, Department of Otorhinolaryngology-Head and Neck Surgery, Chonbuk National University School of Medicine, Kumam-dong, Dukjin-gu, Jeonju, South Korea. Fax: +82 63 250 1986 E-mail: imaima97@naver.com

Abstract

Objective:

Impaired cochlear perfusion appears to be the most important event in the development of sudden sensorineural hearing loss. Methylenetetrahydrofolate reductase gene mutations at nucleotide 677 cause reduced methylenetetrahydrofolate reductase enzyme activity, resulting in vascular impairment.

Methods:

Thirty-three patients and 68 control subjects underwent audiological and haematological investigation.

Results:

No statistically significant association was found between sudden sensorineural hearing loss and the methylenetetrahydrofolate reductase C677T gene mutation. Mean homocysteine and cholesterol concentrations were significantly higher in patients than in controls. Mean folate levels were significantly lower in patients than in controls. Amongst patients with sudden sensorineural hearing loss, no significant differences in mean cholesterol, homocysteine or folate concentration were found, comparing patients with methylenetetrahydrofolate reductase C677T mutation genotypes with those without.

Conclusion:

No statistically significant association was found between the methylenetetrahydrofolate reductase C677T gene mutation and sudden sensorineural hearing loss. There was a statistically significant difference between the homocysteine, folate and cholesterol concentrations of sudden sensorineural hearing loss patients, compared with controls. However, there was no statistically significant difference in these levels, comparing patients with and without the methylenetetrahydrofolate reductase C677T mutation.

Type
Main Articles
Copyright
Copyright © JLO (1984) Limited 2010

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1Lazarini, PR, Cameargo, AC. Idiopathic sudden sensorineural hearing loss: etiopathogenic aspects. Braz J Otorhinolaryngol 2006;72:554–61CrossRefGoogle ScholarPubMed
2Stokroos, RJ, Albers, FW, Schirm, J. The etiology of idiopathic sudden sensorineural hearing loss. Experimental herpes simplex virus infection of the inner ear. Am J Otolaryngol 1998;19:447–52Google ScholarPubMed
3Berrocal, JR, Ramirez-Camacho, R. Sudden sensorineural hearing loss: supporting the immunologic theory. Ann Otol Rhinol Laryngol 2002;111:989–97CrossRefGoogle ScholarPubMed
4Boulassel, MR, Deggouj, N, Tomasi, N, Gersdorff, M. Inner ear autoantibodies and their targets in patients with autoimmune inner ear diseases. Acta Otolaryngol 2001;121:2834Google ScholarPubMed
5Cadoni, G, Agostino, S, Manna, R, De Santis, A, Fetoni, AR, Vulpiani, P et al. Clinical associations of serum antiendothelial cell antibodies in patients with sudden sensorineural hearing loss. Laryngoscope 2003;113:797801CrossRefGoogle ScholarPubMed
6Schweinfurth, JM, Cacace, AT. Cochlear ischemia induced by circulating iron particles under magnetic control: an animal model for sudden hearing loss. Am J Otolaryngol 2000;21:636–40Google ScholarPubMed
7Guo, Y, Zhang, C, Du, X, Nair, U, Yoo, TJ. Morphological and functional alterations of the cochlea in apolipoprotein E gene deficient mice. Hear Res 2005;208:5467CrossRefGoogle ScholarPubMed
8Schuknecht, HF, Kimura, RS, Naufal, PM. The pathology of sudden deafness. Acta Otolaryngol 1973;76:7597CrossRefGoogle ScholarPubMed
9Nagahara, K, Fisch, U, Yagi, N. Perilymph oxygenation in sudden and progressive sensorineural hearing loss. Acta Otolaryngol 1983;96:5768CrossRefGoogle ScholarPubMed
10Suckfull, M. Fibrinogen and LDL apheresis in treatment of sudden hearing loss: a randomized multicentre trial. Lancet 2002;360:1811–17CrossRefGoogle Scholar
11Nakamura, M, Whitlock, G, Aoki, N, Nakashima, T, Hoshino, T, Yokoyama, T et al. Japanese and western diet and risk of idiopathic sudden deafness: a case-control study using pooled controls. Int J Epidemiol 2001;30:608–15CrossRefGoogle ScholarPubMed
12Menachem, G, Gideon, F, Ron, E, Nira, KM, Neta, G, Iman, AA et al. Impact of methionine synthase gene and methylenetetrahydrofolate reductase gene polymorphisms on the risk of sudden sensorineural hearing loss. Audiol Neurotol 2006;11:287–93Google Scholar
13Van Guldenet, C, Stehouwer, CD. Hyperhomocysteinaemia and vascular disease – a role for DNA hypomethylation? Lancet 2003;361:1668–9CrossRefGoogle Scholar
14Friedman, G, Goldschmidt, N, Friedlander, Y, Ben-Yehuda, A, Selhub, J, Babaey, S et al. A common mutation A1298C in human methylenetetrahydrofolate reductase gene: association with plasma total homocysteine and folate concentrations. J Nutr 1999;129:1656–61CrossRefGoogle ScholarPubMed
15Leclerc, D, Campeau, E, Goyette, P, Adjalla, CE, Christensen, B, Ross, M et al. Human methionine synthase: cDNA cloning and identification of mutations in patients of the cblG complementation group of folate/cobalamin disorders. Hum Mol Genet 1996;5:1867–74CrossRefGoogle ScholarPubMed
16Lievers, KJ, Boers, GH, Verhoef, P, den Heijer, M, Kluijtmans, LA, van der Put, NM et al. A second common variant in the MTHFR gene and its relationship to MTHFR enzyme activity, homocysteine, and cardiovascular disease risk. J Mol Med 2001;79:522–8CrossRefGoogle ScholarPubMed
17Capaccio, P, Ottaviani, F, Cuccarini, V, Ambrosetti, U, Fagnani, E, Bottero, A et al. Methylenetetrahydrofolate reductase gene mutations as risk factors for sudden hearing loss. Am J Otolaryngol 2005;26:383–7CrossRefGoogle ScholarPubMed
18Yamasoba, T, Kikuchi, S, Higo, R, O'uchi, T, Tokumaru, A. Sudden sensorineural hearing loss associated with slow blood flow of the vertebrobasilar system. Ann Otol Rhinol Laryngol 1993;102:873–7CrossRefGoogle ScholarPubMed
19Capaccio, P, Ottaviani, F, Cuccarini, V, Bottero, A, Schindler, A, Cesana, BM et al. Genetic and acquired prothrombotic risk factors and sudden hearing loss. Laryngoscope 2007;117:547–51CrossRefGoogle ScholarPubMed
20Mattson, MP, Kruman, II, Duan, W. Folic acid and homocysteine in age-related disease. Ageing Res Rev 2002;1:95111CrossRefGoogle ScholarPubMed
21Hirano, K, Ikeda, K, Kawase, T, Oshima, T, Kekehata, S, Takahashi, S et al. Prognosis of sudden deafness with special reference to risk factors of microvascular pathology. Auris Nasus Larynx 1999;26:111–15CrossRefGoogle ScholarPubMed