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This version was published on July 1, 2008
Clinical and Applied Thrombosis/Hemostasis, Vol. 14, No. 3, 356-359 (2008)
DOI: 10.1177/1076029607306399

The Importance of Thrombotic Risk Factors in the Development of Idiopathic Sudden Hearing Loss

Zuleyha Yildiz, MSc

Department of Pediatric Molecular Genetics, Medical School of Ankara University

Arzu Ulu, MSc

ENT Department, Ankara Social Security Hospital

Armagan Incesulu, MD

Department of Pediatric Molecular Genetics, Medical School of Ankara University

Yalcin Ozkaptan, MD

ENT Department, Gülhane Military Medical School, Ankara, Turkey

Nejat Akar, MD

Department of Pediatric Molecular Genetics, Medical School of Ankara University, akar{at}medicine.ankara.edu.tr

Impaired cochlear blood circulation has been suggested to cause sudden hearing loss. In this study, the role of factor V 1691 G-A (FV 1691 G-A), prothrombin 20210 G-A (PT 20210 G-A), methylene tetrahydrofolate reductase 677 C-T (MTHFR 677 C-T), factor V 4070 A-G (FV 4070 A-G), endothelial cell protein C receptor (EPCR) gene 23-bp insertion, and plasminogen activator inhibitor-1 (PAI-1) 4G/5G mutation was assessed. Fifty-three patients with idiopathic sudden sensorineural hearing loss and 80 individuals comprising the control group were included in this study. The frequency for FV 1691 A was 6.2% in the patient group and 3.7% in the control group, PT 20210 G-A was 1.2% in the patient group and 1.9% in the control group, and FV 4070 A-G was 7.5% in the patient group and 11.3% in the control group. The frequency of MTHFR 677 C-T was significantly higher in the patient group than in the control group, with a P value of .03. PAI-1-675 4G/5G polymorphism was found to be 71.2% and 69.8%, in the control group and the patient group, respectively. The EPCR 23-bp insertion was 0% in the control group and was found in 3 patients (3.7%), which needs further study.

Key Words: idiopathic sudden hearing loss • thrombotic risk factors • vascular impairment • EPCR


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