Oxidative Status in Patients with Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo (BPPV) is the most frequent peripheral vestibular disorder and is particularly seen among older patients suffering from vertigo. The brief vertigo attacks in and imbalance symptoms of BPPV are caused by freely floating otoconia within the semicircular canals. The...

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Bibliographic Details
Published in:The journal of international advanced otology 2018-08, Vol.14 (2), p.299-303
Main Authors: Sahin, Ethem, Deveci, Ildem, Dinc, Mehmet Emre, Yayla Ozker, Berna, Bicer, Cemile, Erel, Ozcan
Format: Article
Language:English
Subjects:
Aging
Antioxidants
Causes of
Development and progression
Disease
Fistula
Health aspects
Hearing loss
Homeostasis
Hospitals
Metabolism
Original
Otolaryngology
Oxidation
Oxidative stress
Physiological aspects
Studies
Surgery
Thiols
Vertigo
Vitamin deficiency
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Summary:Benign paroxysmal positional vertigo (BPPV) is the most frequent peripheral vestibular disorder and is particularly seen among older patients suffering from vertigo. The brief vertigo attacks in and imbalance symptoms of BPPV are caused by freely floating otoconia within the semicircular canals. The aim of this prospective study was to evaluate the role of oxidative stress, using native thiol/disulfide (SH/SS) homeostasis as a novel indicator, in the etiology of BPPV. The 62 participants in the study included 31 patients with BPPV and, as the control group, 31 healthy individuals without any cochleovestibular disorders. Patients with BPPV initially had significantly lower native SH levels and significantly lower SH/total thiol (TT) ratios, as well as significantly higher SS/SH and SS/TT ratios, than the healthy controls. After successful treatment of their vertigo, which was confirmed based on the results obtained from the second blood sample, patients with BPPV still had lower SH levels and SH/TT ratios and significantly higher SS/SH and SS/TT ratios than the healthy controls. Our results suggest a role of oxidative stress in the development of BPPV, through both calcium metabolism and the direct toxic effects of free oxygen radicals, including the triggering of apoptosis.
ISSN:1308-7649
2148-3817
DOI:10.5152/iao.2018.4756