Please use this identifier to cite or link to this item: http://localhost:8080/xmlui/handle/123456789/8115
Title: Ischemia modified albumin level and thiol/disulfide homeostasis in the etiology of tinnitus
Authors: Kurku, Huseyin
Bor, Mehmet Akif
Tulgar, Mustafa Faris
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Keywords: Disulfide
IMA
thiol/disulfide homeostasis
tinnitus
Issue Date: 2022
Publisher: International Journal of Medical Biochemistry
Series/Report no.: Research Article;28-33
Abstract: Objectives: Although many theories about the etiology of tinnitus have been proposed, it has not been fully clarified. In this study, we investigated the role of ischemia in the etiology of tinnitus. Methods: A total of 90 participants, 50 tinnitus patients and 40 controls, were included in this study. Total thiol (TT), native thiol (NT), NT/TT ratio, disulfide, disulfide/TT ratio, disulfide/NT ratio, ischemia-modified albumin (IMA), and IMA/ albumin ratio (IMA/AlbR) values of tinnitus patient group and controls were compared and receiver operating characteristic (ROC) analyses conducted. Results: IMA (0.767±0.06) and IMA/AlbR (17.71±2.46) values were statistically significantly higher in the tinnitus group than in the control group (0.742±0.06 vs. 16.00±2.48 and p=0.040 vs. p=0.002, Independent Samples test). No statistically significant difference was observed between the groups for the other parameters. While albumin was presenting a perfect positive correlation with TT and NT, IMA showed rugged negative parallelism with NT and TT, similar to that of IMA/AlbR. According to ROC analysis, a cut-off value of 14.29 was found to be statistically significant for IMA/AlbR in distinguishing patients with tinnitus from the controls (sensitivity of 96%, specificity of 32.5%, AUC: 0.676, and p=0.002). Conclusion: In the present study, in the tinnitus group, higher values of IMA and IMA/AlbR, which are markers of ischemic status, support the theory specifying that ischemia has an influential role in the etiology of tinnitus.
URI: http://localhost:8080/xmlui/handle/123456789/8115
ISSN: 2618-642X
Appears in Collections:Vol 5 No 1 (2022)

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