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Title: Betahistine exacerbates amikacin ototoxicity. Author: Aksoy F, Dogan R, Ozturan O, Yildirim YS, Veyseller B, Yenigun A, Ozturk B. Journal: Ann Otol Rhinol Laryngol; 2015 Apr; 124(4):280-7. PubMed ID: 25358613. Abstract: OBJECTIVE: Betahistine augments cochlear blood flow and is currently used as an efficient therapeutic agent. Amikacin is used in a wide range of areas, but its ototoxic effect continues to be problematic. This study investigates the effect of betahistine on amikacin-induced ototoxicity. METHODS: Thirty-two healthy rats were randomized to 4 groups of 8 rats in each group (amikacin, amikacin+betahistine, betahistine, and no treatment). Amikacin was administered intramuscularly to groups 1 and 2 for 14 days. Betahistine was delivered by oral gavage to groups 2 and 3 for 21 days. Distortion-product otoacoustic emissions (DPOAE) and auditory brainstem response (ABR) tests were conducted on all rats. RESULTS: There were significant decreases in the DPOAE levels and significant increases in the ABR thresholds of the amikacin and amikacin+betahistine groups on the 7th, 14th, and 21st days, as compared to their basal values. The DPOAE levels of the amikacin+betahistine group significantly decreased on days 7, 14, and 21, and the ABR thresholds significantly increased on the same days, as compared to the amikacin group. CONCLUSION: Our study implies that amikacin's ototoxic effects are augmented by the concurrent use of betahistine. Experimental and clinical research, supported by histopathological studies, is needed to affirm our findings.[Abstract] [Full Text] [Related] [New Search]