Betahistine Exacerbates Amikacin Ototoxicity. (April 2015)

• Record Type: Journal Article
• Authors: Aksoy, Fadlullah; Dogan, Remzi; Ozturan, Orhan; Yildirim, Yavuz Selim; Veyseller, Bayram; Yenigun, Alper; Ozturk, Burak
• Is Part Of: Annals of otology, rhinology & laryngology. Volume 124:Number 4(2015:Apr.)
• Page Start: 280
• Page End: 287
• Publication Date: 2015-04
• Subjects: ABR -- amikacin -- betahistine -- DPOAE -- ototoxicity; Otolaryngology -- Periodicals; 617.51
• DOI: 10.1177/0003489414557020
• Languages: English
• ISSNs: 0003-4894

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.