Betahistine exacerbates amikacin ototoxicity

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.