Comparison of Intratympanic Oxytocin and Dexamethasone in Cisplatin Ototoxicity: An Experimental Study.

Although it is widely used, there is still no valid treatment for ototoxicity caused by the antineoplastic drug cisplatin. In this study, we aimed to investigate the efficacy of intratympanic resveratrol and intratympanic dexamethasone treatment in cisplatin-induced ototoxicity. We also compared intratympanic atosiban (oxytocin antagonist) and oxytocin in cisplatin ototoxicity. In this study, 30 rats (60 ears) were used by separating into 5 groups. Cisplatin, oxytocin, dexamethasone, atosiban and 0.9% NaCl were administered intraperitoneally to all groups separately. Auditory Brainstem Response and Distortion Product Otoacoustic Emission tests were performed on all groups before and 72 h after the procedure. Pre-treatment values were higher than post-treatment values in all groups (p < 0.001). There was no significant prolongation of the post-treatment Auditory Brainstem Response I-IV interval in the oxytocin and dexamethasone groups (p > 0.05). There was no significant decrease in the frequencies of 2832 and 4004 after treatment in the oxytocin and dexamethasone group compared to pre-treatment in Distortion Product Otoacoustic Emission. As a result, it has been shown that intratympanic oxytocin may be an option that can be used in the treatment, although it is not as effective as dexamethasone in preventing cisplatin ototoxicity.

Efficacy of 2 Different Intratympanic Steroid Regimen on Prevention of Cisplatin Ototoxicity: An Experimental Study.

Ototoxicity is the general name of cochlear and vestibular organ injury resulting from encountering various therapeutic agents and chemical substances. Cisplatin is commonly used in the treatment of many cancers. In this study, the efficacy of intratympanic steroids was compared for preventing cisplatin ototoxicity. In this study, 32 (64 ears) rats were used by separating into 4 groups. Cisplatin was administered intraperitoneally to the first group (n = 8). Methylprednisolone and then cisplatin were administered intratympanically to the second group (n = 8). On the third group (n = 8), dexamethasone and then cisplatin were administered intratympanically. To the fourth group (n = 8), 0.9% NaCl and then cisplatin were given intratympanically. Otoacoustic emission (OAE) measurements and auditory brainstem responses (ABRs) tests were performed on all groups before and 72 hours after the procedure. Pretreatment of ABR-IV values were 4.29 ± 0.19 milliseconds in group 2 and 4.27 ± 0.16 milliseconds in group 3, whereas posttreatment ABR-IV values were 4.95 ± 0.35 milliseconds in group 2 and 4.65 ± 0.26 milliseconds in group 3. The ABR-IV values were measured significantly shorter in the rats given dexamethasone and methylprednisolone, according to control and cisplatin groups (P < .001). Pretreatment of ABR I-IV interval values were 2.98 ± 0.34 milliseconds and 3.03 ± 0.42 milliseconds in group 1 and group 4, respectively, and ABR I-IV interval values in group 1 and group 4 posttreatment were 3.49 ± 0.39 milliseconds and 3.5 ± 0.39 milliseconds in group 1 and group 4, respectively. Auditory brainstem responses I-IV interval was significantly longer in the cisplatin and control group than in the rats given dexamethasone and methylprednisolone (P < .001). After cisplatin treatment, OAE amplitudes decreased significantly in group 1 and group 4 for all frequencies, while OAE values were protected in methylprednisolone and dexamethasone group (P < .001). In conclusion, it has been shown that both agents have protective effects on cisplatin ototoxicity, with dexamethasone slightly more than methylprednisolone.

Comparison of the protective efficacy between intratympanic dexamethasone and resveratrol treatments against cisplatin-induced ototoxicity: an experimental study.

PURPOSE: The main aim of this study was to compare the efficacy of intratympanic administration of dexamethasone and resveratrol in preventing cisplatin ototoxicity by measuring acoustic brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). METHODS: Forty rats (80 ears) were divided into five groups. Cisplatin was administered intraperitoneally to the first group (n = 8). Group 2 (n = 8) received cisplatin after resveratrol had been administered intratympanically. Group 3 (n = 8) received cisplatin after dexamethasone had been administered intratympanically. Group 4 (n = 8) received cisplatin after sodium chloride (NaCl) had been given intratympanically. Group 5 (n = 8) received cisplatin after dimethylsulfoxide (DMSO) had been given intratympanically. ABR and DPOAE tests were performed on all groups before and 72 h after the procedure. RESULTS: ABR threshold values in rats that received dexamethasone and resveratrol were found to be less affected than those observed in the other post-cisplatin groups. ABR-IV and ABR-I-IV interval values were significantly reduced in rats that had been given dexamethasone and resveratrol compared to the other groups. After cisplatin treatment, otoacoustic emission (OAE) amplitudes were significantly decreased in Groups 1, 4, and 5 for all frequencies, while OAE values were sustained in the resveratrol and dexamethasone groups (Groups 2 and 3). At OAE frequency 5652, dexamethasone was more significantly associated with protective than resveratrol was, while no significant difference was found between the two groups at other OAE frequencies. CONCLUSION: In conclusion, intratympanic dexamethasone and intratympanic resveratrol treatments may provide a significant protection against cisplatin-induced ototoxicity.