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Abstract Objective: Previous studies have shown that hearing function is also vulnerable to the effects of diabetes mellitus which can be shown by brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of brainstem auditory evoked potential and distortion product otoacoustic emission in hyperglycemia and whether there is a relationship between reactive oxygen substances production and hearing deterioration in the rat model. Methods: 25 streptozotocin induced diabetic rats were divided into three groups: control, high blood glucose, and diabetes mellitus. Brainstem auditory evoked potential and distortion product otoacoustic emission were recorded, and thiobarbituric acid reactive substances levels were measured in the brainstem tissue. Results: At 8 kHz, the latencies of I, II, III, IV, and V brainstem auditory evoked potential waves in high blood glucose and diabetes mellitus groups were elongated, at 16 kHz, only these wave latencies of the diabetes mellitus group were prolonged compared with the control group. A significant decrease was also found in distortion product otoacoustic emission amplitudes at 4, 6, 8, and 10 kHz in the high blood glucose and diabetes mellitus groups compared to the control group. There was a significant increase in thiobarbituric acid reactive substances values due to the increase in blood glucose levels in the high blood glucose and diabetes mellitus groups compared to the control group. Conclusion: These results suggested that high blood glucose levels may cause hearing impairment not only in the diabetic state but also in the period of hyperglycemia before the onset of manifest diabetes mellitus and reactive oxygen substances may play an important role in the pathophysiology of diabetes mellitus. We suggest that regulating high glucose levels even before the onset of manifest diabetes mellitus may prevent hazardous effects on hearing function. Level of evidence: Level 3.

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OBJECTIVE: Previous studies have shown that hearing function is also vulnerable to the effects of diabetes mellitus which can be shown by brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of brainstem auditory evoked potential and distortion product otoacoustic emission in hyperglycemia and whether there is a relationship between reactive oxygen substances production and hearing deterioration in the rat model. METHODS: 25 streptozotocin induced diabetic rats were divided into three groups: control, high blood glucose, and diabetes mellitus. Brainstem auditory evoked potential and distortion product otoacoustic emission were recorded, and thiobarbituric acid reactive substances levels were measured in the brainstem tissue. RESULTS: At 8 kHz, the latencies of I, II, III, IV, and V brainstem auditory evoked potential waves in high blood glucose and diabetes mellitus groups were elongated, at 16 kHz, only these wave latencies of the diabetes mellitus group were prolonged compared with the control group. A significant decrease was also found in distortion product otoacoustic emission amplitudes at 4, 6, 8, and 10 kHz in the high blood glucose and diabetes mellitus groups compared to the control group. There was a significant increase in thiobarbituric acid reactive substances values due to the increase in blood glucose levels in the high blood glucose and diabetes mellitus groups compared to the control group. CONCLUSION: These results suggested that high blood glucose levels may cause hearing impairment not only in the diabetic state but also in the period of hyperglycemia before the onset of manifest diabetes mellitus and reactive oxygen substances may play an important role in the pathophysiology of diabetes mellitus. We suggest that regulating high glucose levels even before the onset of manifest diabetes mellitus may prevent hazardous effects on hearing function. LEVEL OF EVIDENCE: Level 3.

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Abstract Introduction: It is difficult to evaluate the effect of drugs clinically used for idiopathic sudden sensorineural hearing loss, mainly because its underlying mechanism remains unknown. Objective: This study assessed the efficacy of hyperbaric oxygen therapy or ozone therapy in the treatment of idiopathic sudden sensorineural hearing loss, when either therapy was included with steroid treatment. Methods: A retrospective analysis examined 106 patients with idiopathic sudden sensorineural hearing loss seen between January 2010 and June 2012. Those with an identified etiology were excluded. The patients were divided into three treatment groups: oral steroid only (n = 65), oral steroid + hyperbaric oxygen (n = 26), and oral steroid + ozone (n = 17). Treatment success was assessed using Siegel criteria and mean gains using pre- and post-treatment audiograms. Results: The highest response rate to treatment was observed in the oral steroid + ozone therapy group (82.4%), followed by the oral steroid + hyperbaric oxygen (61.5%), and oral steroid groups (50.8%). There were no significant differences in the response to treatment between the oral steroid and oral steroid + hyperbaric oxygen groups (p < 0.355). The oral steroid + ozone group showed a significantly higher response rate to treatment than the oral steroid group (p = 0.019). There were no significant differences between the oral steroid + hyperbaric oxygen and oral steroid + ozone groups (p = 0.146). Conclusion: The efficiency of steroid treatment in patients with severe hearing loss was low. It was statistically ascertained that adding hyperbaric oxygen or ozone therapy to the treatment contributed significantly to treatment success.

Resumo Introdução: É difícil avaliar o efeito dos fármacos clinicamente usados na surdez súbita idiopática, principalmente porque o seu mecanismo subjacente se mantém desconhecido. Objetivo: Avaliar a eficácia da oxigenoterapia hiperbárica ou ozonioterapia no tratamento de surdez súbita, quando uma ou outra terapia é incluída no tratamento com esteroides. Método: Uma análise retrospectiva examinou 106 pacientes com surdez súbita atendidos entre janeiro de 2010 e junho de 2012. Aqueles com uma etiologia identificada foram excluídos. Os pacientes foram divididos em três grupos de tratamento: apenas esteroide oral (n = 65), esteroide por via oral + oxigenoterapia hiperbárica (n = 26) e esteroides por via oral + ozônio (n = 17). O sucesso do tratamento foi avaliado com critérios de Siegel e os ganhos médios com audiogramas pré e pós-tratamento. Resultados: A taxa de resposta mais elevada para o tratamento foi observada no grupo de esteroide + ozonioterapia (82,4%), seguida por grupos de esteroide oral + oxigenoterapia hiperbárica (61,5%) e esteroide oral (50,8%). Não houve diferenças significantes na resposta ao tratamento entre os grupos de esteroide oral e esteroides + oxigenoterapia hiperbárica (p < 0,355). O grupo de esteroide oral + ozônio apresentou uma taxa de resposta significantemente mais elevada ao tratamento do que o grupo de esteroide oral (p = 0,019). Não houve diferenças significantes entre os grupos de esteroide oral + oxigenoterapia hiperbárica e esteroide oral + ozônio (p = 0,146). Conclusão: A eficiência do tratamento com esteroides em pacientes com perda auditiva grave foi baixa. Verificou-se estatisticamente que a adição de oxigenoterapia hiperbárica ou ozonioterapia ao tratamento contribuiu significantemente para o sucesso do tratamento.

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INTRODUCTION: It is difficult to evaluate the effect of drugs clinically used for idiopathic sudden sensorineural hearing loss, mainly because its underlying mechanism remains unknown. OBJECTIVE: This study assessed the efficacy of hyperbaric oxygen therapy or ozone therapy in the treatment of idiopathic sudden sensorineural hearing loss, when either therapy was included with steroid treatment. METHODS: A retrospective analysis examined 106 patients with idiopathic sudden sensorineural hearing loss seen between January 2010 and June 2012. Those with an identified etiology were excluded. The patients were divided into three treatment groups: oral steroid only (n=65), oral steroid+hyperbaric oxygen (n=26), and oral steroid+ozone (n=17). Treatment success was assessed using Siegel criteria and mean gains using pre- and post-treatment audiograms. RESULTS: The highest response rate to treatment was observed in the oral steroid+ozone therapy group (82.4%), followed by the oral steroid+hyperbaric oxygen (61.5%), and oral steroid groups (50.8%). There were no significant differences in the response to treatment between the oral steroid and oral steroid+hyperbaric oxygen groups (p<0.355). The oral steroid+ozone group showed a significantly higher response rate to treatment than the oral steroid group (p=0.019). There were no significant differences between the oral steroid+hyperbaric oxygen and oral steroid+ozone groups (p=0.146). CONCLUSION: The efficiency of steroid treatment in patients with severe hearing loss was low. It was statistically ascertained that adding hyperbaric oxygen or ozone therapy to the treatment contributed significantly to treatment success.

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