Reversible bilateral ototoxicity in a patient with chronic hepatitis B during peginterferon alpha-2a treatment

Gözdaş, Hasan Tahsin; Karabay, Oğuz

doi:10.4103/0253-7613.150377

Cited by 4 publications

(4 citation statements)

References 7 publications

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“…Third, a population-based study cannot clarify the real mechanism underlying the association between HBV/HCV infection and SSNHL because extracting cochlear tissue pathogens or detecting cochlear injury through imaging is very difficult [7, 8]. In addition, patients who developed SSNHL due an ototoxic effect after antiviral drug administration for HVB/HCV infection (which has been reported in some studies) could not be excluded [10, 11]. However, a case–control study revealed pegylated interferon plus ribavirin therapy does not have any impact on the hearing thresholds of patients with HCV [29].…”

Section: Discussionmentioning

confidence: 99%

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Increased risk of sudden sensorineural hearing loss in patients with hepatitis virus infection

et al. 2017

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The etiology of sudden sensorineural hearing loss (SSNHL) remains unclear. Possible causes of SSNHL include vascular diseases, viral infection, and autoimmune disorders. Therefore, we investigated whether hepatitis virus infection is correlated with the risk of SSNHL. Using data from the Taiwan Longitudinal Health Insurance Database, we conducted a retrospective matched-cohort study to compare patients diagnosed with hepatitis B or C virus (HBV/HCV) infections from January 1, 2000, to December 31, 2010, (N = 170,942) with frequency-matched controls (N = 512,826) at a ratio of 1:3 by sex, age, and index year. We followed each patient until the end of 2010 and evaluated the incidence of SSNHL. At the end of the follow-up period, 647 (0.38%, 647/170,942) patients developed SSNHL in the HBV/HCV group compared with 978 (0.19%, 978/512,826) in the control groups, with a statistical significance of P < 0.001 (using the log-rank test). The incidence rate ratio of SSNHL was 5.743-fold higher in the HBV/HCV group than in the control group (283.17 vs. 49.31 per 100,000 person-years, P < 0.001). The risk of SSNHL increased with HBV/HCV infection, and an adjusted hazard ratio of 5.103 (95% CI, 4.585–5.678) was determined using Cox proportional hazards regression. This study contributes to the awareness of the increased risk of SSNHL in HBV/HCV-infected populations. Our findings suggest that an underlying viral infection contributes to the development of SSNHL.

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Section: Discussionmentioning

confidence: 99%

“…Hepatitis virus infection has been correlated with SSNHL in only a small number of case reports [8–11]. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections have emerged as a global health problem, and as many as 350 million and 123 million individuals have been infected with HBV and HCV, respectively, worldwide [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Increased risk of sudden sensorineural hearing loss in patients with hepatitis virus infection

et al. 2017

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“…There is limited data on the ototoxic effects of ribavirin, and it is possible that IFN/ribavirin ototoxicity is due to non-pegylated IFNs alone rather than ribavirin. However, hearing loss caused by IFN therapy is usually reversible ( 61 ), whereas (PEG)-IFN/ribavirin therapy can cause permanent hearing loss ( 62 ), suggesting that ribavirin itself may be ototoxic, with a potentiating or synergistic effect where co-treatment with ribavirin exacerbates IFN ototoxicity.…”

Section: Candidate Covid-19 Pharmacotherapeutics With Known Ototoxicitymentioning

confidence: 99%

“…Recent clinical trials showed that IFN-α therapy significantly reduced viral shedding and levels of inflammatory biomarkers, whereas IFN-β therapy improved virologic clearance; both therapies led to improved recovery in patients with COVID-19 ( 68 , 69 ). Clinical studies have shown reversible hearing loss in patients receiving either IFN-α or IFN-β therapy ( 61 , 70 ) via an unknown mechanism, while co-treatment with IFN and other therapies, such as ribavirin can lead to permanent hearing loss ( 62 ). Elevated ABR thresholds were observed in albino Swiss mice after treatment with IFN-α2A, likely due to fibroblast cell toxicity in the spiral limbus ( 71 ).…”

Section: Candidate Covid-19 Pharmacotherapeutics With Known Ototoxicitymentioning

confidence: 99%

Detecting Novel Ototoxins and Potentiation of Ototoxicity by Disease Settings

Coffin

Boney²,

Hill

et al. 2021

Front. Neurol.

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Over 100 drugs and chemicals are associated with permanent hearing loss, tinnitus, and vestibular deficits, collectively known as ototoxicity. The ototoxic potential of drugs is rarely assessed in pre-clinical drug development or during clinical trials, so this debilitating side-effect is often discovered as patients begin to report hearing loss. Furthermore, drug-induced ototoxicity in adults, and particularly in elderly patients, may go unrecognized due to hearing loss from a variety of etiologies because of a lack of baseline assessments immediately prior to novel therapeutic treatment. During the current pandemic, there is an intense effort to identify new drugs or repurpose FDA-approved drugs to treat COVID-19. Several potential COVID-19 therapeutics are known ototoxins, including chloroquine (CQ) and lopinavir-ritonavir, demonstrating the necessity to identify ototoxic potential in existing and novel medicines. Furthermore, several factors are emerging as potentiators of ototoxicity, such as inflammation (a hallmark of COVID-19), genetic polymorphisms, and ototoxic synergy with co-therapeutics, increasing the necessity to evaluate a drug's potential to induce ototoxicity under varying conditions. Here, we review the potential of COVID-19 therapies to induce ototoxicity and factors that may compound their ototoxic effects. We then discuss two models for rapidly detecting the potential for ototoxicity: mammalian auditory cell lines and the larval zebrafish lateral line. These models offer considerable value for pre-clinical drug development, including development of COVID-19 therapies. Finally, we show the validity of in silico screening for ototoxic potential using a computational model that compares structural similarity of compounds of interest with a database of known ototoxins and non-ototoxins. Preclinical screening at in silico, in vitro, and in vivo levels can provide an earlier indication of the potential for ototoxicity and identify the subset of candidate therapeutics for treating COVID-19 that need to be monitored for ototoxicity as for other widely-used clinical therapeutics, like aminoglycosides and cisplatin.

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