Ototoxic Hearing Loss Research Articles

A retrospective audit of audiology encounters in patients undergoing Cisplatin treatment at a large Australian tertiary cancer care centre.

To identify the number and timing of audiology encounters for adult oncology patients in a tertiary care setting in Australia. A retrospective case review was completed for 149 patients who received Cisplatin chemotherapy (CT) at a large, publicly funded tertiary hospital in Brisbane, Queensland, Australia between 1st January and 31st December 2019. Patient data was extracted from the Queensland Oncology Repository (QOR) provided by Cancer Alliance Queensland (CAQ). The number of audiology encounters was low overall with a median of 0 and interquartile range (IQR) of 0-1. Of the entire patient cohort, there was a mean of 1.2 encounters with 56% of patients not engaging with audiology. Where audiology did occur, encounters were most likely before or early in the CT treatment period. This study has demonstrated engagement with audiology services for patients undergoing CT treatment was limited with the few audiology engagements occurring before or early in the CT treatment period. Further research is needed to identify the barriers and facilitators to accessing audiological ototoxic monitoring (OtoM) during chemotherapy treatment in hospitals in Australia. Early identification of ototoxic hearing loss offers the opportunity to minimise further exposure to the ototoxic agent, minimise functional and communication impacts for the patient and provide early opportunity for discussion, education and counselling with patients, carers and their treating team. This, in turn, is expected to improve health related quality of life.

Practice of Monitoring Cisplatin-Induced Ototoxicity by Audiology, ENT, and Oncology Specialists: A Survey-Based Study in a Single Italian Medical Center.

Ototoxic drugs can result in hearing loss and tinnitus. Early detection of the ototoxic process can help minimize or prevent these consequences. The American Speech-Language-Hearing Association has provided guidelines for monitoring ototoxicity, whereas Italy has not yet implemented a national monitoring protocol. This study aims to assess the current state of ototoxicity monitoring in patients receiving cisplatin therapy. A self-administered survey has been used to gather information from oncologists, audiologists, and ENT specialists. The research was conducted at Santa Maria della Misericordia hospital in Perugia. Two questionnaires were administered, one to ENT/audiology specialists and another to oncology specialists. Both questionnaires were used to collect information on awareness of chemotherapy-induced ototoxicity. A comprehensive understanding of cisplatin-induced ototoxicity has been widely established (100%). The most commonly reported audiological symptoms by patients were hearing loss (100%) and tinnitus (87.5%). The majority of ENT and audiologists (93.8%) and oncologists (92.9%) expressed the need for a specific ototoxic monitoring program. However, they noted the absence of a well-defined ototoxicity monitoring protocol. A well-established and efficient ototoxic monitoring system facilitates early detection of ototoxic hearing loss and subsequent rehabilitation of inevitable hearing impairment.

Mitochondrial redox system: A key target of antioxidant therapy to prevent acquired sensorineural hearing loss.

Noise (noise-induced hearing loss), and ototoxic drugs (drug-induced ototoxicity), and aging (age-related hearing loss) are the major environmental factors that lead to acquired sensorineural hearing loss. So far, there have been numerous efforts to develop protective or therapeutic agents for acquired hearing loss by investigating the pathological mechanisms of each types of hearing loss, especially in cochlear hair cells and auditory nerves. Although there is still a lack of information on the underlying mechanisms of redox homeostasis and molecular redox networks in hair cells, an imbalance in mitochondrial reactive oxygen species (ROS) levels that enhance oxidative stress has been suggested as a key pathological factor eventually causing acquired sensorineural hearing loss. Thus, various types of antioxidants have been investigated for their abilities to support auditory cells in maintenance of the hearing function against ototoxic stimuli. In this review, we will discuss the scientific possibility of developing drugs that target particular key elements of the mitochondrial redox network in prevention or treatment of noise- and ototoxic drug-induced hearing loss.

Aural Diversity: noise control and a sustainable future.

The unquestioned assumption of a "normal" pair of standard healthy ears underpins most sound-related disciplines, from acoustics to engineering, from music to sound studies, from medicine to hearing science. Yet, the reality is that everybody hears differently. Our ears are uniquely shaped. We all experience temporary changes in hearing, such as during a cold. Everybody goes through presbyacusis (age-related hearing loss) at varying rates after the teenage years. More specific aural divergences are the result of an array of hearing differences or impairments which affect roughly one sixth of the world's population (Lancet, 2013). These include noise-related, genetic, ototoxic, traumatic, and disorder-based hearing loss, some of which may cause full or partial deafness. Moreover, "loss" is not the only form of difference: auditory perceptual disorders such as tinnitus, hyperacusis and misophonia involve an increased sensitivity to sound. This paper presents findings from the AHRC-funded Aural Diversity Network, which explores the consequences of these differences for noise-related engineering and many other fields. How may we ensure a sustainable future that acknowledges aural diversity?

Prevention and management of hearing loss in patients receiving ototoxic medications.

Following the efforts of patient advocates, the World Health Organization published updated guidelines for management of multidrug-resistant tuberculosis in 2018 that advised against the routine use of ototoxic second-line injectable drugs (amikacin, capreomycin and kanamycin). Although hearing loss is no longer considered an unavoidable harm for patients with multidrug-resistant tuberculosis, ototoxic medications continue to be used for several infectious and oncological disorders around the world. These drugs contribute to more than a half a million cases of hearing loss worldwide annually. Currently, there are no international standards for preventing and managing hearing loss associated with ototoxic medications. We present recent data on the prevention and management of hearing loss related to these drugs and highlight the variability in care across settings. More importantly, we aim to provide an evidence-based framework for evaluating, screening and preventing ototoxicity. Finally, we identify avenues for future research so that patients no longer have to choose between hearing loss and a disease cure. There remain significant gaps in our understanding about optimal screening and treatment of ototoxic hearing loss. Here we aim to inspire future international guidelines to address gaps in ototoxicity care and establish research agendas for eliminating ototoxic medications.

Intratympanic Administration of Dieckol Prevents Ototoxic Hearing Loss.

Objective. Systemic administration of dieckol reportedly ameliorates acute hearing loss. In this study, dieckol was delivered to the inner ear by the intratympanic route. The functional and anatomic effects and safety of dieckol were assessed using the rat ototoxicity model. Materials and methods. Dieckol in a high-molecular-weight hyaluronic acid vehicle (dieckol+vehicle group) or vehicle without dieckol (vehicle-only group) were randomly delivered into 12 ears intratympanically. Ototoxic hearing loss was induced by intravenous administration of cisplatin, gentamicin, and furosemide. The hearing threshold and surviving outer hair cells (OHC) were enumerated. Biocompatibility was assessed by serial endoscopy of the tympanic membrane (TM), and the histology of the TM and the base of bulla (BB) mucosa was quantitatively assessed. Results. The hearing threshold was significantly better (difference of 20 dB SPL) in the dieckol+vehicle group than in the vehicle-only group. The number of surviving OHCs was significantly greater in the dieckol+vehicle group than in the vehicle-only group. There were no signs of inflammation or infection in the ear. The thickness of the TM and the BB mucosa did not differ between the two groups. Conclusion. Intratympanic local delivery of dieckol may be a safe and effective method to prevent ototoxic hearing loss.

Cichoric Acid May Play a Role in Protecting Hair Cells from Ototoxic Drugs.

Ototoxic hearing loss due to antibiotic medication including aminoglycosides and excess free radical production causes irreversible hair cell injury. Cichoric acid, a naturally occurring phenolic acid, has recently been found to exert anti-oxidative and anti-inflammatory properties through its free radical scavenging capacity. The present study aimed to investigate the protective effects of cichoric acid against neomycin-induced ototoxicity using transgenic zebrafish (pvalb3b: TagGFP). Our results indicated that cichoric acid in concentrations up to 5 μM did not affect zebrafish viability during the 2 h treatment period. Therefore, the otoprotective concentration of cichoric acid was identified as 5 μM under 2 h treatment by counting viable hair cells within the neuromasts of the anterior- and posterior-lateral lines in the study. Pretreatment of transgenic zebrafish with 5 μM of cichoric acid for 2 h significantly protected against neomycin-induced hair cell death. Protection mediated by cichoric acid was, however, lost over time. A terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and FM4-64 staining, respectively, provided in situ evidence that cichoric acid ameliorated apoptotic signals and mechanotransduction machinery impairment caused by neomycin. A fish locomotor test (distance move, velocity, and rotation frequency) assessing behavioral alteration after ototoxic damage revealed rescue due to cichoric acid pretreatment before neomycin exposure. These findings suggest that cichoric acid in 5 μM under 2 h treatment has antioxidant effects and can attenuate neomycin-induced hair cell death in neuromasts. Although cichoric acid offered otoprotection, there is only a small difference between pharmacological and toxic concentrations, and hence cichoric acid can be considered a rather prototypical compound for the development of safer otoprotective compounds.

Auditory assessment of neonates at high risk of hearing impairment admitted to the intensive care unit

Background: Permanent hearing loss is a common neonatal health problem which leads to deleterious effects on language, speech development and academic outcome. Its prevalence is much higher in newborns that need neonatal intensive care admission. Methods: This is a cross-sectional study included 314 neonates admitted to neonatal intensive care unit. The inclusion criteria included neonates with risk factors of hearing loss. They were all evaluated by Transient Evoked Otoacoustic Emissions (TEOAE). Automated auditory brainstem response (AABR) was done at 3 months of age for those who failed TEOAE screening. Results: Out of 314 neonates, 4.5% were diagnosed by permanent hearing loss. No statistical significance was detected between hearing loss and gender (P = 0.61), prematurity (P = 0.529) and birth weight (P = 0.076). The most common risk factor detected was ototoxic drug intake, with aminoglycosides being the most frequent. There was a significant P value between ototoxic medications and hearing loss (P = 0.018). The highest percentage of cases with hearing loss was detected among neonates who received both aminoglycosides and vancomycin. Conclusion: The prevalence of permanent hearing loss among admitted neonates at risk of hearing loss are high.

Curcumin-Encapsulated Chitosan-Coated Nanoformulation as an Improved Otoprotective Strategy for Ototoxic Hearing Loss.

Overexpression of apoptotic factors in the inner ear is generally proven to induce ototoxicity. This has aroused research interest in various antiapoptotic drugs, the most representative of which is curcumin (CUR). In this study, two nanoformulations of CUR were developed with sustained-release behavior to improve their protective effects against ototoxic hearing loss (HL), which were the nanoparticles of CUR-loaded poly(lactic acid-glycolic acid) (CUR-PLGA NPs) and CUR-loaded chitosan-coated PLGA NPs (CUR-CS/PLGA NPs). The obtained results revealed that both CUR-NPs provided otoprotection in vitro and in vivo, and their effective doses in guinea pigs were much less than that of dexamethasone, which was clinically used to treat HL. Moreover, relative to CUR and CUR-PLGA NPs, CUR-CS/PLGA NPs exhibited the highest accumulation in HEI-OC1 cells and guinea pigs' cochlea. In pharmacodynamic experiments, the optimal administration timing was investigated, and CUR-CS/PLGA NPs showed sustained efficacy and the best hearing improvement at all tested sound frequencies. Lastly, the protective effect of CUR nanoformulations was further validated via inhibition of Caspase-3 and Bax activation, thereby reducing the concentration of reactive oxygen species and protecting mitochondrial integrity in hair cells. Collectively, CUR-CS/PLGA NPs demonstrated potent and lasting effects against ototoxic HL, making our novel formulation a promising candidate for the alleviation of sensorineural HL.

Protective Effects of Vitamin C against Neomycin-Induced Apoptosis in HEI-OC1 Auditory Cell.

Ototoxic hearing loss results from hair cell death via reactive oxygen species (ROS) overproduction and consequent apoptosis. We investigated the effects of vitamin C (VC) on neomycin-induced HEI-OC1 cell damage, as well as the mechanism of inhibition. HEI-OC1 cells were treated with neomycin or with vitamin C (VC). The results indicated that VC had a protective effect on neomycin-induced HEI-OC1 cell death. Mechanistically, VC decreased neomycin-induced ROS generation, suppressed cell death, and increased cell viability. VC inhibited neomycin-induced apoptosis, ameliorated neomycin reduced antiapoptotic Bcl-2 expression, and suppressed neomycin increased expression of proapoptotic Bax, caspase-3 cleavage and caspase-8. TUNEL labeling demonstrated that VC blocked neomycin-induced apoptosis. Further study revealed that the effect of VC on neomycin-induced hair cell death was through interference with JNK activation and p38 phosphorylation. These results indicate that VC via suppressed ROS generation, which inhibited cell death by counteracting apoptotic signaling induced by neomycin in cells. Hence, VC is a potential candidate for protection agent against neomycin-induced HEI-OC1 cell ototoxicity.

Ototoxic hearing loss in the multi-drug resistant tuberculosis era

Objective: To determine the prevalence of hearing loss in tuberculosis patients using Ototoxic medicines and association with demographic and clinical variables.
 Methods: This cross sectional study recruited a sample of n= 65 diagnosed cases of tuberculosis on ototoxic chemotherapy, of both genders, aged 12 to 70 years, using non-probability convenience sampling. Study was conducted at Audiology Department of Civil Hospital Bahawalpur, over a period of 6 months from 1st May, 2019 to 31st October 2019. Screening was performed using medical history sheet, otoscopy and hearing assessment. Data collected was analyzed using SPSS- Version 21.0.
 Results: Results revealed a gender proportion of 43 (66.2%) males and 22(33.8%) females with mean age of 35.87+9.35 years. The prevalence of hearing loss was 23.1% (n=15) with mild hearing loss in 73.33% cases and moderate hearing loss 26.67%. Hearing loss was associated with drug, its duration and associated symptoms of tinnitus and vertigo with p=0.000.
 Discussion: It is concluded that hearing loss is quite prevalent (23.1%) with multidrug resistant tuberculosis treatment in this region and is significantly associated with the drug used, its duration and associated symptoms.

A longitudinal community-based ototoxicity monitoring programme and treatment effects for drug-resistant tuberculosis treatment, Western Cape.

BackgroundSouth Africa has a high burden of drug-resistant tuberculosis (DRTB) and until recently, ototoxic aminoglycosides were predominant in treatment regimens. Community-based ototoxicity monitoring programmes (OMPs) have been implemented for early detection of hearing loss and increased patient access.ObjectivesA longitudinal study was conducted to describe the service delivery characteristics of a community-based OMP for DRTB patients facilitated by CHWs as well as observed ototoxic hearing loss in this population.MethodA descriptive retrospective record review of longitudinal ototoxicity monitoring of 194 DRTB patients undergoing treatment at community-based clinics in the city of Cape Town between 2013 and 2017.ResultsFollow-up rates between consecutive monitoring assessments reached as high as 80.6% for patients assessed by CHWs. Few patients (14.2% – 32.6%) were assessed with the regularity (≥ 6 assessments) and frequency required for effective ototoxicity monitoring, with assessments conducted, on average, every 53.4–64.3 days. Following DRTB treatment, 51.5% of patients presented with a significant ototoxic shift meeting one or more of the American Speech-Language-Hearing Association (ASHA) criteria. Deterioration in hearing thresholds was bilateral and most pronounced at high frequencies (4 kHz – 8 kHz). The presence of pre-existing hearing loss, human immunodeficiency virus co-infection and a history of noise exposure were significant predictors of ototoxicity in patients.ConclusionDRTB treatment with kanamycin resulted in significant deterioration of hearing longitudinally, predominantly at high frequencies. With ongoing training and supportive supervision, CHWs can facilitate community-based ototoxicity monitoring of DRTB patients. Current protocols and guidelines may require reassessment for appropriate community-based ototoxicity monitoring.

Dual Viscosity Mixture Vehicle for Intratympanic Dexamethasone Delivery Can Block Ototoxic Hearing Loss.

Clinically there is no effective method to prevent drug induced hearing loss in patients undergoing chemotherapy and anti-tuberculosis therapy. In this study, we developed an intratympanic (IT) local drug delivery vehicle featuring hyaluronic acid-based dual viscosity mixture encapsulation of dexamethasone (D), named dual-vehicle + D, and assessed its protective effect in ototoxic hearing loss. We assessed the residence time, biocompatibility, and treatment outcome of the novel vehicle compared with the current standard of care vehicle (saline) and control conditions. The hearing threshold and hair cell count were significantly better in the dual-vehicle + D group compared to the other two groups. The final hearing benefit in the dual-vehicle group was approximately 25–35 dB, which is significant from a clinical point of view. Morphologic evaluation of the cochlear hair cells also supported this finding. Due to the high viscosity and adhesive property of the vehicle, the residence time of the vehicle was 49 days in the dual-vehicle + D group, whereas it was less than 24 h in the saline + D group. There was no sign of inflammation or infection in all the animals. From this study we were able to confirm that dual viscosity mixture vehicle for IT D delivery can effectively block ototoxic hearing loss.

Protective effect of MSC-derived exosomes against cisplatin-induced apoptosis via heat shock protein 70 in auditory explant model

Therapeutics based on stem cell technology, including stem cell-derived exosomes, have emerged in recent years for the treatment of what were otherwise considered incurable diseases. In this study, we evaluated the efficacy of human MSC-derived exosomes for protection against cisplatin induced ototoxic hearing loss. Incubation of cochlear explants with MSC-derived exosomes prior to addition of cisplatin induced a reduction in cisplatin-induced drug toxicity in auditory hair cells but not when the exosomes were introduced simultaneously with or after cisplatin. The delivery of MSC-derived exosomes to cochlear explants was confirmed by the increasing protein levels of the exosome markers CD63 and HSP70 to reduce apoptosis. These results were consistent with those from a model in which MSC-derived exosomes protect auditory hair cells from cisplatin-induced drug toxicity in an ex vivo cochlear explant model and support future studies into the therapeutic benefits of stem cell-derived exosomes in clinical applications.

Feasibility and first results of a prospective cohort study to investigate cisplatin-associated ototoxicity amongst cancer patients in South Africa

BackgroundCervical cancer, one of the most common cancers affecting females in South Africa, commonly requires a cisplatin-based-treatment regimen, which has been associated with ototoxic side effects. However, cisplatin-associated ototoxicity is largely under-reported in South Africa, despite its impact of hearing loss having serious overt ramifications on the quality of life of these patients. Hence, a prospective cohort study was undertaken to assess the audiological changes in female cervical cancer patients receiving cisplatin therapy.ObjectiveTo present details of the feasibility study and initial results on hearing patterns in cervical cancer patients receiving cisplatin chemotherapy. .MethodsFifty cervical cancer patients commencing with cisplatin chemotherapy underwent audiological assessments at a hospital in South Africa at various time intervals. Assessments included case history, otoscopic examination, immittance audiometry, pure tone audiometry (including high-frequency audiometry), speech audiometry, and distortion product otoacoustic emission testing. Data analysis involved the use of descriptive statistics and the Cochran-Armitage trend test for a linear trend in proportions.ResultsFifty participants, aged between 32 and 79 years (Mean: 53 years; SD = 11.00), were recruited. Clinical findings revealed an incidence of 100% ototoxic hearing loss at the one-month post-treatment, i.e., 98% after three cycles of cisplatin and 2% at one-month post-chemotherapy. Sensorineural hearing loss and high-frequency tinnitus were most common. Deterioration in hearing thresholds was more evident in the extended high-frequency range, with the number of “no-responses,” from 11,200 Hz to 20,000 Hz, increasing with each successive audiological evaluation. This study further indicated that recruitment and follow-up of study participants within a limited resource setting are possible. However, cognizance must be given to a multidisciplinary approach and constant engagement with participants through regular contact either telephonically or via a short-message-system.ConclusionExposure to cisplatin treatment contributed to hearing loss in females with cervical cancer, highlighting the need for ototoxicity monitoring during chemotherapy treatments. Furthermore, the results indicate that it is possible to conduct prospective cohort studies, using a multidisciplinary approach in limited-resource environments with appropriate planning and training strategies, as this study was able to achieve its aim successfully.

Deletion of Clusterin Protects Cochlear Hair Cells against Hair Cell Aging and Ototoxicity.

Hearing loss is a debilitating disease that affects 10% of adults worldwide. Most sensorineural hearing loss is caused by the loss of mechanosensitive hair cells in the cochlea, often due to aging, noise, and ototoxic drugs. The identification of genes that can be targeted to slow aging and reduce the vulnerability of hair cells to insults is critical for the prevention of sensorineural hearing loss. Our previous cell-specific transcriptome analysis of adult cochlear hair cells and supporting cells showed that Clu, encoding a secreted chaperone that is involved in several basic biological events, such as cell death, tumor progression, and neurodegenerative disorders, is expressed in hair cells and supporting cells. We generated Clu-null mice (C57BL/6) to investigate its role in the organ of Corti, the sensory epithelium responsible for hearing in the mammalian cochlea. We showed that the deletion of Clu did not affect the development of hair cells and supporting cells; hair cells and supporting cells appeared normal at 1 month of age. Auditory function tests showed that Clu-null mice had hearing thresholds comparable to those of wild-type littermates before 3 months of age. Interestingly, Clu-null mice displayed less hair cell and hearing loss compared to their wildtype littermates after 3 months. Furthermore, the deletion of Clu is protected against aminoglycoside-induced hair cell loss in both in vivo and in vitro models. Our findings suggested that the inhibition of Clu expression could represent a potential therapeutic strategy for the alleviation of age-related and ototoxic drug-induced hearing loss.

Roles of Bak and Sirt3 in Paraquat-Induced Cochlear Hair Cell Damage.

Paraquat, a superoxide generator, can damage the cochlea causing an ototoxic hearing loss. The purpose of the study was to determine if deletion of Bak, a pro-apoptotic gene, would reduce paraquat ototoxicity or if deletion of Sirt3, which delays age-related hearing loss under caloric restriction, would increase paraquat ototoxicity. We tested these two hypotheses by treating postnatal day 3 cochlear cultures from Bak±, Bak-/-, Sirt3±, Sirt3-/-, and WT mice with paraquat and compared the results to a standard rat model of paraquat ototoxicity. Paraquat damaged nerve fibers and dose-dependently destroyed rat outer hair cells (OHCs) and inner hair cells (IHCs). Rat hair cell loss began in the base of the cochlea with a 10μM dose and as the dose increased from 50 to 500μM, the hair cell loss increased near the base of the cochlea and spread toward the apex of the cochlea. Rat OHC losses were consistently greater than IHC losses. Unexpectedly, in all mouse genotypes, paraquat-induced hair cell lesions were maximal near the apex of the cochlea and minimal near the base. This unusual damage gradient is opposite to that seen in paraquat-treated rats and in mice and rats treated with other ototoxic drugs. However, paraquat always induced greater OHC loss than IHC loss in all mouse strains. Contrary to our hypothesis, Bak deficient mice were more vulnerable to paraquat ototoxicity than WT mice (Bak-/- > Bak± > WT), suggesting that Bak plays a protective role against hair cell stress. Also, contrary to expectation, Sirt3-deficient mice did not differ significantly from WT mice, possibly due to the fact that Sirt3 was not experimentally upregulated in Sirt3-expressing mice prior to paraquat treatment. Our results show for the first time a gradient of ototoxic damage in mice that is greater in the apex than the base of the cochlea.

Baseline audiological profiling of South African females with cervical cancer: an important attribute for assessing cisplatin-associated ototoxicity

BackgroundCisplatin is a popular antineoplastic agent used to treat cervical cancer in women from low and middle-income countries. Cisplatin treatment is associated with ototoxicity, often resulting in hearing loss. In light of this, it is crucial to conduct baseline audiological assessments prior to treatment initiation in order to evaluate the extent of cisplatin-associated-ototoxicity. Additionally, the identification of inherent risk factors and hearing patterns in specific patient cohorts is needed, especially in South Africa, a middle-income country characterized by the quadruple burden of disease (Human Immunodeficiency Virus (HIV), Tuberculosis (TB), Diabetes and Hypertension).MethodsThis study aimed to describe a profile of risk factors and hearing in a cohort of females with cervical cancer before cisplatin treatment commenced. A descriptive study design that included 82 cervical cancer patients, who underwent audiological evaluation prescribed for ototoxicity monitoring was conducted.ResultsAll participants (n = 82) presented with risk factors (diabetes, hypertension, HIV, and antiretroviral therapy) for cisplatin ototoxicity and/or pre-existing sensorineural hearing loss. High-frequency tinnitus was the most common otological symptom experienced by 25 (31%) participants. Fifty-nine (72%) participants presented with normal hearing, twenty-two (27%) with a sensorineural hearing loss, and 36% were diagnosed with mild hearing loss. Abnormal Distortion Product Otoacoustic Emissions (DPOAE) findings were obtained bilaterally in two participants (2.4%), in the right ear only of another two (2.4%) participants and the left ear of three participants (3.7%). Most participants (94%) had excellent word recognition scores, demonstrating an excellent ability to recognize words within normal conversational levels under optimal listening conditions. Age was significantly associated with hearing loss at all thresholds. Among the co-morbidities, an HIV positive status significantly triggered hearing loss, especially at higher frequencies.ConclusionThis study demonstrated that South African females with cervical cancer present with various co-morbidities, which may predispose them to develop cisplatin-associated -ototoxic hearing loss. Identification of these co-morbidities and hearing loss is essential for the accurate monitoring of cisplatin toxicities. Appropriate management of these patients is pivotal to reduce the adverse effects that hearing impairment can have on an individual’s quality of life and to facilitate informed decision-making regarding the commencement of cisplatin chemotherapy.

The Ototoxicity of Antimalarial Drugs-A State of the Art Review.

This review summarizes current knowledge about the occurrence of hearing and balance disorders after antimalarial drugs treatment. It also examines the clinical applications of antimalarials, their mechanisms behind this ototoxicity and how it can be monitored. It includes studies with larger numbers of patients and those in which auditory function was assessed using audiological tests. Some antimalarials have been repurposed for other conditions like autoimmune disorders, rheumatic diseases, some viral diseases and cancers. While old antimalarial drugs, such as quinoline derivatives, are known to demonstrate ototoxicity, a number of new synthetic antimalarial agents particularly artemisinin derivatives, demonstrate unknown ototoxicity. Adverse audiovestibular effects vary depending on the medication itself, its dose and route of administration, as well as the drug combination, treated disease and individual predispositions of the patient. Dizziness was commonly reported, while vestibular symptoms, hearing loss and tinnitus were observed much less frequently, and most of these symptoms were reversible. As early identification of ototoxic hearing loss is critical to introducing possible alternative treatments with less ototoxic medications, therefore monitoring systems of those drugs ototoxic side effects are much needed.

Ototoxicity: A review of South African studies

BackgroundOtotoxicity is damage to cells in the inner ear after administering a toxic drug, with a resultant hearing loss. Drugs used to treat illnesses such as cancer, tuberculosis, human immuno-deficiency virus (HIV) and infections are potentially ototoxic. South Africa has one of the highest rates of HIV and tuberculosis, and thus a potentially greater degree of the population is being affected by hearing loss from the medications used to treat these illnesses.MethodsTo determine the current status of research in ototoxicity, a systematic literature review was carried out to determine the focus areas of South African studies for the period 1989–2019. From the database search engines used (Science Direct, Ebscohost and Proquest), a total of 33 relevant articles were identified, including the themes of pharmacology, audiology and knowledge.ResultsStudies were conducted in the three most resourced provinces in South Africa. Findings indicate that there is a need for educating doctors regarding ototoxicity and a delineation of the role of the audiologist in monitoring and management of ototoxic hearing loss. There is a resultant need for audiology training on the pharmacology of ototoxic medication, otoprotective strategies and adherence to recommended guidelines. This has implications for university audiology training programmes and curriculum planning. The need for development of South Africa-specific audiology guidelines was highlighted.ConclusionWhilst it is noted that there is a lack of resources for effective implementation of ototoxicity-monitoring protocols, it is also noted that there are measures and otoprotective strategies that can be put in place without additional resources.