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Children can suffer from hearing loss due to viral diseases like chicken pox, mumps and influenza. As hearing loss after viral infection is possible, measures should be taken to reduce the risk of infection. Allow your Audiologist to professionally evaluate the type and severity of your hearing loss.
However, if the infection causes fluid build in the ear due to a viral ear infection, then the hearing loss is not sensorineural.Sensorineural hearing loss is permanent in nature, and the only recourse the child or the adult would have is to wear a hearing aid or a cochlear implant if the loss is severe. In fact, according to health experts, cytomegalovirus infection is one of the most common causes of hearing loss among children. Researchers have also found that adults can lose their hearing due to an unidentified viral infection. It allows us to listen to sounds around us, and it also helps us to communicate with people.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractBackground. Hearing loss after viral infection can occur while the woman is pregnant, in childhood or even adulthood. If the source of the hearing loss is not known, then it is known as idiopathic hearing loss.
If any hearing impairment is noticed, it should immediately be brought to a doctor's attention. Therefore, hearing loss or suffering from a lower capacity of hearing can affect the way we mix, connect and behave with people.
Cisplatin is a well known platinum-based chemotherapeutic agent used for the treatment of various malignant tumours. Experimental, clinical studies and reviews published between 2004 and 2014 in the English medical literature concerning ototoxicity were selected using Medline, PubMed, and Google Scholar databases. Inclusion criteria were cisplatin-induced ototoxicity and therapy aimed at preventing or curing this disorder.
Molecular mechanisms and clinical, audiological, and histological markers of cisplatin-induced ototoxicity are described. Hyppolito, “Mechanisms of cisplatin ototoxicity: theoretical review,” Journal of Laryngology and Otology, vol.
Moreover, experimental and clinical strategies for prevention or treatment of hearing loss were also reviewed. Experimental studies demonstrate a wide range of otoprotective molecules and strategies efficient against cisplatin-induced hearing loss. Further research must be completed to bring future therapeutic options into clinical setting.1.
Introduction Cisplatin (cis-diamminedichloroplatinum II) is a well-known chemotherapeutic alkylating agent very effective in the treatment of various malignant tumors, especially squamous cell cancers of the head and neck regions, in both the pediatric and adult age groups [1]. Though synthesized already since 1845 by Peyrone owing to him its name of Peyrone’s salt, only in the late 1960s was it used clinically in oncologic therapy for head and neck, lung, bladder, cervical, ovarian, testicular, and gastrointestinal cancers, as well as malignant gliomas and metastatic cancers such as melanoma, mesothelioma, and those of the prostate and breast [2]. One of its major side effects is irreversible neurosensorial hearing loss which affects ears symmetrically: high frequencies in the first place followed by low, speech range frequencies in a dose related and cumulative fashion.
Rybak, “Cisplatin and aminoglycoside antibiotics: hearing loss and its prevention,” The Anatomical Record, vol.
Cisplatin-induced hearing loss is favoured either by preexisting afflictions like hypoalbuminemia, anaemia, renal failure, and noise-induced hearing loss or by risk factors like therapy with loop diuretics, aminoglycoside antibiotics, radiotherapy fields which includes the inner ear, extreme ages (very young or very old), duration and dose schedule of cisplatin infusion, and genetic factors. As subsequent multiple cisplatin regimens for the control of cancer may be necessary, side effects should be prevented or treated without reducing the efficacy of the antitumor mechanisms.2. Material and MethodsA review of the literature from 2004 to 2014 was performed, using the Medline, PubMed, and Google Scholar databases. The search terms included cisplatin-induced hearing loss, protective therapy for inner ear diseases, intratympanic therapy, systemic therapy, and gene therapy.
Mechanisms of Cisplatin OtotoxicityCisplatin inflicts injuries mainly to outer hair cells, progressing from the third to the first row and to some extent to inner hair cells of the organ of Corti in the basal turn of the cochlea followed by alterations in sensorial cells situated in the apex. Cisplatin also targets supporting cells, marginal cells of the stria vascularis, and the spiral ligament [4]. The vestibular organs are not spared, nor are spiral ganglion cells in experimental conditions [5]. The ensuing hearing loss may be very disabling to patients whose communication is already impaired due to cancers of the head and neck. Cochlear tissues fight the oxidative stress by means of antioxidant defence systems including glutathione, glutathione reductase, superoxide dismutase, and catalase [1]. Cisplatin-induced disturbance of potassium uptake and secretion in the stria vascularis has also been suggested, leading to impairment of the function of outer and inner hair cells in the organ of Corti, with alteration of the endocochlear potential and subsequent hearing loss [1]. Daniel, “Systemic dexamethasone for the prevention of cisplatin-induced ototoxicity,” European Archives of Oto-Rhino-Laryngology, vol. The former include pure tone (normal frequency and extended high-frequency range), speech and impedance audiometry, auditory brainstem responses, and Distortion Product Otoacoustic Emissions (DPOAEs) testing.
DPOAEs reflect early injuries to outer hair cells in the organ of Corti thereby allowing monitoring and early detection of cisplatin ototoxicity during cancer treatment [9, 10].
Since DPOAEs measurement is based on the integrity of outer hair cells which is affected by cisplatin therapy before elevation of auditory threshold as measured by pure tone audiometry, DPOAE testing is more sensitive than the latter for the detection of cisplatin-induced ototoxicity. Moreover, the results provided by DPOAEs, as an objective testing, are not influenced by the ability of the deteriorating cancerous patient to respond to the sound stimulus [9].
Light microscopy of cochlear samples obtained from animals receiving cisplatin shows loss of hair cells with collapse of the tunnel of Corti and Nuel’s space.
Akcay, “The role of thiamine pyrophosphate in prevention of cisplatin ototoxicity in an animal model,” The Scientific World Journal, vol. In cisplatin treated animals’ cochlea the scanning electron microscopy detects damage and loss of stereocilia of the hair cells as well as rupture of the cuticular plate [13]. The amount of free chemotherapeutic agent reaching targets in the cochlea is responsible for the ototoxic effect and consequent hearing loss. Reducing the total amount of cisplatin by limitation of the total dose per cycle, dose intensity and the cumulative dose would diminish the antitumor effect which is not desirable. Iseri, “Possible protective effect of sertraline against cisplatin-induced ototoxicity: an experimental study,” The Scientific World Journal, vol. If given systemically, they should be nontoxic, must attain efficient concentrations in the inner ear to protect labyrinthine tissues from cisplatin ototoxicity, and should not hamper the antitumor effect of cisplatin.
Higher concentrations of otoprotective molecules can be achieved by intratympanic administration. Experimental StudiesSeveral otoprotective molecules and strategies against cisplatin-induced ototoxicity have been tested in experimental animals.
Hinduja, “Is S-nitrosylation of cochlear proteins a critical factor in cisplatin-induced ototoxicity?” Antioxidants & Redox Signaling, vol.
Its main effect is tissue hyperoxygenation through plasma dissolved oxygen and was successfully tested in guinea pigs as a protective agent against cisplatin ototoxicity. Efficacy of otoprotection by hyperbaric oxygen therapy after cisplatin administration was evaluated by otoacoustic emissions following hyperbaric treatment and by scanning electron microscopy examination.
The study confirmed that cisplatin induces dose-dependent cochlear alterations consisting of cellular lesions and significant hair damage in outer hair cells. Analysis of anatomical changes in cochlear outer hair cells indicated signs of otoprotection against cisplatin in animals treated with hyperbaric oxygen therapy although in functional studies distortion product acoustic emission were absent reflecting a certain degree of hearing loss, most probably reversible and related to experimental artefacts. The study concluded that hyperbaric oxygen therapy has otoprotective effects against cisplatin-induced ototoxicity.
However, further studies are necessary to test other effects of high pressure oxygen on the cochlea [17].Another study investigated the effect of epigallocatechin gallate (EGCG) on the transcription factor STAT1, an important mediator of cell death. STAT1 phosphorylation is involved in both hair cells and support cells transformation after experimental exposure of mouse utricule to cisplatin. Oshima et al., “Cisplatin-induced apoptotic cell death in Mongolian gerbil cochlea,” Hearing Research, vol.
EGCG proved its efficiency as an otoprotective agent against cisplatin ototoxicity due to its inhibition of STAT1.
The hypothesis was further supported by the failure of EGCG to provide protection against cisplatin in STAT1-deficient mice [18].Former studies showed that lactate injected intratympanically in guinea pigs treated with ototoxic levels of cisplatin allowed near total preservation of otoacoustic emissions [19]. Since lactate is a part of Ringer solution, safely used in human subjects, and has the smallest molecular weight among other antioxidants which facilitates transport across the round window membrane, a further study was conducted to prove its otoprotective effect against cisplatin ototoxicity when injected intratympanically, before intraperitoneal cisplatin administration.
The molecular protective mechanism is based on the enzyme lactate dehydrogenase located in the mitochondria of outer hair cells.

The conversion of lactate to pyruvate in the presence of the enzyme leads to the formation of nicotinamide adenine dinucleotide (NADH) which is a natural antioxidant that may be involved in reducing toxic effects of oxygen reactive species resulted at cellular level following cisplatin therapy.
The study used auditory brainstem responses recordings which is a more sensible method than otoacoustic emissions testing, a fact that explains the differences in otoprotective effect reported by previous studies.
Hiraumi et al., “Effect of cisplatin on distortion product otoacoustic emissions in Japanese patients,” Laryngoscope, vol. The same study investigated the otoprotective effect of intratympanic N-acetylcysteine injections as well as its systemic diffusion following the administration. The results showed that high concentration of intratympanic N-acetylcysteine is not reliable for otoprotection against cisplatin ototoxicity since it caused more middle and inner ear damage than cisplatin alone. This was confirmed by high-performance liquid chromatography testing of blood samples taken from the venous system of the experimental animals after intratympanic injections of N-acetylcysteine. This latter outcome proves that the intratympanic route of administration would be safe and prevent inactivation of antitumor effect of cisplatin by binding between the thiol moiety of N-acetylcysteine and the platinum-containing molecule of the chemotherapeutic drug [20].Most of the existing studies focus on exogenous administration of antioxidants. Pharmacological activation of intrinsic defence mechanisms against oxidative stress in the inner ear caused by cisplatin therapy also proved helpful as showed by an experimental animal study using systemic administration of thiamine pyrophosphate (TPP). Thiamine pyrophosphate functions as coenzyme for peroxisomes being a crucial factor for energy metabolism, antioxidation, and myelinisation of nerve cells.
Its intraperitoneal injection increased the level of natural antioxidants like glutathione and antioxidant enzymes (superoxide dismutase, glutathione peroxidase and glutathione reductase) and reduced the content of malonildialdehyde, an indicator of lipid peroxidation following increased levels of oxygen reactive species resulting from cisplatin toxicity.
The histologic evaluation of cochleae harvested from TPP treated animals showed preservation of the morphology of the organ of Corti and outer hair cells and no destruction of spiral ganglion cells and stria vascularis following cisplatin therapy [5].The wide range of therapeutic molecules studied for their otoprotective effect against cisplatin-induced ototoxicity also includes sertraline, an antidepressant with neuroprotective effects in rats [6].
The selective serotonin reuptake inhibitor also has antioxidant effects, stimulates neurogenesis, and increases antiapoptotic protein levels [21].
It has been documented by distorsion product otoacoustic emissions recordings that oral administration of sertraline in cisplatin-treated rats prevented hearing loss above 5000 Hz, in a statistically significant manner. Neuwelt, “Early changes in auditory function as a result of platinum chemotherapy: Use of extended high-frequency audiometry and evoked distortion product otoacoustic emissions,” Journal of Clinical Oncology, vol.
Besides, sertraline would be beneficial to patients whose communication abilities are already deteriorated either by the cancer itself or by the treatment modalities and, therefore, feel depressed [6].An experimental single dose model of cisplatin ototoxicity in guinea pigs showed the otoprotective effect of systemic histone deacetylase inhibitor sodium butyrate. Distortion product otoacoustic emissions testing were chosen to provide a sensitive assay of the functional state of outer hair cells after systemic cisplatin insult on the cochlea. The systemic administration of the otoprotective agent avoided the side effects of the more invasive tympanic local route of administration. Moreover, sodium butyrate did not interfere with the tumoricidal effect of cisplatin providing both protections from reactive oxygen species and a certain degree of antitumor activity according to former reports. Acetylation of different cell proteins, including histones, is responsible both for the protective effect against oxidative stress and for the cell division inhibition and subsequent anticancer activity. Auditory brainstem responses were used to certify reduced threshold shifts in cisplatin treated animals who received transtympanic NOX3 siRNA. Since cisplatin administration has been previously associated with upregulation of NOX3 in the inner ear, Nox3 is thought to be a major source of free radicals in the cochlea following cisplatin exposure. The resulting free radicals initiate the inflammatory process in the cochlea by activating signal transducer and activator of transcription-1 (STAT1), followed by activation of p53 and increase in inflammatory mediators like TNF-alpha and interleukin-1 [23].
A single transtympanic injection of siRNA attenuated cisplatin ototoxicity by suppressing inflammation in a dose-related manner.
It hampered cisplatin-induced auditory brainstem responses threshold shift and higher doses allowed for complete morphological preservation of outer hair cells as proven by scanning electron microscopy examinations of the rat cochleae [24].Among various strategies that have been devised in experimental settings to prevent cisplatin ototoxicity, minocycline, a tetracycline derivative, proved its partial efficacy in vivo and in vitro. The anti-inflammatory and neuroprotective properties of minocycline have been previously reported. Lansdaal et al., “Audiometric patterns in ototoxicity of intra-arterial cisplatin chemoradiation in patients with locally advanced head and neck cancer,” Audiology and Neurotology, vol.
The biochemical mechanisms involve caspase-1 and caspase-3 inhibition, which decreases the amount of interleukin-1 and prevents apoptosis. The protective effect of minocycline has been tested both on cisplatin treated cell cultures and in experimental animals which underwent cisplatin intraperitoneal therapy after systemic administration of the otoprotective agent.
Cell viability assays showed that minocycline had a protective effect against cisplatin toxic action. Recordings of auditory brainstem responses and evaluation of the scanning electron microscopy sections of inner ears harvested from minocycline plus cisplatin treated animals indicated a partial preservation of the function and morphology of the outer hair cells as compared to those from animals treated with cisplatin alone [25].The effect of intraperitoneal administration of erdosteine on cisplatin-induced ototoxicity in a guinea pig model was also studied.
Erdosteine is a thiol derivative with established antioxidant properties due to its active sulfhydryl groups following liver first-pass metabolism.
Pre- and posttreatment auditory brainstem responses measurements were performed in living animals while outer hair cell counts were analyzed by scanning electron microscopy of the cochleae removed from euthanized animals. Apparently, cisplatin had deleterious effects on outer and inner ear cells situated in the basal turn of the cochlea despite intratympanic administration of protective dexamethasone [27].
Further experimental studies supported the finding that cisplatin exerts its damaging effect in a base to apex gradient, lower frequencies being spared for long.
Craver, “Cisplatin and cranial irradiation-related hearing loss in children,” The Ochsner Journal, vol. Moreover, lower doses of cisplatin allow the naturally present antioxidants to annihilate the resulting reactive oxygen species, explaining the spontaneous hearing threshold recovery even in the absence of protective dexamethasone administration [28].The intratympanic administration of dexamethasone avoids diminishing the tumoricidal activity of cisplatin. Downregulating apoptosis genes in tumour cells are responsible for this common side effect of systemic steroid therapy [29]. An experimental study conducted on cisplatin treated guinea pigs asserted the safety of intratympanic dexamethasone based on audiologic and histologic results. Auditory brainstem responses testing, optic microscopic and scanning electron microscopic examinations of cochleae showed no significant differences between intratympanic dexamethasone-treated animals and saline-treated controls. Dexamethasone administered intratympanically proved efficacious in protecting the labyrinth against cisplatin-induced ototoxicity as shown by reduced auditory brainstem responses threshold shifts and unaltered histological inner ear structures. The study’s results also suggest that giving the intratympanic dexamethasone one hour before the cisplatin administration provides the best protection (total protection) against the ototoxic insult by the alkylating agent compared to dexamethasone injections one day prior to cisplatin administration (partial protection) [14].
According to another study, in order for the dexamethasone to exert a protective effect against cisplatin ototoxicity, the timing of administration of the two drugs should be highly synchronized so that the peak concentration of dexamethasone in the perilymph should correlate with the peak concentration of the chemotherapeutic agent [3].Otoprotection with dexamethasone against cisplatin-induced age-related hearing loss was investigated in a guinea pig model following observations that persons older than 65 years account for more than half of the newly diagnosed malignancies.
A single dose of cisplatin was administered intraperitoneally in old mice preceded and followed by dexamethasone injected intratympanically to counteract the cisplatin toxic effect on inner ear hair cells. Pre- and posttreatment auditory brainstem responses were recorded to evaluate hair cell function. The results of the study pointed out that no synergistic action between age related hearing loss and cisplatin-induced hearing loss exists since threshold shifts were smaller in older animals than those in young mice.
Another finding of the study was that the protective effect of dexamethasone against cisplatin-induced ototoxicity was a function of stimulus frequency in old mice.
Age-related changes of the mechanism of distribution of dexamethasone in scala tympani perilymph after round window membrane application in guinea pigs seem to account for the frequency dependent otoprotective effect [30].Intratympanic dexamethasone failed to protect against cisplatin-induced ototoxicity in a multidose cisplatin ototoxicity mouse model. The study was prompted by typical clinical protocols of cancer treatments which require administration of multiple, smaller cisplatin doses, exerting their curative effect through cumulative dosing. Contrary to previous experimental studies, the mice received five doses of cisplatin throughout five days, mimicking the cumulative exposure seen in malignant tumours treatment. Intratympanic dexamethasone was administered on the same days as the intraperitoneal cisplatin.
Only a slight decrease of TNF-alpha expression in the cochlea was demonstrated by immunohistochemical staining of anatomical samples harvested from systemic cisplatin plus dexamethasone treated animals. Dexamethasone also seemed to protect stria vascularis from morphological alterations, probably owing this effect to higher concentrations of steroid in the lateral cochlear wall following increased cochlear flow and a naturally highly vascularised stria vascularis. Kalleny, “Effect of intratympanic dexamethasone administration on cisplatin-induced ototoxicity in adult guinea pigs,” Auris Nasus Larynx, vol.
Still, a functional otoprotective effect of systemic dexamethasone against cisplatin-induced hearing loss was not observed [4].Among naturally occurring molecules, Rosmarinic acid, a water-soluble polyphenolic compound extracted from Dansam-Eum, was tested for its protective effect against cisplatin-induced ototoxicity in laboratory settings. The results of the study showed that Rosmarinic acid inhibited cisplatin-induced caspase-1 activation providing protection against stereocilia loss in the primary organ of Corti explants [32].Another natural remedy, the Maytenus ilicifolia aqueous extract, was evaluated for its possible otoprotection in guinea pigs. Despite the well-known South America plant’s antioxidant effects (due to the presence of flavonoids and alkaloids), functional tests did not demonstrate any protective action on the cisplatin exposed cochleae. Yet, the extract improved the clinical status and weight of guinea pigs and diminished mortality after cisplatin exposure [33].Resveratrol, a polyphenol found in grape skin and seed, has antioxidant, neuroprotective, and dose dependent antiapoptotic properties [34].
Recent experimental research pointed out the preventive effect of resveratrol against cisplatin induced ototoxicity. An in vitro study on House Ear Institute-Organ of Corti 1 cell line showed that resveratrol in low doses prevented ototoxicity mainly influencing apoptotic gene expression but proved cytotoxic effect in high doses [34]. Laurell, “Cochlear pharmacokinetics of cisplatin: an in vivo study in the guinea pig,” The Laryngoscope, vol. Clinical StudiesIntratympanic dexamethasone was clinically tested for its otoprotective effect in patients suffering from neoplastic diseases for which the treatment protocol included cisplatin.

Intratympanic dexamethasone has already been tested clinically for the treatment of idiopathic sudden sensorineural hearing loss and Meniere disease [37]. Intratympanic administration of steroids avoids significant systemic side effects like hyperglycaemia, peptic ulcers, hypertension, osteoporosis, and psychosis. The intratympanic route also provides higher concentrations of drug in the inner ear fluids and prevents significant interference between dexamethasone, which is known to reduce efficacy of chemotherapeutic agents, and cisplatin.
Patients enrolled in the study underwent unilateral intratympanic dexamethasone administration prior to every cisplatin treatment session, with the contralateral ear used as a control. Serial follow-up audiometry and distorsion product otoacoustic emissions testing were performed to check the functional state of both study and control ears.
The conclusion of the study is that intratympanic dexamethasone has minimal effect towards reducing cisplatin ototoxicity. Further studies using different concentrations of dexamethasone and a perfect timing of administration are necessary to investigate its role in preventing hearing loss after cisplatin therapy [3].Transtympanic L-N-acetylcysteine was also clinically tested in head and neck cancer patients undergoing cisplatin therapy. Ramkumar, “Cisplatin ototoxicity and protection: clinical and experimental studies,” Tohoku Journal of Experimental Medicine, vol. Thiol compounds are known to either directly bind cisplatin or act as free radical scavengers.
Based on that, their intratympanic administration was suggested to avoid the decrease of oncologic effectiveness of cisplatin and to reduce the oxidative stress caused by it.
Intratympanic L-N-acetylcysteine was well tolerated by patients receiving multiple doses of cisplatin as part of their oncologic treatment.
The study protocol required the L-NAC injection to be approximately 1 hour before systemic administration of cisplatin, for the sake of better timing. The outcome of the pure tone audiometry testing at 1 and 2 months after the last cycle of cisplatin showed that L-N-acetylcysteine was overall not significantly otoprotective. The study protocol had several challenges like the difficulty in maintaining high enough concentrations of aqueous solution of L-N-acetylcysteine in the middle ear due to the technique of administration.
Another study flaw was the different initial hearing thresholds due to preexisting hearing loss [38].Few clinical studies tested systemic otoprotective molecules for preventing cisplatin-induced hearing loss. Amifostine, a phosphorylated aminothiol designed to protect against radiation damage, was known to counteract the toxic effect of different anticancer treatments without interfering with the tumoricidal effect. Féres, “The role of hyperbaric oxygen therapy (hot) as an otoprotection agent against cisplatin ototoxicity,” Acta Cirurgica Brasileira, vol. Although significant protection of amifostine against haematological toxicity after high dose carboplatin therapy in a child with medulloblastoma was reported [39], a clinical study considering systemic administration of amifostine failed to prove any otoprotective effect against cisplatin-induced hearing loss in a group of pediatric patients treated with cisplatin associated with other chemotherapeutic agents [40].
OtopharmacogeneticsThe well-isolated inner ear organ makes it prone to targeted genetic therapies.
Viral or nonviral gene vectors can be delivered through a transtympanic route without the risk of dispersing them and reaching other tissues with subsequent undesirable genetic alteration.
Long term effects after single administration, cellular selectivity, and replacement of genetically flawed nucleic acid sequences are the main benefits of gene therapy. Common viral vectors include herpes simplex virus, recombinant adenoassociated virus, recombinant adenovirus, and adenovirus, used to amplify the expression of targeted genes.
Cells are infected with the vectors (transfection) which transfer genes whose expressed proteins influence important processes like growth, oxidative stress, and apoptosis. Nathanson, “Cisplatin-induced hair cell death requires STAT1 and is attenuated by epigallocatechin gallate,” Journal of Neuroscience, vol.
Clinical applications require further studies regarding safety, immunogenicity, and consequences of genetic manipulation [41].Another strategy to avoid cisplatin-induced hearing loss would be the pretreatment genotyping to find out patients at risk for the ototoxic effect of cisplatin [42].
DiscussionForty-three publications were reviewed concerning prevention or treatment of cisplatin induced ototoxicity. Experimental studies sustained the efficiency of hyperbaric oxygen therapy, epigallocatechin therapy, and intratympanic lactate. The latter two therapies provide exogenous antioxidants while pharmacologic activation of endogenous antioxidants by means of intratympanic thiamine pyrophosphate was consistent with higher levels of natural antioxidants. Oral sertraline, besides its otoprotective effect against cisplatin induced ototoxicity, also has therapeutic value concerning the depression occurring frequently in oncologic patients. Chang, “Prevention of cisplatin ototoxicity using transtympanic N-acetylcysteine and lactate,” Otology and Neurotology, vol. Sodium butirate proved its efficiency against cisplatin induced hearing loss in a monodose cisplatin model. The production of endogenous radicals of oxygen species was reduced after intratympanic administration of short interfering RNA which reduces the expression of NOX3 in the cochlea. Minocycline appeared to be efficient only at low doses of cisplatin while systemic erdosteine showed promising results. Dexamethasone in experimental studies combined efficiency against cisplatin induced ototoxicity with preservation of the tumoricidal activity of cisplatin.
When older mice were treated, the dexamethasone was more otoprotective at higher frequencies compared to experiments including younger subjects. Rosmarinic acid also proved to be otoprotective while the Maytenus ilicifolia aqueous extract was not. Saliba, “The role of intratympanic lactate injection in the prevention of cisplatin-induced ototoxicity,” Laryngoscope, vol. Resveratrol had contradictory effects, systemic low doses, and in vitro administration preventing ototoxicity, whereas high oral doses seem to enhance cisplatin ototoxicity.
There also were experimental studies which showed inefficiency of intratympanic N-acetylcysteine and intratympanic and systemic dexamethasone. N-Acetylcysteine also had a damaging effect on middle and inner ear structures.Clinical studies proved a minor otoprotective effect of intratympanic dexamethasone and no effect of systemic amifostine and intratympanic L-N-acetylcysteine.
New perspectives are brought about by genetic therapy using viral vectors and genotyping to anticipate interindividual variability in cisplatin ototoxicity.5. ConclusionHearing loss prevention and treatment during cisplatin therapy for cancer needs further research to find new strategies and optimize old ones.
Blendy, “Antidepressant action: to the nucleus and beyond,” Trends in Pharmacological Sciences, vol. Roberson, “The histone deacetylase inhibitor sodium butyrate protects against cisplatin-induced hearing loss in guinea pigs,” The Laryngoscope, vol. Ramkumar, “Short interfering RNA against STAT1 attenuates cisplatin-induced ototoxicity in the rat by suppressing inflammation,” Cell Death and Disease, vol.
Rybak, “Transtympanic administration of short interfering (si)RNA for the NOX3 isoform of NADPH oxidase protects against cisplatin-induced hearing loss in the rat,” Antioxidants and Redox Signaling, vol. Cho, “Protective effect of minocycline against cisplatin-induced ototoxicity,” Clinical and Experimental Otorhinolaryngology, vol.
Daniel, “Protective effect of erdosteine against cisplatin-induced ototoxicity in a guinea pig model,” Otolaryngology—Head and Neck Surgery, vol. Herzer et al., “Glucocorticoid cotreatment induces apoptosis resistance toward cancer therapy in carcinomas,” Cancer Research, vol. Parham, “Can intratympanic dexamethasone protect against cisplatin ototoxicity in mice with age-related hearing loss?” Otolaryngology—Head and Neck Surgery, vol.
Parham, “Dexamethasone otoprotection in a multidose cisplatin ototoxicity mouse model,” Otolaryngology—Head and Neck Surgery, vol. Kim et al., “Rosmarinic acid, active component of dansam-eum attenuates ototoxicity of cochlear hair cells through blockage of caspase-1 activity,” PLoS ONE, vol. Coelho, “The use of Maytenus ilicifolia to prevent cisplatin-induced ototoxicity,” Brazilian Journal of Otorhinolaryngology, vol.
Aktas, et al., “Molecular mechanisms of protective effect of resveratrol against cisplatinium induced ototoxicity,” Journal of International Advanced Otology, vol.
Sari et al., “Protective role of resveratrol against cisplatin induced ototoxicity in guinea pigs,” International Journal of Pediatric Otorhinolaryngology, vol. McKenna, “Drug delivery for treatment of inner ear disease: current state of knowledge,” Ear and Hearing, vol.
Oster, “Administration of Ethyol (amifostine) to a child with medulloblastoma to ameliorate hematological toxicity of high dose carboplatin,” Anti-Cancer Drugs, vol.
Malogolowkin et al., “Amifostine does not protect against the ototoxicity of high-dose cisplatin combined with etoposide and bleomycin in pediatric germ-cell tumors,” Cancer, vol. Jayne, “Cisplatin-induced ototoxicity and the role of pharmacogenetic testing,” Journal of Pediatric Pharmacology and Therapeutics, vol.

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