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To assess the role of DNA repair in maintenance of hearing function and neurological integrity, we examined hearing status, neurological function, DNA repair complementation group and history of acute burning on minimal sun exposure in all patients with xeroderma pigmentosum, who had at least one complete audiogram, examined at the National Institutes of Health from 1971 to 2012.
Xeroderma pigmentosum is a heterogeneous disease associated with several different defects in DNA repair.
We investigated the role of DNA repair in the maintenance of auditory and neurological integrity by examining hearing status, complementation group, neurological function and burning phenotype in patients with xeroderma pigmentosum seen at the National Institutes of Health between 1971 and 2012. We conducted a retrospective follow-up study of 84 patients with xeroderma pigmentosum examined at the National Institutes of Health, from 1971 to 2012, who had audiometric data available. All patients who had an audiometric examination between 1 January 1971 and 18 January 2012 were included in the study. Neurological involvement was ranked using the scale of xeroderma pigmentosum-type neurological degeneration developed by Nishigori et al.
Linear regressions predicting hearing threshold by age were calculated for the xeroderma pigmentosum-type neurological degeneration and xeroderma pigmentosum without neurological involvement groups. Standard deviations (Std Dev) of the means are shown to indicate the extent of threshold variation observed among mice within each class. AbstractBackground : Cisplatin-induced ototoxicity shows high interindividual variability and is often accompanied by transient or permanent tinnitus. Materials and Methods : Fifty-seven patients scheduled for cisplatin-based chemotherapy were included in the study.
Results : The subjective hearing loss was found in seven patients, while six patients had tinnitus during the chemotherapy.
Conclusion : As use of high-frequency audiometry is still limited in research work only, we need a strict protocol of adding high-frequency audiometry in the cisplatin-based chemotherapy regimen. IntroductionCisplatin contributed significantly in the early success of modern chemotherapy for solid tumors and today, cisplatin is a primary drug for testicular cancer, medulloblastoma, osteogenic sarcoma, cervix and ovarian cancers.
During follow-up, seven patients complained of subjective hearing loss and six had tinnitus at the time of first follow-up but none had both complaints. DiscussionCisplatin induced ototoxicity compromises, [11] development of language, cognitive functions, learning ability, communication and quality of life in terms of isolation and depression.
Ultrasound is defined as cyclic sound pressure above the frequency limit of human hearing, approximately 20 kHz. For many audio devices, the size and shape of the device makes little difference for audio performance. For this reason, an ultrasonic microphone is directional, though it has only one acoustic port.
Ultrasound also loses energy quickly due to absorption effects, with absorption increasing along with frequency and humidity.
Place the test microphone and reference microphone with the sound ports at 90 degree incidence to the speaker at a distance of 1 m. Sweep the sound source through the frequency range of interest, and compare the reference microphone output to test the microphone output. Equipment used for ultrasonic recording must have adequate frequency bandwidth to avoid filtering out frequencies of interest. Microphone level signals require pre-amplification, so check the specifications for any pre-amplifier used for listening or recording.
If using a PC to record ultrasonic signals, verify that the sound card supports sampling rates of at least twice the maximum frequency of interest.
The frequency response for the SPM0404UD5 covers a wide frequency band — from subsonic to ultrasonic (see Figure 2).
If using the SPM0404UD5 for low frequencies in addition to high frequencies, uniform phase performance may be important for array performance or consistency in feed-forward systems. Condition monitoring: ultrasonic acoustic sensing may be an attractive option for condition monitoring of objects such as bearings, valves, motors, gears, and pumps for a prediction of failure or need for replacement. Leak detection: an ultrasonic sensor may listen for leak detection in pressure and vacuum systems such as boilers, heat exchangers, condensers, chillers, tanks, pipes, hatches, and hydraulic systems. Event detection: one or more SPM0404UD5 ultrasonic MEMS sensors may be used to detect an event that creates ultrasonic energy, such as an impulse or acoustic shock wave.
Totonchy1 Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USA2 Clinical Research Training Programme, National Institutes of Health, Bethesda, MD 20892, USADeborah Tamura1 Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USAMatthew S. Although all patients with xeroderma pigmentosum are sensitive to ultraviolet radiation damage, only a portion experience acute burning on minimal sun exposure after only a few minutes in direct sunlight.
Patients were referred to the National Institutes of Health Clinical Centre by outside health care professionals and were enrolled into protocols approved by the National Cancer Institute Institutional Review Board. Masking was used for air and bone conduction testing when appropriate to ensure ear-specific results. ANOVA was used to compare the 4F-PTA by degree of neurodegeneration for those patients with xeroderma pigmentosum with neurodegeneration. Patients with non-xeroderma pigmentosum-type neurological involvement were not included in the analysis based on the heterogeneity of their neurological disease. One audiogram per patient (the earliest complete audiogram) was used to determine a cross-sectional relationship between age and hearing threshold. Radial section of cochlea showing missing IHC, but intact nerve fibers in the habenula perforata. IHC loss, attributed to failure of differentiation, was caused by a mutation in the Srrm4 gene, which affects tissue-specific alternative splicing [92]. The Slc19a2- [90] and Ggt1dwg mutations are on mouse strain backgrounds that do not have the ahl susceptibility allele of the Cdh23 gene [112], which is associated with accelerated hearing loss and a primary loss of OHC [14]. It is not possible to identify the susceptible individuals before commencement of the treatment. All patients were divided into three groups depending on the dose of cisplatin infused in 3 weeks. The hearing loss was sensorineural, dose dependent, symmetrical, bilateral and irreversible. Cisplatin is a cell cycle-nonspecific cytotoxic drug and has a toxic profile that is different from other important cytotoxic drugs.
No patient had distant metastasis, and hence none underwent cranial radiation for treatment. The tinnitus was present in one subject of Group 1 (50-year-old male) and group 3 (34-year-old male), while group 2 had 4 patients (mean age 50 years). Eight patients had significant hearing loss at Fisher′s scale and this loss was observed in 11 of 12 patients at 4 and 6 KHz.


In all three groups, hearing loss was sensorineural, irreversible and symmetrical, and there was no sex predilection. Predicting cisplatin ototoxicity in children: The influence of age and the cumulative dose. Ototoxicity of high-dose cisplatin by bolus administration in patients with advanced cancers and normal hearing.
Evoked otoacoustic emissions--an approach for monitoring cisplatin induced ototoxicity in children. Ototoxicity in children receiving platinum chemotherapy: Underestimating a commonly occurring toxicity that may influence academic and social development.
Platinum compound-related ototoxicity in children: Long-term follow-up reveals continuous worsening of hearing loss. Left-right asymmetry in hearing loss following cisplatin therapy in children--the left ear is slightly but significantly more affected.
Ototoxicity of cis-diamminedichloroplatinum (II): influence of dose, schedule and mode of administration. The role of hyperbaric oxygen therapy (hot) as an otoprotection agent against cisplatin ototoxicity. Ototoxicity in a randomized phase III trial of intra-arterial compared with intravenous cisplatin chemoradiation in patients with locally advanced head and neck cancer. Early changes in auditory function as a result of platinum chemotherapy: use of extended high-frequency audiometry and evoked distortion product otoacoustic emissions. Detection of late ototoxic side effect of cisplatin by distortion otoacoustic emission (DPOAE).
Set an adequate sampling rate in the record settings of the recorder program used (such as Adobe Audition or similar). Specialized equipment is required for measurements at both extremes of the frequency range. Noise is measured in a sealed heavy steel enclosure that rests on a cushion to limit vibration transmission (see Figure 4). The measurement in Figure 5 compares the SPM0404UD5 phase noise with the phase noise of a laboratory reference microphone in a sealed cavity.
Pantell2 Clinical Research Training Programme, National Institutes of Health, Bethesda, MD 20892, USA3 Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, Bethesda, MD 20892, USAChristopher Zalewski4 Otolaryngology Branch, National Institute on Deafness and other Communication Disorders, Bethesda, MD 20892, USAPorcia T. Patients with xeroderma pigmentosum variant have defects in DNA polymerase eta involved in translesional DNA synthesis. Written informed consent was obtained from each participant or parents of minor participants.
Fischer’s exact test was used to determine the odds ratio for developing xeroderma pigmentosum-type neurological degeneration. Chow tests taking into account the combination of the slope and intercept of these regression lines were used to compare these data against the ISO 7029 50th percentile line of hearing threshold by age. If either of these mutations were examined in a strain that has the Cdh23 susceptibility variant, the results likely would show OHC loss as well as IHC loss. We conducted a prospective, randomized and observational study in a tertiary care centre and evaluated the effects of different doses of cisplatin on hearing.
High doses of cisplatin cause nephrotoxicity, gastrointestinal toxicity, neurotoxicity and ototoxicity.
During radiation for the head and neck cancers, ipsilateral temporal bone and ear of patients were protected by beam-modification devices (shielding block made up of lead) so as to avoid any affect of radiation on hearing.
A polar response measurement is required to determine the exact directional pattern at a specific frequency.
Bradford5 Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USASaumil N. DNA damage induced by oxidative metabolism is thought to contribute to the progressive loss of non-dividing neurons in the brain (Brooks et al., 2008).
We obtained outside audiometric records for review and included these (35 additional audiograms) in our analysis only if the examining audiologist rated reliability as good. Duration of audiometric monitoring ranged from a single test (n = 45) to a 39-year period (n = 1).
If neurological evaluation was not completed at the time of audiometric testing, neurological ranking was assigned from the assessment closest to the date of audiometric evaluation. Ototoxicity is one of the dose-limiting side effects of cisplatin because it increases with increase in the dose. Of 9 patients, 6 had significant hearing loss at 8 and 12 KHz, while only 4 of 7 patients showed significant hearing loss at 16 KHz. Cisplatin blocks transduction channels within the outer hair cells of the cochlea and causes progressive destruction of outer hair cells, inner hair cells and supporting cells within the organ of Corti.
Merchant6 Department of Otology and Laryngology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USAJoseph Nadol6 Department of Otology and Laryngology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USASikandar G.
Of the 17 patients with xeroderma pigmentosum-type neurological degeneration, 13 (76%) developed hearing loss, and all 17 were in complementation groups xeroderma pigmentosum type A or type D and reported acute burning on minimal sun exposure.
Death typically occurs in the third or fourth decades of life in patients with xeroderma pigmentosum with neurodegeneration (Bradford et al., 2011). However, not all patients with mutations in these genes develop neurodegeneration, making prediction of neurological disease clinically difficult. To examine the hearing phenotype directly attributable to xeroderma pigmentosum, ears with a history of otological surgery other than myringotomy tube placement (n = 1) were excluded from analysis.
For each subject, we defined the reference audiogram as the most recent complete audiogram. Patients with neurological involvement atypical of that observed in xeroderma pigmentosum were classified as non-xeroderma pigmentosum-type neurological involvement. All statistical tests were two-sided, and the 95% confidence interval was calculated for each test.
Of those reporting acute burning on minimal sun exposure, 25 were non-Hispanic whites, five were African American, one was Asian and one was of other ethnicity.
Interestingly, metformin, a drug that inhibits mTOR, attenuated aminoglycoside-induced hair cell loss in vitro, but it did not reduce hearing loss and hair cell damage in vivo [70]. It was hypothesized that GLAST in supporting cells protects IHC by taking up excess glutamate, converting it to glutamine, which is neuroprotective, and then transferring it to IHC, similar to what occurs between glia and neurons [95-100].
Oxidative stress has been shown to play a major role in the pathophysiology of thiamine deficiency [107] and thiamine deficiency was shown to reduce GSH levels and induce oxidative stress in brain mitochondria of mice [108].


Khan1 Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USARaphael Schiffmann7 National Institute of Neurological Diseases and Stroke, Bethesda, MD 20892, USATyler Mark Pierson7 National Institute of Neurological Diseases and Stroke, Bethesda, MD 20892, USAEdythe Wiggs7 National Institute of Neurological Diseases and Stroke, Bethesda, MD 20892, USAAndrew J. Xeroderma pigmentosum complementation groups and mutations in the xeroderma pigmentosum variant gene were determined using cell fusion, host cell reactivation, western blotting or DNA sequencing (Bradford et al., 2011). Cisplatin-induced ototoxicity is often accompanied by transient or permanent tinnitus [4],[5] and shows high interindividual variability. All included patients underwent a detailed history, clinical examination, hearing (tuning fork tests and pure tone audiometry) and vestibular functions assessment (bithermal caloric, positioning and positional tests), blood (complete hemogram, liver and renal function tests) and urine analysis.
Cisplatin ototoxicity is also associated with the generation of reactive oxygen species, depletion of intracellular glutathione and interference with antioxidant enzymes within the cochlea. Griffith4 Otolaryngology Branch, National Institute on Deafness and other Communication Disorders, Bethesda, MD 20892, USAJohn J.
Temporal bone histology in a patient with severe xeroderma pigmentosum-type neurological degeneration revealed marked atrophy of the cochlear sensory epithelium and neurons. Patient data were collected from medical records at the National Institutes of Health Clinical Centre, from records of outside institutions, research records at the National Cancer Institute, previous publications (Bradford et al., 2011) and personal correspondence. When bone-conduction was not tested, hearing loss was classified as sensorineural, but only if tympanometry was normal (Margolis and Heller, 1987), and acoustic stapedial reflexes were present at levels commensurate with the degree of hearing loss (Gelfand et al., 1990).
Three patients had otitis media at a single audiometric test session, none of which were at the time of the most recent complete (reference) audiogram. In this study, hearing assessment was done before starting cisplatin therapy and at one and three months after cisplatin infusion.
DiGiovanna1 Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USAKenneth H. The 19-year mean age of detection of clinically significant hearing loss in the patients with xeroderma pigmentosum with xeroderma pigmentosum-type neurological degeneration was 54 years younger than that predicted by international norms. Hearing loss type was classified as unknown when there were insufficient audiological data to categorize the hearing loss as sensorineural, mixed or conductive. Identification of susceptible individuals before commencement of the treatment is not possible; however, early ototoxic effects can be detected by high-frequency audiometry [7] and otoacoustic emission.
In patients with xeroderma pigmentosum, aged 4–30 years, a four-frequency pure-tone average ?10 dB hearing loss was associated with a 39-fold increased risk (P = 0.002) of having xeroderma pigmentosum-type neurological degeneration. Materials and MethodsThis study was conducted in the Departments of Otolaryngology- Head and Neck Surgery, and Radiation-Oncology (Regional Cancer Centre). Severity of hearing loss parallels neurological decline in patients with xeroderma pigmentosum-type neurological degeneration. Pure-tone hearing sensitivity for singe frequencies and the 4F-PTA was analysed using age- and gender-specific reference ranges for hearing levels from a large population of otologically screened adults reported in International Organization for Standardization (ISO) 7029 (International Standard Organization, 2000).
Audiometric findings, complementation group, acute burning on minimal sun exposure and age were important predictors of xeroderma pigmentosum-type neurological degeneration. Sensory thresholds of the worse hearing ear were determined from bone-conduction thresholds or from air-conduction thresholds, in cases where bone-conduction was not tested and both tympanometry and acoustic reflexes were normal.
Few studies [14],[15] involving follow-up to two years had also found irreversible hearing loss by cisplatin.
These results provide evidence that DNA repair is critical in maintaining neurological integrity of the auditory system.
The sensory thresholds were compared with and plotted against the 5th, 50th and 95th percentile of combined male and female age-matched ISO 7029 data.
We found no correlation between age and hearing loss or between baseline hearing level and cisplatin-induced hearing loss. Group 2 comprised 35 patients (21 male and 14 female) of whom 23 had various head and neck cancer (excluding larynx) and the remaining 12 were suffering from carcinoma of the cervix. The maximum increase in the hearing threshold after cisplatin administration was 45 dB at 8 KHz in both ears of a 43-year-old patient. In Group 2, cisplatin caused a maximum increase of 40 dB in the hearing threshold at 12 KHz in the hearing threshold of right ear in a 19-year-old patient.
In the left ear, uniform increase of about 30 dB was observed in hearing threshold at all frequencies in all age groups. Few authors [20],[21] have found relationship between free circulating cisplatin in plasma with time. They found that cisplatin infusion during afternoon and evening results in low plasma levels of free cisplatin, and hence cisplatin administrated during the early evening hours results in fewer side effects including ototoxicity. Measurement of correlation between time and plasma concentration was beyond the scope of this study. We found no correlation of tinnitus with the dose of cisplatin or age, which was comparable to the study by Moroso et al . The risk of permanent hearing damage from platinum chemotherapy is stimulating the development of otoprotectants for coadministration with platinum to reduce hearing damage without affecting the antitumor activity of the platinum agent.
There are numerous otoprotectant agents under research, which include aspirin, antioxidants, [24] intratympanic dexamethasone [25] and hyperbaric oxygen therapy, [26] Ginkgo biloba extract, [27] diethyldithiocarbamate, [28] lipoic acid, [29] adenosine agonist, [30] vitamin E [31] and sodium thiosulfate. Although, the importance of high-frequency audiometry in cisplatin chemotherapy was established about 25 years earlier, [33] but in majority of the centers including our department, it is used only during research work.
However, lack of infrastructure, non-availability of high-frequency audiometer and audiologist is a major problem in these centers, especially in our country. To conclude, we all know that cancer patients are living in physical and mental agony and cisplatin-induced ototoxicity further enhances this morbidity. Audiological monitoring is an essential part of the management of adults and children receiving platinum-based chemotherapy.
Although few authors [12],[34],[35] found distortion product otoacoustic emission as a better method of detecting cisplatin-induced early ototoxicity but high-frequency pure-tone audiometry is the first choice due to its high sensitivity. High-frequency monitoring alerts the physician of early ototoxic effects, who has opportunity to change a patient′s course of treatment.
Therefore, high-frequency audiometry should be included in the cisplatin-based chemotherapy regimen.
Increase in the dose of cisplatin lead to increase in ototoxicity that warrants further research to find therapeutic efficacy of low-dose cisplatin or a better substitute of cisplatin.
Otoprotective drugs are still at experimental level but may be beneficial in cisplatin ototoxicity.AcknowledgmentDr RS Minhas provided general help in this research work.



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