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Head & Neck Feb 2015Both radiotherapy (RT) and cisplatin-based chemoradiotherapy (CRT) in patients with head and neck cancer may cause sensorineural hearing loss (SNHL). The purpose of this... (Review)
Review
BACKGROUND
Both radiotherapy (RT) and cisplatin-based chemoradiotherapy (CRT) in patients with head and neck cancer may cause sensorineural hearing loss (SNHL). The purpose of this review was to provide more insight into SNHL because of CRT compared to RT.
METHODS
Comprehensive search of Medline and Embase with the terms "radiotherapy" combined with "ototoxicity," "head and neck squamous cell carcinoma," and synonyms.
RESULTS
Of the 2507 studies found, 21 were included in this study. Pooled analysis could not be committed because of heterogeneity. Incidence rates of SNHL after RT and CRT varied considerably, with percentages ranging from 0% to 43% and 17% to 88%, respectively. Factors that influenced the risk of SNHL were radiation dose to the cochlea, follow-up time, age, baseline hearing level, and cisplatin dose.
CONCLUSION
The wide range of SNHL incidence rates makes it impossible to draw any conclusions on the severity of RT- and CRT-induced ototoxicity. To allow for future comparison of study outcomes, development of uniform criteria is of utmost importance.
Topics: Age Factors; Antineoplastic Agents; Chemoradiotherapy; Cisplatin; Cochlea; Dose-Response Relationship, Drug; Head and Neck Neoplasms; Hearing Loss, Sensorineural; Humans; Radiotherapy; Radiotherapy Dosage
PubMed: 24478269
DOI: 10.1002/hed.23551 -
Cancer Epidemiology Aug 2022Platinum-based chemotherapeutic agents cisplatin and carboplatin are widely used in cancer treatment worldwide and may result in ototoxic hearing loss. The high... (Meta-Analysis)
Meta-Analysis Review
Platinum-based chemotherapeutic agents cisplatin and carboplatin are widely used in cancer treatment worldwide and may result in ototoxic hearing loss. The high incidence of cancer and salient ototoxic effects of platinum-based compounds pose a global public health threat. The purpose of this study was twofold. First, to estimate the prevalence of ototoxic hearing loss associated with treatment with cisplatin and/or carboplatin via a systematic review and meta-analysis. Second, to estimate the annual global burden of ototoxic hearing loss associated with exposure to cisplatin and/or carboplatin. For the systematic review, three databases were searched (Ovid Medline, Ovid Embase, and Web of Science Core Collection) and studies that reported prevalence of objectively measured ototoxic hearing loss in cancer patients were included. A random effects meta-analysis determined pooled prevalence (95% confidence intervals [CI]) of ototoxic hearing loss overall, and estimates were stratified by treatment and patient attributes. Estimates of ototoxic hearing loss burden were created with published global estimates of incident cancers often treated with platinum-based compounds and cancer-specific treatment rates. Eighty-seven records (n = 5077 individuals) were included in the meta-analysis. Pooled prevalence of ototoxic hearing loss associated with cisplatin and/or carboplatin exposure was 43.17% [CI 37.93-48.56%]. Prevalence estimates were higher for regimens involving cisplatin (cisplatin only: 49.21% [CI 42.62-55.82%]; cisplatin & carboplatin: 56.05% [CI 45.12-66.43%]) versus carboplatin only (13.47% [CI 8.68-20.32%]). Our crude estimates of burden indicated approximately one million individuals worldwide are likely exposed to cisplatin and/or carboplatin, which would result in almost half a million cases of hearing loss per year, globally. There is an urgent need to reduce impacts of ototoxicity in cancer patients. This can be partially achieved by implementing existing strategies focused on primary, secondary, and tertiary hearing loss prevention. Primary ototoxicity prevention via otoprotectants should be a research and policy priority.
Topics: Antineoplastic Agents; Carboplatin; Cisplatin; Hearing Loss; Humans; Neoplasms; Ototoxicity; Platinum
PubMed: 35724557
DOI: 10.1016/j.canep.2022.102203 -
International Journal of Pediatric... May 2019Aminoglycosides are a well-known clinically relevant antibiotic family used to treat bacterial infections in humans and animals and can produce toxic side effects....
INTRODUCTION
Aminoglycosides are a well-known clinically relevant antibiotic family used to treat bacterial infections in humans and animals and can produce toxic side effects. Aminoglycoside-induced hearing loss (HL) has been shown to have a genetic susceptibility. Mitochondrial DNA mutations have been implicated in inherited and acquired hearing impairment.
OBJECTIVE
Literature review of genetic mutations associated with aminoglycoside-induced ototoxicity.
METHODS
PubMed was accessed from 1993 to 2017 using the search terms "aminoglycoside, genetic, ototoxicity, hearing loss". Exclusion criteria consisted of a literature in a language other than English, uncompleted or ongoing studies, literature with non-hearing related diseases, literature on ototoxicity due to cisplatin/carboplatin based chemotherapy, literature on ototoxicity from loop diuretics, animal studies, literature studying oto-protective agents, and literature without documented aminoglycoside exposure.
RESULTS
108 articles were originally identified, and 25 articles were included in our review. Mitochondrial 12S rRNA mutations were identified in all 25 studies in a total of 220 patients. Eight studies identified A1555G mutation as primary genetic factor underlying HL in cases of aminoglycoside-induced ototoxicity. The next most common mutation identified was C1494T.
DISCUSSION
Mitochondrial 12s rRNA mutation A1555G was present in American, Chinese, Arab-Israeli, Spanish and Mongolian ethnicities. All mutations leading to aminoglycoside ototoxicity were mitochondrial mutations.
CONCLUSIONS
Consideration of preexisting genetic defects may be valuable in treatments involving aminoglycosides. In particular populations such as those of Chinese origin, clinicians should continue to consider the increased susceptibility to aminoglycosides.
Topics: Aminoglycosides; Anti-Bacterial Agents; Female; Genetic Predisposition to Disease; Hearing Loss, Sensorineural; Humans; Male; Mutation; RNA, Ribosomal
PubMed: 30743189
DOI: 10.1016/j.ijporl.2019.02.002 -
Iranian Journal of Otorhinolaryngology Sep 2022Noise-induced hearing loss (NIHL) is defined as the sensorineural hearing loss caused by acute acoustic trauma or chronic exposure to high-intensity noises. Exposure to...
INTRODUCTION
Noise-induced hearing loss (NIHL) is defined as the sensorineural hearing loss caused by acute acoustic trauma or chronic exposure to high-intensity noises. Exposure to noises can lead to irreversible damage to the inner ear and, consequently, to a permanent shift of the hearing threshold. Police officers are particularly at risk of acute or chronic hearing damages. The aim of this study is to evaluate the hearing loss of police officers in relation to the occupational risk factors and clinical-anamnestic characteristics by collecting and analyzing existing data and evidence available in public databases.
MATERIALS AND METHODS
A systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses group (PRISMA). Studies were included if they met inclusion and exclusion criteria. Study selection, data extraction, and quality assessment were conducted independently by two researchers.
RESULTS
Our initial literature search yielded 29 peer-reviewed articles. Out of 29 papers, only 10 were included in the review, after inclusion and exclusion criteria were applied the.
CONCLUSIONS
Hypertension, smoking and alcohol intake significantly affect hearing performance. In addition, a history of acoustic trauma, use of ototoxic drugs, exposure to noise in leisure-time activities and failure to use ear protectors are often found in a fair number of subjects. NIHL is also related to the age of the subjects as well as the extent and duration of noise exposure. Furthermore, NIHL is also influenced by shooting practice sessions police officers are required to undertake as well as by the chronic exposure to traffic noise, especially in motorcycle police officers.
PubMed: 36246192
DOI: 10.22038/IJORL.2022.64036.3198 -
Antioxidants (Basel, Switzerland) Apr 2019Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing... (Review)
Review
Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing loss, as well as hearing loss due to mitochondrial gene mutation. Mitochondria are the main sources of reactive oxygen species (ROS) and ROS-induced oxidative stress is involved in cochlear damage. Moreover, the release of ROS causes further damage to mitochondrial components. Antioxidants are thought to counteract the deleterious effects of ROS and thus, may be effective for the treatment of oxidative stress-related diseases. The administration of mitochondria-targeted antioxidants is one of the drug delivery systems targeted to mitochondria. Mitochondria-targeted antioxidants are expected to help in the prevention and/or treatment of diseases associated with mitochondrial dysfunction. Of the various mitochondria-targeted antioxidants, the protective effects of MitoQ and SkQR1 against ototoxicity have been previously evaluated in animal models and/or mouse auditory cell lines. MitoQ protects against both gentamicin- and cisplatin-induced ototoxicity. SkQR1 also provides auditory protective effects against gentamicin-induced ototoxicity. On the other hand, decreasing effect of MitoQ on gentamicin-induced cell apoptosis in auditory cell lines has been controversial. No clinical studies have been reported for otoprotection using mitochondrial-targeted antioxidants. High-quality clinical trials are required to reveal the therapeutic effect of mitochondria-targeted antioxidants in terms of otoprotection in patients.
PubMed: 31022870
DOI: 10.3390/antiox8040109 -
European Journal of Hospital Pharmacy :... Jul 2023Updated European Committee on Antimicrobial Susceptibility Testing (EUCAST) amikacin breakpoints for Enterobacterales and included revised dosing recommendations of... (Review)
Review
BACKGROUND
Updated European Committee on Antimicrobial Susceptibility Testing (EUCAST) amikacin breakpoints for Enterobacterales and included revised dosing recommendations of 25-30 mg/kg to achieve key pharmacokinetic/pharmacodynamic parameters, higher than recommended in the British National Formulary. The objectives of this review were to identify clinical evidence for high-dose amikacin regimens and to determine drug exposures that are related to adverse events and toxicity.
METHODS
The literature search was conducted in October 2021 and updated in May 2022 using electronic databases for any study reporting adult participants treated with amikacin at doses ≥20 mg/kg/day. Reference lists of included papers were also screened for potential papers. Data were extracted for pharmacokinetic parameters and clinical outcomes, presented in a summary table and consolidated narratively. Meta-analysis was not possible. Each study was assessed for bias before, during and after the intervention using the ROBINS-I tool.
RESULTS
Nine studies (total 501 participants in 10 reports) were identified and included, eight of which were observational studies. Assessment of bias showed substantial flaws. Dosing regimens ranged from 25 to 30 mg/kg/day. Six studies adjusted the dose in obesity when participants had a body mass index of ≥30 kg/m. Target peak serum concentrations ranged from 60 mg/L to 80 mg/L and 59.6-81.8% of patients achieved these targets, but there was no information on clinical outcomes. Two studies reported the impact of high-dose amikacin on renal function. No studies reporting auditory or vestibular toxicity were identified.
CONCLUSION
All included papers were limited by a significant risk of bias, while methodological and reporting heterogeneity made drawing conclusions challenging. Lack of information on the impact on renal function or ototoxicity means high-dose regimens should be used cautiously in older people. There is a need for a consensus guideline for high-dose amikacin to be written.
TRIAL REGISTRATION NUMBER
PROSPERO (CRD42021250022).
Topics: Adult; Aged; Humans; Amikacin; Clinical Protocols
PubMed: 36344247
DOI: 10.1136/ejhpharm-2022-003421 -
Discovery Medicine 2015Cisplatin-based chemoradiation (CRT) offers head and neck squamous cell carcinoma (HNSCC) patients better overall survival when compared to radiation alone. However, it... (Review)
Review
BACKGROUND
Cisplatin-based chemoradiation (CRT) offers head and neck squamous cell carcinoma (HNSCC) patients better overall survival when compared to radiation alone. However, it also increases acute and late toxicity (LT). Here we aimed to review the main aspects of diagnosis and treatment of long-term toxicities in HNSCC patients after CRT.
METHODS
We crossed-searched PubMed MeshTerms: Survivors, Deglutition Disorders, Xerostomia, Hypothyroidism, Cisplatin, Kidney, Hearing, and Osteoradionecrosis, with keywords: "Head and Neck Neoplasms" and "Chemoradiotherapy." A total of 5,541 publications were retrieved and 48 were selected for this systematic review.
RESULTS
Dysphagia (25%), xerostomia (40-80%, depending on the technique used), hypothyroidism (42%), ototoxicity (27%), and osteoradionecrosis (4%) were the most commonly reported LT and were related to compromised quality of life aspects in HNSCC patients. Concurrent cisplatin and higher radiation doses, especially to normal tissue, increased the rates of LT.
CONCLUSIONS
Late CRT toxicities were reported mostly in retrospective studies. Addressing these adverse effects as endpoints in future clinical trials is necessary to provide tools to prevent and treat them adequately, allowing better quality of life and survival results.
Topics: Carcinoma, Squamous Cell; Chemoradiotherapy; Cisplatin; Head and Neck Neoplasms; Humans
PubMed: 26321088
DOI: No ID Found -
Critical Reviews in Oncology/hematology Mar 2019Tinnitus can occur during and after treatment for childhood cancer. Studies on the occurrence of, and risk factors for tinnitus during and after childhood cancer...
BACKGROUND
Tinnitus can occur during and after treatment for childhood cancer. Studies on the occurrence of, and risk factors for tinnitus during and after childhood cancer treatment are scarce. The aim of this study is to get insight into the frequency and risk factors of tinnitus during and after childhood cancer therapy, based on a review of all previously reported literature.
MATERIALS AND METHODS
Systematic electronic literature searches that combined childhood cancer with different treatments and tinnitus terms were performed in the databases EMBASE, Medline, Cochrane, Web of Science, and Google Scholar. Studies were included based on reporting the frequency of tinnitus during and/or after childhood cancer, with 75% of participants being under the age of 25 at time of diagnosis, diagnosed with any type of childhood malignancy and treated with any type of chemotherapy and/or radiotherapy. A risk of bias assessment per research question was performed.
RESULTS
Tinnitus incidence rates were reported up to 15.9 (95% CI 11.8-21.4) during therapy and up to 5.4 (95% CI 4.3-6.9) more than 5 years after diagnosis. The relative risk of developing tinnitus as compared to siblings during and after childhood cancer therapy were reported up to 17.2 (95% CI 11.8-25.0) during therapy and up to 3.7 (95% CI 2.7-5.1) more than 5 years after diagnosis. Independent risk factors for tinnitus development included high dose cranial radiation and platinum based chemotherapy.
CONCLUSION
The frequency of and risk to develop tinnitus seems to be higher in childhood cancer patients and survivors as compared to the normal population. Regular tinnitus screening before, during and after therapy with standardized questionnaires for early detection seems therefore reasonable in order to identify high-risk patients and eventually develop successful clinical preventive, supportive and management strategies.
Topics: Antineoplastic Agents; Cancer Survivors; Child; Cranial Irradiation; Humans; Incidence; Neoplasms; Platinum Compounds; Risk Factors; Tinnitus
PubMed: 30819438
DOI: 10.1016/j.critrevonc.2019.01.004 -
International Journal of Audiology Sep 2018Define clinical trials and adverse event (AE) monitoring from the perspective of the audiologist. Rationalise the importance of audiology's involvement before, during...
OBJECTIVES
Define clinical trials and adverse event (AE) monitoring from the perspective of the audiologist. Rationalise the importance of audiology's involvement before, during and after monitoring. Identify strengths and weaknesses in toxicity grading scales, and discuss factors that may influence these.
DESIGN
Literature involving commonly cited grading scales used to capture ototoxicity is reviewed. Current regulations and language associated with clinical trial implementation and AE monitoring are described. Personal observations based on a variety of clinical populations are drawn from years of experience developing and employing ototoxicity monitoring protocols in a complex medical setting.
RESULTS
Six commonly used grading scales for ototoxicity are systematically reviewed for strengths and weaknesses. Necessary considerations that inform selection of grading scales are presented. A review of and historical context for clinical trial development and AE monitoring is provided.
CONCLUSIONS
The audiologist's role in therapeutic decision making goes beyond collection of the audiogram. Clear communication to stakeholders in ototoxicity monitoring is paramount, and toxicity grading scales are one tool to facilitate this exchange. Various factors should be considered in advance of selecting the most appropriate scale to capture hearing loss, and no scale is without limitation.
Topics: Adverse Drug Reaction Reporting Systems; Age Factors; Attitude of Health Personnel; Audiologists; Clinical Decision-Making; Clinical Trials as Topic; Dose-Response Relationship, Drug; Drug Monitoring; Health Knowledge, Attitudes, Practice; Hearing; Hearing Loss; Hearing Tests; Humans; Predictive Value of Tests; Professional Role; Prognosis; Reproducibility of Results; Research Design; Risk Factors; Severity of Illness Index
PubMed: 29276851
DOI: 10.1080/14992027.2017.1417644 -
Antimicrobial Agents and Chemotherapy Aug 2022To systematically evaluate the relationships between vancomycin trough serum concentrations and clinical outcomes in children using meta-analysis. Several databases,... (Meta-Analysis)
Meta-Analysis
To systematically evaluate the relationships between vancomycin trough serum concentrations and clinical outcomes in children using meta-analysis. Several databases, including PubMed, Elsevier, Web of Science, EMBASE, Medline, clinicaltrials.gov, the Cochrane Library, and three Chinese databases (Wanfang Data, China National Knowledge Infrastructure, and SINOMED), were comprehensively searched to obtain research articles on vancomycin use in children from inception through December 2021. All studies were screened and evaluated using the Cochrane systematic review method. Then, the feature information was extracted for meta-analysis. The evaluated results included clinical efficacy, vancomycin-associated nephrotoxicity, hepatotoxicity, ototoxicity, mortality, and microbial clearance. A total of 35 studies involving 4820 children were included in the analysis. The meta-analysis showed that compared with children with vancomycin trough concentrations <10 μg/mL, those with vancomycin trough concentrations ≥10 μg/mL had a higher clinical efficacy rate [OR: 2.23, 95% CI: 1.29 to 3.84, = 0.004] and higher incidences of nephrotoxicity [OR: 2.76, 95% CI: 1.51 to 5.07, = 0.001], ototoxicity [OR: 1.87, 95% CI: 1.08 to 3.23, = 0.02] and microbial clearance [OR: 2.36, 95% CI: 1.53 to 3.64, = 0.0001]. All-cause mortality [OR: 1.07, 95% CI: 0.45 to 2.53, = 0.88] and hepatotoxicity [OR: 0.84, 95% CI: 0.46 to 1.53, = 0.57] were similar between the two groups. Subgroup analysis showed that compared with children with vancomycin trough concentrations of 10 to 15 μg/mL, those with vancomycin trough concentrations >15 μg/mL had a higher incidence of nephrotoxicity [OR: 2.64, 95% CI: 1.28 to 5.43, = 0.008], but there was no significant difference in clinical efficacy [OR: 0.85, 95% CI: 0.30 to 2.44, = 0.76]. A vancomycin trough concentration of 10 to 15 μg/mL can improve clinical efficacy in children. Additionally, avoidance of trough concentrations >15 μg/mL can reduce the incidence of adverse reactions.
Topics: Anti-Bacterial Agents; Chemical and Drug Induced Liver Injury; Child; Humans; Ototoxicity; Renal Insufficiency; Retrospective Studies; Vancomycin
PubMed: 35862741
DOI: 10.1128/aac.00138-22