2018, Number 1
Rev Cubana Pediatr 2018; 90 (1)
Quintero NJ, Hernández CMC, de León ONE, Meléndez QL
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ABSTRACTIntroduction: hearing loss induced by ototoxic drugs was approached as a serious, frequent problem with an impact on the daily work of otolaryngologists and pediatricians. A review was conducted about the relationship of ototoxicity to aminoglycosides, antineoplastic treatments, salicylates, quinines and some diuretics.
Objective: analyze the most updated current approaches about ototoxicity, risk factors, genetic predisposition and prevention.
Methods: a retrospective review was conducted of the literature on the topic published in Spanish and English, as well as the most interesting and thoughtprovoking reports, from an open start date until February 2017, by means of a search on the Internet and in the databases Google, Cochrane and PubMed-MEDLINE.
Results: more than 100 papers were obtained. The exact ototoxicity mechanisms by aminoglycosides and cisplatin were an area of active research. An analysis was made of the relationship between ototoxicity and caspases 8, 9 and 3, essential mediators in the apoptosis of ciliated cells in the cochlea, and hearing loss. A description is provided of the relationship between mutations of the MTRNR1 gene, which codifies for the ribosomal subunit 12s, and hearing loss by ototoxicity. A connection was established with hearing loss and mitochondrial nonsyndromic deafness, exclusively maternal transmission, and increased susceptibility to ototoxicity by aminoglycosides, a key predisposing factor.
Final considerations: ototoxic drugs induce cochlear toxicity and bilaterally symmetric or asymmetric hearing loss at high frequencies, secondary to irreversible destruction of external ciliated cells in the organ of Corti. Recent research about cisplatin has identified the susceptible population, and may offer new, less aggressive treatment alternatives. Current criteria are presented about audiological surveillance and ototoxicity grades. Prevention implies strict surveillance.