Abstract

Platinum-based treatments can trigger ototoxicity during cancer treatment. Patients commonly develop bilateral, irreversible sensorineural hearing loss, which is especially critical in the pediatric population, requiring long-term follow-up due to potential detrimental hearing-loss effects on language and social development. The prevalence of ototoxicity following platinum-based chemotherapy in this group is not well established, but incidences as high as 90% have been reported. Among the adult population, it has been reported that up to 80% of patients may develop ototoxicity. Thus, this condition may be an important cause of decreasing quality of life in cancer survivors. From a clinical point of view, ototoxicity induced by platinum-based chemotherapy exhibits auditory manifestations as well as vestibular symptoms and tinnitus. Ototoxicity can clinically manifest within hours to days following the first chemotherapy cycle or even years after treatment. High-frequency hearing loss typically occurs first, and it can evolve to involve middle frequencies in a dose-dependent manner. Mechanistically, platinum-based chemotherapy induced ototoxicity is mainly caused from the production of pathological levels of reactive oxygen species (ROS) rather than DNA-adduct formation, which has led to test strategies based on direct ROS scavengers to ameliorate hearing loss. Clinically controversial data have been obtained from several trials and thus have increased interest in the development of strategies to protect patients from ototoxicity without altering the anticancer effects of platinum-based treatments.