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Understanding Cisplatin-Induced Hearing Loss

Understanding Cisplatin-Induced Ototoxicity

Unfortunately, at commonly used doses and administration schedules, Cisplatin frequently causes ototoxicity through progressive loss of outer and inner hair cells in the organ of Corti. This process appears to be mediated by reactive oxygen species and depletion of antioxidants in the microenvironment (Blakley et al, 2002; Rybak and Somani, 1999). Irreversible hearing loss, typically in the high frequency (4 to 8 kHz) and very high frequency (9 to 20 kHz) ranges, has been documented as early as following the first platinum chemotherapy dose. The hearing loss normally worsens, affecting progressively lower frequencies in a cumulative, dose-dependent fashion (Berg et al, 1999; Punnett et al, 2004; Bertolini et al, 2004). Factors that significantly increase a child’s risk for moderate to severe hearing loss include age < 5 years at treatment and a cumulative CIS dose of ≥ 400 mg/m2 (Li et al, 2004). Cisplatin-induced hearing loss is often clinically significant, especially in young children who are critically dependent upon normal hearing for cognitive, psychosocial, and speech development (Gilmer-Knight et al, 2005; Fausti et al, 1993; Hindley, 1997).

In the U.S., it is estimated that over 3,000 children receive platinum based chemotherapy for localized cancers and globally approximately 10,000.  Of these, 40% to 90% develop profound and irreversible ototoxicity.  The incidence of hearing loss in these children depends upon the dose and duration of chemotherapy, and many of these children require lifelong hearing aids. There is currently no established preventive agent for this hearing loss and only expensive, technically difficult and sub-optimal cochlear (inner ear) implants have been shown to provide some benefit. Infants and young children at critical stages of development lack speech language development and literacy, and older children and adolescents lack social-emotional development and educational achievement.

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