Subsequent studies have shown similar benefit when STS is administered intravenously to humans. Several studies have demonstrated the otoprotective effects of intravenous STS in animal models. The thiol compound may also act to scavenge reactive oxygen species produced by the platinum, thus preventing the initiation of the apoptotic pathway. The chelating properties of the sulfur-thiol functional group are believed to be responsible for the otoprotective effects of STS, binding to, and inactivating the platinum. STS has been shown to act as both an antioxidant as well as a chelating agent in vivo. STS is approved by the US Food and Drug Administration (FDA) as an antidote for cyanide and nitroprusside toxicity and for calciphylaxis. Among these, sodium thiosulfate (STS) has shown particular promise as an otoprotective agent. These numbers are higher for those receiving high dose cisplatin, children, those with prior irradiation and those with prior hearing loss.Ī number of agents have been investigated in animal models as otoprotection against the toxic effects of cis- and carboplatin.
Rates of ototoxicity are approximately 80% with audiologic findings of hearing loss, and 20% with symptomatic hearing loss. Cisplatin causes ototoxicity through the formation of reactive oxygen species and activation of the apoptotic pathway in outer hair cells and the stria vascularis.
Vestibular function can also be damaged by platinum-based toxicity.
With increasing doses, the hearing loss worsens to include the speech frequencies. Cisplatin is associated with a dose-dependent, high frequency sensorineural hearing loss. Examples of such tumors include: osteosarcoma, Wilms' tumor, rhabdomyosarcoma, neuroblastoma, Ewing's sarcoma, primary brain tumors, carcinoma, and various other solid tumors. Platinum-based chemotherapeutic agents are used to treat a number of malignant tumors, both in children and adults. Why Should I Register and Submit Results?.
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