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Vol. 286, Issue 1, 77-84, July 1998
Oregon Health Sciences University and Veterans Administration;
Portland, Oregon
Sodium thiosulfate (STS) provides protection against
carboplatin-induced ototoxicity in an animal model. The purpose of this study was to determine the STS dose required for otoprotection, in
patients with malignant brain tumors treated with carboplatin in
conjunction with osmotic blood-brain barrier disruption. Twenty-nine patients received STS intravenously 2 hr after carboplatin. Doses were
escalated from 4 g/m2 to 8, 12, 16 and 20 g/m2
on consecutive months. Audiologic assessment was performed at baseline
and monthly. The audiograms were compared with those of 19 similarly
treated historical control patients who did not receive STS. The
incidence of ototoxicity in the historical control group of patients
was 79% (15/19). This group had an average loss of 20.8 ± 5.9 dB
(n = 19) at 8 kHz after one treatment with
carboplatin, whereas the STS treatment group lost only 3.7 ± 2 dB
(n = 15) after one treatment. This difference was
statistically significant as assessed by Student's t
test (P < .05). Furthermore, patients in the STS treatment group
with excellent base-line hearing showed little change in hearing
thresholds at 8 kHz after the second treatment (8.0 ± 8.3 dB)
(n = 5) compared with the historical control
patients with excellent base-line hearing, (40.5 ± 8.6 dB)
(n = 11). Our data support that doses of 16 or 20 g/m2 of STS decrease carboplatin-induced hearing loss
without central nervous system entry. Clinical demonstration of an
otoprotective effect with a two-compartment system to prevent
drug-induced hearing loss, while preserving central nervous system
cytotoxicity, has not been reported previously.
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