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Risk factors contributing to the development of carboplatin-related delayed hypersensitivity reactions in Japanese patients with gynecologic cancers

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Abstract

Purpose

The rate of hypersensitivity reactions in patients receiving carboplatin (CBDCA) has been reported to increase after multiple doses of the agent. However, risk factors for these onsets have not been well described. In this study, we investigated the contribution of the reported risk factors to the onset of CBDCA-related delayed hypersensitivity reactions.

Methods

We reviewed the records of gynecologic cancer patients receiving CBDCA of more than 7 cycles in Mie University Hospital from March 2006 to July 2009. The patients were divided into two groups on the basis of whether hypersensitivity reactions developed (13 patients) or not (43 patients). Thereafter, the potential influences of the patients’ characteristics on the development of CBDCA-related delayed hypersensitivity reactions were explored using logistic regression analyses.

Results

The median CBDCA-free interval (10 months) in patients with hypersensitivity reactions was significantly higher than that (3 months) in patients without hypersensitivity reactions. Logistic regression analyses revealed a CBDCA-free interval >13 months (odds ratio 22.2, 95% confidence interval 2.57–192, p < 0.01) and a maximum dose of CBDCA > 650 mg (odds ratio 9.52, 95% confidence interval 1.04–93.9; p < 0.05) were significantly correlated with the incidence of CBDCA-related delayed hypersensitivity reactions.

Conclusions

Careful attention should be paid to the onset of delayed hypersensitivity reactions for recurrent gynecologic cancer patients receiving CBDCA > 650 mg after an interval of more than 13 months from the previous CBDCA administration.

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No author has any conflict of interest.

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Correspondence to Masahiro Okuda.

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Sugimoto, H., Iwamoto, T., Murashima, Y. et al. Risk factors contributing to the development of carboplatin-related delayed hypersensitivity reactions in Japanese patients with gynecologic cancers. Cancer Chemother Pharmacol 67, 415–419 (2011). https://doi.org/10.1007/s00280-010-1338-5

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  • DOI: https://doi.org/10.1007/s00280-010-1338-5

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