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Association between N-desethylamiodarone/amiodarone ratio and amiodarone-induced thyroid dysfunction

  • Pharmacodynamics
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Abstract

Purpose

We used a retrospective data mining approach to explore the association between serum amiodarone (AMD) and N-desethylamiodarone (DEA) concentrations and thyroid-related hormone levels.

Methods

Laboratory data sets from January 2012 to April 2016 were extracted from the computerized hospital information system database at the National Cerebral and Cardiovascular Center (NCVC). Data sets that contained serum AMD and DEA concentrations and thyroid function tests, including thyroid-stimulating hormone (TSH), free thyroxine (FT4), and free triiodothyronine (FT3), were analyzed.

Results

A total of 1831 clinical laboratory data sets from 330 patients were analyzed. Data sets were classified into five groups (euthyroidism, hyperthyroidism, subclinical hyperthyroidism, hypothyroidism, and subclinical hypothyroidism) based on the definition of thyroid function in our hospital. Most abnormal levels of thyroid hormones were observed within the therapeutic range of serum AMD and DEA concentrations. The mean DEA/AMD ratio in the hyperthyroidism group was significantly higher than that in the euthyroidism group (0.95 ± 0.42 vs. 0.87 ± 0.28, p = 0.0209), and the mean DEA/AMD ratio in the hypothyroidism group was significantly lower than that in the euthyroidism group (0.77 ± 0.26 vs. 0.87 ± 0.28, p = 0.0038). The suppressed TSH group (0.98 ± 0.41 vs. 0.87 ± 0.28, p < 0.001) and the elevated FT4 level group (0.90 ± 0.33 vs. 0.84 ± 0.27, p = 0.0037) showed significantly higher DEA/AMD ratios compared with normal level groups. The elevated TSH group showed a significantly lower DEA/AMD ratio compared with the normal group (0.81 ± 0.25 vs. 0.87 ± 0.28, p < 0.0001).

Conclusions

High and low DEA/AMD ratios were associated with AMD-induced hyperthyroidism and hypothyroidism, respectively. The DEA/AMD ratio may be a predictive marker for AMD-induced thyroid dysfunction.

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Acknowledgements

None.

Authors’ contributions

Mitsutaka Takada conceived the study and design. Mikie Yamato, Kyoichi Wada, and Akira Oita acquired data. Mikie Yamato, Kyoichi Wada, and Mitsutaka Takada analyzed and interpreted data. Mikie Yamato, Kyoichi Wada, and Mitsutaka Takada drafted the manuscript. Mai Fujimoto, Kouichi Hosomi, and Tomohiro Hayashi revised the manuscript. Mikie Yamato and Mistukata Takada analyzed statistical data. Mistutaka Takada did supervision.

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Authors and Affiliations

  1. Division of Clinical Drug Informatics, School of Pharmacy, Kindai University, 3-4-1, Kowakae, Higashi-osaka, Osaka, 577-8502, Japan

    Mikie Yamato, Mai Fujimoto, Kouichi Hosomi & Mitsutaka Takada

  2. Department of Pharmacy, National Cerebral and Cardiovascular Center, Suita, Japan

    Mikie Yamato, Kyoichi Wada & Akira Oita

  3. Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan

    Tomohiro Hayashi

  4. Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan

    Tomohiro Hayashi

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  1. Mikie Yamato
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Correspondence to Mitsutaka Takada.

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The authors declare that they have no conflicts of interest.

Ethical approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. This study was approved by the Ethics Committees of the NCVC and Kindai University. For this type of study, formal consent is not required.

Additional information

This study was carried out in the Department of Pharmacy, National Cerebral and Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka, Japan.

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Yamato, M., Wada, K., Fujimoto, M. et al. Association between N-desethylamiodarone/amiodarone ratio and amiodarone-induced thyroid dysfunction. Eur J Clin Pharmacol 73, 289–296 (2017). https://doi.org/10.1007/s00228-017-2195-5

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  • DOI: https://doi.org/10.1007/s00228-017-2195-5

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