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Department of Clinical Pharmacology, Bispebjerg Hospital
Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
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Background: Little is known about the whole body oxidative stress burden following radioactive iodine (<sup>131</sup>I) therapy of thyroid diseases. Methods: We studied 17 patients with benign nodular goiter treated with <sup>131</sup>I therapy. The targeted thyroid dose was 50 Gy in 11 patients pretreated with 0.1 mg of recombinant human TSH (rhTSH). In 6 patients, the applied thyroid dose was 100 Gy without rhTSH prestimulation. Well-established biomarkers of oxidative stress to RNA (8-oxo-7,8-dihydroguanosine; 8-oxoGuo) and DNA (8-oxo-7,8-dihydro-2'-deoxyguanosine; 8-oxodG) were measured in freshly voided morning urine (normalized against the creatinine concentration) at baseline, and 7 and 21 days after rhTSH (not followed by <sup>131</sup>I), and 7 and 21 days after <sup>131</sup>I therapy, respectively. Results: The baseline urinary excretions of 8-oxoGuo and 8-oxodG were 2.20 ± 0.84 and 1.63 ± 0.70 nmol/mmol creatinine, respectively. We found no significant changes in the excretion of any of the metabolites, neither after rhTSH stimulation alone nor after <sup>131</sup>I therapy. Also, no significant differences were found between the rhTSH group (low dose, median <sup>131</sup>I: 152 MBq) and the non-rhTSH group (high dose, median <sup>131</sup>I: 419 MBq; 8-oxoGuo: p = 0.66, 8-oxodG: p = 0.71). Conclusion: Systemic oxidative stress, as detected by nucleic acids metabolites in the urine, is not increased after thyroid stimulation with 0.1 mg of rhTSH, or after <sup>131</sup>I therapy. Our method cannot quantify the oxidative stress induced locally in the thyroid gland, but the study supports that <sup>131</sup>I therapy of benign nodular goiter carries no or only a minute risk of developing subsequent malignancies. It remains to be explored whether our findings also apply to hyperthyroid disorders.
