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Increased Cardiovascular and Cancer Mortality after Radioiodine Treatment for Hyperthyroidism

Department of Internal Medicine (S.M., P.J., H.O., J.S.) and Research Unit (H.H.), Tampere University Hospital, FIN-33521 Tampere, Finland; Medical School (S.M., P.J.) and Tampere School of Public Health (H.H., A.A.), University of Tampere, FIN-33014 Tampere, Finland; and STUK-Radiation and Nuclear Safety Authority (A.A.), Research and Environmental Surveillance, FIN-00881 Helsinki, Finland

Address all correspondence and requests for reprints to: Saara Metso, M.D., Department of Internal Medicine, Tampere University Hospital, P.O. Box 2000, FIN-33521 Tampere, Finland. E-mail: saara.metso{at}pshp.fi.

Context: Patients treated with radioiodine (RAI) for hyperthyroidism have been reported to be at increased risk for death. It is not clear whether the increased mortality is due to hyperthyroidism itself or the effect of RAI.

Objective: Our objective was to compare the mortality of hyperthyroid patients treated with RAI with that of an age- and gender-matched reference population.

Design: We conducted a population-based cohort study.

Participants: A total of 2793 patients who received RAI treatment for hyperthyroidism in Tampere University Hospital between 1965 and 2002, and 2793 reference subjects were followed for a median of 9 yr.

Results: Record linkage with Statistics Finland identified all-cause mortality of 453 vs. 406 per 10,000 person-years in the patients and controls [rate ratio (RR) 1.12; 95% confidence interval 1.03–1.20]. Cerebrovascular diseases accounted for most of the increased mortality among patients (RR 1.40), and mortality from cancer increased (RR 1.29) as well. The risk of death increased in patients older than 60 yr at treatment. Mortality increased with the dose of RAI and was elevated in patients with nodular thyroid disease, but not in those with Graves’ disease. Previous treatment with partial thyroidectomy decreased, whereas antithyroid medication did not affect mortality. In Cox regression analysis, RAI-treated hyperthyroidism (RR 1.56) and age (RR 1.10/1 yr) increased, and the development of hypothyroidism (RR 0.52) reduced mortality significantly.

Conclusions: Hyperthyroidism per se probably accounts for the increased cerebrovascular mortality after RAI treatment. Our results of increased cerebrovascular and cancer mortality emphasize the need for long-term vigilance concerning patients treated with RAI.

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