Modeling the absorbed dose to the common carotid arteries following radioiodine treatment of benign thyroid disease

Jeppe Lerche la Cour, Per Hedemann-Jensen, Jens Søgaard-Hansen, Birte Nygaard, Lars Thorbjørn Jensen

4 Citationer (Scopus)

Abstract

Introduction: External fractionated radiotherapy of cancer increases the risk of cardio- and cerebrovascular events, but less attention has been paid to the potential side effects on the arteries following internal radiotherapy with radioactive iodine (RAI), i.e. 131-iodine. About 279 per million citizens in the western countries are treated each year with RAI for benign thyroid disorders (about 140,000 a year in the EU), stressing that it is of clinical importance to be aware of even rare radiation-induced side effects. In order to induce or accelerate atherosclerosis, the dose to the carotid arteries has to exceed 2 Gy which is the known lower limit of ionizing radiation to affect the endothelial cells and thereby to induce atherosclerosis. Objective: To estimate the radiation dose to the carotid arteries following RAI therapy of benign thyroid disorders. Methods: Assuming that the lobes of the thyroid gland are ellipsoid, that the carotid artery runs through a part of the lobes, that there is a homogeneous distribution of RAI in the lobes, and that the 24 h RAI uptake in the thyroid is 35 % of the 131I orally administrated, we used integrated modules for bioassay analysis and Monte Carlo simulations to calculate the dose in Gy/GBq of administrated RAI. Results: The average radiation dose along the arteries is 4-55 Gy/GBq of the 131I orally administrated with a maximum dose of approximately 25-85 Gy/GBq. The maximum absorbed dose rate to the artery is 4.2 Gy/day per GBq 131I orally administrated. Conclusion: The calculated radiation dose to the carotid arteries after RAI therapy of benign thyroid disorder clearly exceeds the 2 Gy known to affect the endothelial cells and properly induce atherosclerosis. This simulation indicates a relation between the deposited dose in the arteries following RAI treatment and an increased risk of atherosclerosis and subsequent cerebrovascular events such as stroke.

OriginalsprogEngelsk
TidsskriftAnnals of Nuclear Medicine
Vol/bind27
Udgave nummer9
Sider (fra-til)862-866
Antal sider5
ISSN0914-7187
DOI
StatusUdgivet - nov. 2013

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