REVIEW  UPDATE ON DIAGNOSIS AND TREATMENT OF HYPERTHYROIDISM 

The Quarterly Journal of Nuclear Medicine and Molecular Imaging 2021 June;65(2):132-7

DOI: 10.23736/S1824-4785.21.03337-9

Copyright © 2021 EDIZIONI MINERVA MEDICA

language: English

Radioiodine therapy of Graves’ disease

Arnoldo PICCARDO ¹ ✉, Martina UGOLINI ¹, Vania ALTRINETTI ¹, Sergio RIGHI ², Francesco FIZ ³, Luca FOPPIANI ⁴, Luca GIOVANELLA ⁵

¹ Department of Nuclear Medicine, E.O. Ospedali Galliera, Genoa, Italy; ² Department of Medical Physics, E.O. Ospedali Galliera, Genoa, Italy; ³ Humanitas Clinical and Research Center, Rozzano, Milan, Italy; ⁴ Department of Internal Medicine, E.O. Ospedali Galliera, Genoa, Italy; ⁵ Clinic of Nuclear Medicine and Molecular Imaging, Imaging Institute of Southern Switzerland, Bellinzona, Switzerland

Graves’ disease (GD), the most common cause of hyperthyroidism, is an autoimmune disease directly caused by circulating autoantibodies that bind and activate the TSH receptor, inducing metabolic activation of the thyroid gland; this may be associated with important cardiac (atrial fibrillation) and ocular (ophthalmopathy) complications. Treating GD with real curative intent implies the full elimination of the functioning thyroid parenchyma using surgery or radioactive iodine therapy (RAI). RAI has been used in humans with hyperthyroidism since 1941, thanks to the pioneering work of a physician (Dr. Saul Hertz) and a physicist (Dr. Arthur Roberts). The rationale of RAI is based on the effect of radiation of ¹³¹I on target cells leading to DNA damage, both directly, through breakage of molecular bonds, and indirectly through the formation of free radicals. In particular, irradiation causes a broad spectrum of cellular damage due to the production of reactive oxygen species and lipid peroxidation of the plasma membrane. Thus, RAI-related cellular death takes place through both apoptosis and necrosis. The aim of this review was to summarize indications, efficacy, safety profile, and dosimetric aspects of RAI treatment in patients affected by GD.

KEY WORDS: Iodohippuric acid; Hyperthyroidism; Therapeutics; Review