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      Misdiagnosis of Paraganglioma by 123I-mIBG Without Stable Iodine Blockade of Thyroidal Radioiodine Uptake

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          Abstract

          Iodine-123/iodine-131 ( 123I/ 131I)-metaiodobenzylguanidine (mIBG) scan is an established tool for the localization and treatment of neuroendocrine tumors such as paragangliomas (PGL). To minimize thyroid irradiation by the radioactive iodine in the mIBG preparation, blockade of thyroidal iodine uptake with high doses of stable iodine used to be given routinely as part of all mIBG protocols. As 123I is now more frequently utilized than 131I, concern about thyroid radiation has lessened and thyroid blockade is often considered unnecessary. However, in certain situations, the lack of thyroid blockade can significantly impact treatment decisions. This report describes 2 patients who had mediastinal masses incidentally discovered on CT scans, and on further evaluation were found to have symptoms suggesting catecholamine excess with mildly elevated plasma normetanephrine levels. 123I-mIBG scans were performed without thyroid blockade, which demonstrated accumulation of tracer in the masses that were therefore deemed positive for PGL. Both patients underwent surgical resection of the masses with their surgical pathology revealing ectopic thyroid tissue (ETT). These cases illustrate that if appropriate thyroid blockade is not performed, ETT concentrating radioiodine from mIBG can lead to falsely positive mIBG scans and unnecessary surgical procedures. We conclude that in the setting of a mass suspicious for PGL in a location potentially representing ETT, such as the mediastinum, thyroid blockade should be employed for mIBG protocols to avoid false positive scans caused by ETT.

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          Most cited references16

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          Plasma inorganic iodide as a homeostatic regulator of thyroid function.

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            Escape from the acute Wolff-Chaikoff effect is associated with a decrease in thyroid sodium/iodide symporter messenger ribonucleic acid and protein.

            In 1948, Wolff and Chaikoff reported that organic binding of iodide in the thyroid was decreased when plasma iodide levels were elevated (acute Wolff-Chaikoff effect), and that adaptation or escape from the acute effect occurred in approximately 2 days, in the presence of continued high plasma iodide concentrations. We later demonstrated that the escape is attributable to a decrease in iodide transport into the thyroid, lowering the intrathyroidal iodine content below a critical inhibitory threshold and allowing organification of iodide to resume. We have now measured the rat thyroid sodium/iodide symporter (NIS) messenger RNA (mRNA) and protein levels, in response to both chronic and acute iodide excess, in an attempt to determine the mechanism responsible for the decreased iodide transport. Rats were given 0.05% NaI in their drinking water for 1 and 6 days in the chronic experiments, and a single 2000-microg dose of NaI i.p. in the acute experiments. Serum was collected for iodine and hormone measurements, and thyroids were frozen for subsequent measurement of NIS, TSH receptor, thyroid peroxidase (TPO), thyroglobulin, and cyclophilin mRNAs (by Northern blotting) as well as NIS protein (by Western blotting). Serum T4 and T3 concentrations were significantly decreased at 1 day in the chronic experiments and returned to normal at 6 days, and were unchanged in the acute experiments. Serum TSH levels were unchanged in both paradigms. Both NIS mRNA and protein were decreased at 1 and 6 days after chronic iodide ingestion. NIS mRNA was decreased at 6 and 24 h after acute iodide administration, whereas NIS protein was decreased only at 24 h. TPO mRNA was decreased at 6 days of chronic iodide ingestion and 24 h after acute iodide administration. There were no iodide-induced changes in TSH receptor and thyroglobulin mRNAs. These data suggest that iodide administration decreases both NIS mRNA and protein expression, by a mechanism that is likely to be, at least in part, transcriptional. Our findings support the hypothesis that the escape from the acute Wolff-Chaikoff effect is caused by a decrease in NIS, with a resultant decreased iodide transport into the thyroid. The observed decrease in TPO mRNA may contribute to the iodine-induced hypothyroidism that is common in patients with Hashimoto's thyroiditis.
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              EANM procedure guidelines for 131I-meta-iodobenzylguanidine (131I-mIBG) therapy.

              Meta-iodobenzylguanidine, or Iobenguane, is an aralkylguanidine resulting from the combination of the benzyl group of bretylium and the guanidine group of guanethidine (an adrenergic neurone blocker). It is a noradrenaline (norepinephrine) analogue and so-called "false" neurotransmitter. This radiopharmaceutical, labeled with 131I, could be used as a radiotherapeutic metabolic agent in neuroectodermal tumours, that are derived from the primitive neural crest which develops to form the sympathetic nervous system. The neuroendocrine system is derived from a family of cells originating in the neural crest, characterized by an ability to incorporate amine precursors with subsequent decarboxylation. The purpose of this guideline is to assist nuclear medicine practitioners to evaluate patients who might be candidates for 131I-meta-iodobenzylguanidine to treat neuro-ectodermal tumours, to provide information for performing this treatment and to understand and evaluate the consequences of therapy.
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                Author and article information

                Contributors
                Journal
                J Endocr Soc
                J Endocr Soc
                jes
                Journal of the Endocrine Society
                Oxford University Press (US )
                2472-1972
                01 September 2020
                17 July 2020
                17 July 2020
                : 4
                : 9
                : bvaa099
                Affiliations
                [1 ] Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine , Baltimore, Maryland
                [2 ] Department of Pathology, The Johns Hopkins University School of Medicine , Baltimore, Maryland
                Author notes
                Correspondence:  Stanley Chen Cardenas, MD, Division of Endocrinology, Diabetes, and Metabolism, Johns Hopkins University School of Medicine, 1830 E. Monument Street, Suite 333, Baltimore, Maryland 21217. E-mail: schenca1@ 123456jhmi.edu , stanmc14@ 123456gmail.com
                Author information
                http://orcid.org/0000-0001-7719-4729
                http://orcid.org/0000-0002-4392-3206
                http://orcid.org/0000-0001-5636-9753
                http://orcid.org/0000-0003-4822-2705
                http://orcid.org/0000-0002-9406-6400
                http://orcid.org/0000-0002-9737-7159
                Article
                bvaa099
                10.1210/jendso/bvaa099
                7414919
                5591282c-56b0-48e0-a47a-908f06db135c
                © Endocrine Society 2020.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 11 May 2020
                : 13 July 2020
                : 08 August 2020
                Page count
                Pages: 9
                Categories
                Case Reports
                AcademicSubjects/MED00250

                131i/123i-metaiodobenzylguanidine,ectopic thyroid tissue,paraganglioma metanephrine,normetanephrine

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