Lugol’s solution and other iodide preparations: perspectives and research directions in Graves’ disease

Calissendorff, Jan; Falhammar, Henrik

doi:10.1007/s12020-017-1461-8

Cited by 41 publications

(35 citation statements)

References 57 publications

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“…On the other side, applying our model 1 for cases of acute or continuous exposure seems to indicate that protective efficacy could be improved by increasing the dosage of stable iodine over the usually recommended dose of 100 mg. Lugol's solution has been used for a long time in patients planned for thyroidectomy and historically Plummer used 80-320 mg daily for 10 days as a well established treatment [59]. Even higher daily dosages up to 800 mg daily have been reported in the literature [60,61]. However, for the purpose of iodine blockade aimed at a large heterogeneous population including vulnerable persons without prior individual medical assessment the systemic chemical toxicity of iodine should be carefully considered.…”

Section: Iodine Dosagementioning

confidence: 99%

Development of New Biokinetic-Dosimetric Models for the Simulation of Iodine Blockade in the Case of Radioiodine Exposure in Man

et al. 2019

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In the case of nuclear incidents, radioiodine may be liberated. After incorporation it accumulates in the thyroid and by internal irradiation enhances the risk of cancer occurrence. By administering a large dose of non-radioactive iodine the uptake of radioiodine into the gland can be inhibited (“iodine blockade”). Biokinetic models using first order kinetics are not suited to simulate iodine blockade, as the uptake into the gland is mediated by a saturable active transport. Therefore, we integrated an uptake mechanism described by a Michaelis-Menten kinetic into a simple ICRP biokinetic model. We moreover added a total uptake blocking mechanism representing the Wolff-Chaikoff effect becoming active when the gland is saturated with iodine. The validity of the model was ascertained by comparison with IMBA software. The competition of radioiodine and stable iodine at the membrane carrier site was modeled according to the rate law for monomolecular reactions for competing substrates. Our simulations show that competition for the uptake at the membrane carrier site accounts for about 60% and the saturation of the gland with iodine for over 35% of the total protective efficacy that exceeds 95%. Following acute radioiodine exposure, it is preferable to administer a single large dose of stable iodine. In the case of continuous radioiodine exposure, a single dose of stable iodine is less effective than after an acute exposure and splitting the total available dose and shortening the dosage intervals enhance efficacy. Model-based simulations may be a useful tool to develop antidote dosage schemes for uncommon emergencies.

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Section: Iodine Dosagementioning

confidence: 99%

Development of New Biokinetic-Dosimetric Models for the Simulation of Iodine Blockade in the Case of Radioiodine Exposure in Man

et al. 2019

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“…Therefore, it seems prudent to take into account well-documented experiences from treatments with iodine or drugs containing and liberating iodine, e.g., amiodarone. High doses up to several hundred mg of iodine per day up to several weeks have been used for the treatment of Grave’s disease and/or prior to thyroidectomy (Calissendorf et al 2017 ). Historically, Plummer used 80–320 mg daily for 10 days (Plummer 1924 ).…”

Section: Discussionmentioning

confidence: 99%

A comparison of thyroidal protection by stable iodine or perchlorate in the case of acute or prolonged radioiodine exposure

et al. 2020

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In the case of a nuclear power plant accident, repetitive/prolonged radioiodine release may occur. Radioiodine accumulates in the thyroid and by irradiation enhances the risk of cancer. Large doses of non-radioactive iodine may protect the thyroid by inhibiting radioiodine uptake into the gland (iodine blockade). Protection is based on a competition at the active carrier site in the cellular membrane and the Wolff–Chaikoff effect, the latter being, however, only transient (24–48 h). Perchlorate may alternatively provide protection by a carrier competition mechanism only. Perchlorate has, however, a stronger affinity to the carrier than iodide. Based on an established biokinetic–dosimetric model developed to study iodine blockade, and after its extension to describe perchlorate pharmacokinetics and the inhibition of iodine transport through the carrier, we computed the protective efficacies that can be achieved by stable iodine or perchlorate in the case of an acute or prolonged radioiodine exposure. In the case of acute radioiodine exposure, perchlorate is less potent than stable iodine considering its ED 50. A dose of 100 mg stable iodine has roughly the same protective efficacy as 1000 mg perchlorate. For prolonged exposures, single doses of protective agents, whether stable iodine or perchlorate, offer substantially lower protection than after acute radioiodine exposure, and thus repetitive administrations seem necessary. In case of prolonged exposure, the higher affinity of perchlorate for the carrier in combination with the fading Wolff–Chaikoff effect of iodine confers perchlorate a higher protective efficacy compared to stable iodine. Taking into account the frequency and seriousness of adverse effects, iodine and perchlorate at equieffective dosages seem to be alternatives in case of short-term acute radioiodine exposure, whereas preference should be given to perchlorate in view of its higher protective efficacy in the case of longer lasting radioiodine exposures.

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“…Potassium iodine has been used as a beneficial adjunct to ATDs therapy for Graves' disease, because it attenuates organification and release of thyroid hormones as well as thyroid vascularity and intraoperative blood loss during thyroidectomy (Calissendorff & Falhammar 2017). Compared with MMI alone, potassium iodine together with MMI results in better control of thyrotoxicosis and fewer adverse reactions.…”

Section: Treatmentmentioning

confidence: 99%

Thyrotoxicosis with concomitant thyroid cancer

Cheng

Jin

et al. 2019

Endocrine-Related Cancer

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Thyrotoxicosis with concomitant thyroid cancer is rare and poorly recognized, which may result in delayed diagnosis, inappropriate treatment and even poor prognosis. To provide a comprehensive guidance for clinicians, the etiology, pathogenesis, diagnosis and treatment of this challenging setting were systematically reviewed. According to literatures available, the etiologies of thyrotoxicosis with concomitant thyroid cancer were categorized into Graves’ disease with concurrent differentiated thyroid cancer (DTC) or medullary thyroid cancer, Marine–Lenhart Syndrome with coexisting DTC, Plummer’s disease with concomitant DTC, amiodarone-induced thyrotoxicosis with concomitant DTC, central hyperthyroidism with coexisting DTC, hyperfunctioning metastases of DTC and others. The underlying causal mechanisms linking thyrotoxicosis and thyroid cancer were elucidated. Medical history, biochemical assessments, radioiodine uptake, anatomic and metabolic imaging and ultrasonography-guided fine-needle aspiration combined with pathological examinations were found to be critical for precise diagnosis. Surgery remains a mainstay in both tumor elimination and control of thyrotoxicosis, while anti-thyroid drugs, beta-blockers, 131I, glucocorticoids, plasmapheresis, somatostatin analogs, dopamine agonists, radiation therapy, chemotherapy and tyrosine kinase inhibitors should also be appropriately utilized as needed.

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Lugol’s solution and other iodide preparations: perspectives and research directions in Graves’ disease

Cited by 41 publications

References 57 publications

Development of New Biokinetic-Dosimetric Models for the Simulation of Iodine Blockade in the Case of Radioiodine Exposure in Man

Development of New Biokinetic-Dosimetric Models for the Simulation of Iodine Blockade in the Case of Radioiodine Exposure in Man

A comparison of thyroidal protection by stable iodine or perchlorate in the case of acute or prolonged radioiodine exposure

Thyrotoxicosis with concomitant thyroid cancer

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