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Thyroid Hormones and Calcium Metabolism
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Iodide in the blood is actively taken up into the thyroid follicular cells. The basolateral membrane has a secondary active transport system of iodide (via both Na+/I− co-transporters and Na+/K+-ATPase), which actively pumps iodide into the interior of the cell, a process called iodide trapping (Figure 62.1). The iodide pump concentrates the iodide to about 30 times its blood concentration. The transport mechanism is stimulated by TSH and inhibited by perchlorate and thiocyanate ions. A high circulating iodide concentration can also reduce the iodide trapping mechanism (Wolff–Chaikoff effect).
Drug-induced thyroid dysfunction
Published in David S. Cooper, Jennifer A. Sipos, Medical Management of Thyroid Disease, 2018
Victor Bernet, Robert C. Smallridge
Acute exposure to excess iodine leads to the Wolff-Chaikoff effect, a transient decline in thyroid hormone synthesis from thyroid peroxidase inhibition, resulting in decreased sodium-iodine symporter (NIS) activity, followed by an “escape” from this phenomenon and the resumption of thyroid hormone production (3, 4). Thyrotoxicosis related to iodine exposure is also known as the Jod-Basedow (Jod is German for iodine) phenomenon and typically occurs in patients with underlying thyroid disorders such as nodular goiter, a state of chronic iodine deficiency, or dormant Graves’ disease (5). Iodine-induced thyrotoxicosis may be either short-lived or chronic in nature (6).
Physiology of the Thyroid and Parathyroid Glands
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Excess iodide acutely inhibits the synthesis of thyroid hormones, the Wolff–Chaikoff effect.23 Possible mechanisms include inhibiting the production of H2 O2 and thus blocking the iodination of TG.24 Importantly, this effect is typically short-lived, often lasting for several days only (escape from the Wolff–Chaikoff effect). Thereafter, in patients with pre-existing goitre, excess iodine can cause severe thionamide-resistant thyrotoxicosis. Blocking an overactive thyroid with high-dose iodine before surgery is therefore not encouraged by all centres; if this procedure is chosen, thyroid surgery should be performed within the next few days. Thyrotoxic effects of excess iodine can also be observed in thyrotoxicosis type-1 induced by amiodarone (an antiarrhythmic drug that contains 75 000 Âεg of iodine per tablet) and in patients with goitre following the use of iodine-containing contrast medium when performing computer tomographic (CT) scans.
Stable thyroid function despite regular use of povidone-iodine throat spray for SARS-CoV-2 prophylaxis
Published in Annals of Medicine, 2022
Amy May Lin Quek, Mei Yen Ng, Ooiean Teng, Nicole-Ann Lim, Geelyn Jeng Lin Ng, Samantha Peiling Yang, Mikael Hartman, Paul Anantharajah Tambyah, Alex R. Cook, Raymond Chee Seong Seet
Our findings are consistent with one study that observed no change in thyroxine levels among 24 men following irrigation of the oral cavity with povidone-iodine compared with those who irrigated with chlorhexidine gluconate [21]. The lack of change in thyroid function suggests that any increase in circulatory iodine is likely compensated by the autoregulatory function known as the Wolff-Chaikoff effect which prevents thyroid tissues from synthesizing thyroid hormones despite the increased availability of iodine [22]. Although most povidone-iodine product labels caution against its use among individuals with thyroid disease, we did not observe differences in thyroid function between cases and controls in the lowest and highest TSH quartiles (Figure 2). Data from the current study support the overall safety of povidone-iodine use among those with subclinical thyroid disease which could argue against the need to screen prospective users for asymptomatic thyroid disease. Further studies are needed to examine the effect of povidone-iodine on thyroid function among those with symptomatic thyroid disease.
Modeling principles of protective thyroid blocking
Published in International Journal of Radiation Biology, 2022
Alexis Rump, Stefan Eder, Cornelius Hermann, Andreas Lamkowski, Manabu Kinoshita, Tetsuo Yamamoto, Junya Take, Michael Abend, Nariyoshi Shinomiya, Matthias Port
The Wolff-Chaikoff effect as the second protective mechanism is modeled by a total thyroidal net uptake block (‘switched on’ by setting Tmax at 0, i.e. no transport into the thyroid) becoming effective when the additional iodine content in the gland has reached the saturation level. This has been reported with + 350 µg (2.7581 µmol) (from 8000 µg total iodine content to 8350 µg) (Ramsden et al. 1967). We previously determined this amount with + 448 µg using the data from Blum and Eisenbud (1967), but much higher values have been reported for Japanese (+5000 µg, from 15,000 µg to saturation at 20,000 µg) (Matsunaga and Kobayashi 2001). During the time of total thyroidal uptake block, the renal excretion of iodide is going on unaffected. The thyroidal uptake block is terminated (’switched off’) after a defined period of time that is reasonably set between 24–48 h after onset. Different duration can be used for sensitivity analyses.
Serum thyroid-stimulating hormone receptor antibody levels and thyroid dysfunction after hysterosalpingography: a case-control study
Published in Gynecological Endocrinology, 2021
Shuhei So, Koshi Hashimoto, Masatomo Mori, Shigeki Endo, Wakasa Yamaguchi, Naomi Miyano, Nao Murabayashi, Fumiko Tawara
The thyroid gland utilizes dietary iodine for the secretion of two thyroid hormones, namely, triiodothyronine and thyroxine, that are essential for regulating metabolic processes throughout the body. The recommended daily iodine intake for thyroid hormone synthesis is 150 μg [1]. The thyroid gland has an intrinsic mechanism wherein excessive iodine intake acutely suppresses thyroid hormone synthesis while it inhibits iodine organization; this regulatory phenomenon is known as the Wolff-Chaikoff effect [2]. This inhibitory effect is transient, as the thyroid hormone synthesis returns to the normal level after approximately 48 h; this is known as an escape from the Wolff–Chaikoff effect. These intrinsic regulatory mechanisms for excess iodine management are necessary to maintain normal thyroid function, and disruption in these mechanisms leads to thyroid disorders. Thyroid dysfunction, such as in Hashimoto’s disease and Graves’ disease (GD), is a risk factor for excess iodine-induced hypothyroidism that could possibly occur due to the failure of escape from the Wolff–Chaikoff effect [3]. However, a history of GD and the presence of thyroid nodules are known risk factors for excess iodine-induced thyrotoxicosis [3,4]. This effect is typically the converse of the Wolff–Chaikoff effect and is known as the Jod-Basedow phenomenon [5].