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1
Hardley, Macy T., Andrew H. Chon, Jorge Mestman, Caroline T. Nguyen, Mitchell E. Geffner, and Ramen H. Chmait. "Iodine-Induced Fetal Hypothyroidism: Diagnosis and Treatment with Intra-Amniotic Levothyroxine." Hormone Research in Paediatrics 90, no. 6 (2018): 419–23. http://dx.doi.org/10.1159/000488776.
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Background: Iodine is necessary for fetal thyroid development. Excess maternal intake of iodine can cause fetal hypothyroidism due to the inability to escape from the Wolff-Chaikoff effect in utero. Case Report: We report a case of fetal hypothyroid goiter secondary to inadvertent excess maternal iodine ingestion from infertility supplements. The fetus was successfully treated with intra-amniotic levothyroxine injections. Serial fetal blood sampling confirmed fetal escape from the Wolff-Chaikoff effect in the mid third trimester. Early hearing test and neurodevelopmental milestones were normal. Conclusion: Intra-amniotic treatment of fetal hypothyroidism may decrease the rate of impaired neurodevelopment and sensorineural hearing loss.
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Johnson, T. M. "The Wolff-Chaikoff effect: hypothyroidism due to potassium iodide." Archives of Dermatology 124, no. 8 (August 1, 1988): 1184–85. http://dx.doi.org/10.1001/archderm.124.8.1184.
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Clemens, P. C. "The Wolff-Chaikoff effect: hypothyroidism due to iodine application." Archives of Dermatology 125, no. 5 (May 1, 1989): 705. http://dx.doi.org/10.1001/archderm.125.5.705.
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Johnson, Timothy M. "The Wolff-Chaikoff Effect: Hypothyroidism due to Potassium Iodide." Archives of Dermatology 124, no. 8 (August 1, 1988): 1184. http://dx.doi.org/10.1001/archderm.1988.01670080010005.
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Clemens, Peter C. "The Wolff-Chaikoff Effect: Hypothyroidism due to Iodine Application." Archives of Dermatology 125, no. 5 (May 1, 1989): 705. http://dx.doi.org/10.1001/archderm.1989.01670170121022.
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Heymann, Warren R. "Potassium iodide and the Wolff-Chaikoff effect: Relevance for the dermatologist." Journal of the American Academy of Dermatology 42, no. 3 (March 2000): 490–92. http://dx.doi.org/10.1016/s0190-9622(00)90224-x.
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Aliefendioğlu, Didem, Cihat Şanli, Murat Çakmak, Ayça Ağar, Meryem Albayrak, and Olcay Evliyaoğlu. "Wolff-Chaikoff effect in a newborn: is it an overlooked problem?" Journal of Pediatric Surgery 41, no. 12 (December 2006): e1-e3. http://dx.doi.org/10.1016/j.jpedsurg.2006.08.041.
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Serrano-Nascimento, Caroline, Jamile Calil-Silveira, and Maria Tereza Nunes. "Posttranscriptional regulation of sodium-iodide symporter mRNA expression in the rat thyroid gland by acute iodide administration." American Journal of Physiology-Cell Physiology 298, no. 4 (April 2010): C893—C899. http://dx.doi.org/10.1152/ajpcell.00224.2009.
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Iodide is an important regulator of thyroid activity. Its excess elicits the Wolff-Chaikoff effect, characterized by an acute suppression of thyroid hormone synthesis, which has been ascribed to serum TSH reduction or TGF-β increase and production of iodolipids in the thyroid. These alterations take hours/days to occur, contrasting with the promptness of Wolff-Chaikoff effect. We investigated whether acute iodide administration could trigger events that precede those changes, such as reduction of sodium-iodide symporter (NIS) mRNA abundance and adenylation, and if perchlorate treatment could counteract them. Rats subjected or not to methylmercaptoimidazole treatment (0.03%) received NaI (2,000 μg/0.5 ml saline) or saline intraperitoneally and were killed 30 min up to 24 h later. Another set of animals was treated with iodide and perchlorate, in equimolar doses. NIS mRNA content was evaluated by Northern blotting and real-time PCR, and NIS mRNA poly(A) tail length by rapid amplification of cDNA ends–poly(A) test (RACE-PAT). We observed that NIS mRNA abundance and poly(A) tail length were significantly reduced in all periods of iodide treatment. Perchlorate reversed these effects, indicating that iodide was the agent that triggered the modifications observed. Since the poly(A) tail length of mRNAs is directly associated with their stability and translation efficiency, we can assume that the rapid decay of NIS mRNA abundance observed was due to a reduction of its stability, a condition in which its translation could be impaired. Our data show for the first time that iodide regulates NIS mRNA expression at posttranscriptional level, providing a new mechanism by which iodide exerts its autoregulatory effect on thyroid.
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García Rincón, Cristian Iván, Luz Yaneth Becerra Salazar, Germán Alberto Moreno Gómez, and Henry Mauricio Arenas Quintero. "Disfunción tiroidea posexposición a medio de contraste yodado." Revista Colombiana de Endocrinología, Diabetes & Metabolismo 2, no. 1 (March 25, 2017): 5–9. http://dx.doi.org/10.53853/encr.2.1.64.
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La exposición a cantidades excesivas de yodo bloquea la actividad de la enzima peroxidasa tiroidea (TPO), un fenómeno conocido como efecto de Wolff-Chaikoff. Clínicamente, éste puede llevar a hipotiroidismo. Por el contrario, cuando un tirocito contiene valores bajos de yodo y es expuesto a elevadas concentraciones del mismo, aumenta de forma significativa la producción de hormona tiroidea, llevando frecuentemente a hipertiroidismo clínico y bioquímico, fenómeno conocido como efecto de Jod-Basedow. Tanto el hiper como el hipotiroidismo aumentan el riesgo de enfermedad arterial coronaria, miopatía ventricular izquierda, anormalidades electrofisiológicas, además de incrementar la mortalidad cardiovascular y por todas las causas.Abstract Exposure to excessive amounts of iodine blocks the activity of the enzyme thyroid peroxidase (TPO), a phenomenon known as Wolf-Chaikoff effect. Clinically, this effect can lead to hypothyroidism. On the other hand, when thyrocites have low iodine levels and are exposed to a high iodine concentration, they increase significantly their production of thyroid hormone thus leading to hyperthyroidism, a phenomenon known as Jod-Basedow effect. Both hypothyroidism and hyperthyroidism increase the risk of coronary artery disease, left cardiomyopathy, electrophysiological abnormalities, and all-cause mortality.
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Khopkar, Uday, Bhushan Madke, Siddhi Chikhalkar, Sunanda Mahajan, and Vidya Kharkar. "Ulcerative subcutaneous zygomycosis: Development of hypothyroidism induced by potassium iodide (Wolff-Chaikoff effect)." Indian Journal of Dermatology, Venereology, and Leprology 76, no. 4 (2010): 431. http://dx.doi.org/10.4103/0378-6323.66604.
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Arora, Pooja, M. Raihan, Asha Kubba, and RamK Gautam. "Lymphocutaneous sporotrichosis treated with potassium iodide with development of subclinical hypothyroidism: wolff-chaikoff effect?" Indian Dermatology Online Journal 8, no. 6 (2017): 475. http://dx.doi.org/10.4103/idoj.idoj_3_17.
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Calil-Silveira, Jamile, Caroline Serrano-Nascimento, Peter Andreas Kopp, and Maria Tereza Nunes. "Iodide excess regulates its own efflux: a possible involvement of pendrin." American Journal of Physiology-Cell Physiology 310, no. 7 (April 1, 2016): C576—C582. http://dx.doi.org/10.1152/ajpcell.00210.2015.
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Adequate iodide supply and metabolism are essential for thyroid hormones synthesis. In thyrocytes, iodide uptake is mediated by the sodium-iodide symporter, but several proteins appear to be involved in iodide efflux. Previous studies demonstrated that pendrin is able to mediate apical efflux of iodide in thyrocytes. Acute iodide excess transiently impairs thyroid hormone synthesis, a phenomenon known as the Wolff-Chaikoff effect. Although the escape from this inhibitory effect is not completely understood, it has been related to the inhibition of sodium-iodide symporter-mediated iodide uptake. However, the effects of iodide excess on iodide efflux have not been characterized. Herein, we investigated the consequences of iodide excess on pendrin abundance, subcellular localization, and iodide efflux in rat thyroid PCCl3 cells. Our results indicate that iodide excess increases pendrin abundance and plasma membrane insertion after 24 h of treatment. Moreover, iodide excess increases pendrin half-life. Finally, iodide exposure also increases iodide efflux from PCCl3 cells. In conclusion, these data suggest that pendrin may have an important role in mediating iodide efflux in thyrocytes, especially under conditions of iodide excess.
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Corvilain, Bernard, Jacqueline Van Sande, and Jacques E. Dumont. "Inhibition by iodide of iodide binding to proteins: The “Wolff-Chaikoff” effect is caused by inhibition of H2O2 generation." Biochemical and Biophysical Research Communications 154, no. 3 (August 1988): 1287–92. http://dx.doi.org/10.1016/0006-291x(88)90279-3.
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Khalifa, Maram, Hassaan B. Aftab, and Vitaly Kantorovich. "“Fueling the Fire” - Irish Sea-Moss Resulting in Jod-Basedow Phenomenon in a Patient With Grave’s Disease." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A906. http://dx.doi.org/10.1210/jendso/bvab048.1849.
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Abstract Background: Jod-Basedow phenomenon is a rare cause of thyrotoxicosis due to excess iodine intake. Herbal supplements containing sea-moss have high iodine amount which may precipitate thyrotoxicosis in patients with underlying Grave’s disease or autonomous thyroid nodules. Clinical Case: A seemingly healthy 28-year-old female presented to the ED with chief complaint of fatigue with associated anxiety, palpitations and weight loss. On admission her temperature was 100.4 F, pulse 126 bpm and blood pressure 116/56 mmHg. Exam was unremarkable for thyroid goiter or orbitopathy. Labs revealed WBC count 3.4 x103/µL (ref range 4.0-11.0) with neutropenia, hemoglobin 4.3 g/dL (11.7-15.7), platelet 49 x103/µL (150-450). Liver transaminases (AST, ALT, and alkaline phosphatase) were elevated with levels up to 4 times the upper limit of normal. She was diagnosed with hemolytic anemia secondary to severe Vitamin B12 deficiency due to pernicious anemia. TSH was <0.01 mIU/L (0.27-4.20), free T4 2.46 ng/dL (0.8-1.9) and total T3 139 ng/dL (76-181). The patient subsequently endorsed remote history of hyperthyroidism diagnosed 7 years ago however she could not recall the underlying etiology or the name of medication she was treated with. She reportedly stopped this medication after 1 month due to developing goiter. She also endorsed intermittent use of store-bought supplement of Irish sea moss and bladderwrack in last 2 years. Further workup revealed elevated TSI and TBII antibody titers establishing diagnosis of Grave’s disease. Thyroid ultrasound showed normal sized heterogeneous hypervascular gland with no nodules. I-123 thyroid uptake and scan showed diffuse moderately elevated radioiodine uptake of 16.8% and 40.8% at 4 and 24 hours, respectively. Thionamide therapy was withheld due to concern of neutropenia and transaminitis. She was treated with beta-blocker after which her vital signs normalized. Labs 1 week after stopping sea moss showed TSH 0.01 mIU/L and free T4 1.4 ng/dL. Conclusion: Irish sea moss is a readily available herbal supplement with high, variable amounts of iodine. Despite little scientific evidence, it is often marketed to improve goiter amongst other health benefits. The recommended daily iodine intake per the FDA is 150 mcg. Higher amounts are expected to initially cause a short-lived suppression of thyroid function; the Wolff-Chaikoff effect, followed by “escape” and accelerated production of thyroid hormone in abnormal thyroid gland, known as Jod-Basedow phenomenon. In our case, the patient unknowingly worsened her underlying Grave’s disease due to the Jod-Basedow effect. Of note, apparantly she had a longer than expected course of Wolff-Chaikoff effect preceding the thyrotoxic state due to sporadic irregular intake of sea moss. Discontinuing sea moss led to clinical and biochemical improvement of hyperthyroidism without requiring thionamide therapy.
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Sato, Kaori, Ken Okamura, Mototaka Yoshinari, Takeo Kuroda, Hiroshi Ikenoue, Kaeko Okazawa, Tetsuya Mizokami, Kaoru Onoyama, and Masatoshi Fujishima. "Reversible primary hypothyroidism and elevated serum iodine level in patients with renal dysfunction." Acta Endocrinologica 126, no. 3 (March 1992): 253–59. http://dx.doi.org/10.1530/acta.0.1260253.
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Recovery of thyroid function in patients with both thyroid and renal dysfunction was studied. Among 245 patients with primary hypothyroidism (serum TSH >10 mU/l), 36 had mild to severe renal dysfunction (serum urea nitrogen >7.1 mmol/l and creatinine >106 μmol/l). Of these 36 patients, recovery of the thyroid function after iodine restriction was observed in 30(83%), in whom an elevated serum non-hormonal iodine level (median 236, range 67–15591 μg/l, N=19) and a high thyroidal radioactive iodine uptake (51.5±29.3%at24h, N = 26) were observed. The perchlorate discharge test was positive in 7 of 13 patients examined, suggesting an iodide organification defect rather than an atrophic or destructive change in the thyroid. Antithyroid antibodies were negative in 22 patients (73%) and an almost normal thyroid gland or colloid goitre was confirmed histologically in 8 of them. After a 13.2 mg potassium iodide loading test, 24 h urinary excretion of iodine was about 60% in normal controls, but only 10% in a different group of six euthyroid patients with renal dysfunction. These findings suggest that impaired renal handling of iodine rather than autoimmune mechanism may have a significant role in the pathogenesis of reversible hypothyroidism found in patients with renal dysfunction, probably through a prolonged Wolff-Chaikoff effect.
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Arriagada, Alejandro A., Eduardo Albornoz, Ma Cecilia Opazo, Alvaro Becerra, Gonzalo Vidal, Carlos Fardella, Luis Michea, et al. "Excess Iodide Induces an Acute Inhibition of the Sodium/Iodide Symporter in Thyroid Male Rat Cells by Increasing Reactive Oxygen Species." Endocrinology 156, no. 4 (April 1, 2015): 1540–51. http://dx.doi.org/10.1210/en.2014-1371.
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Abstract Na+/I− symporter (NIS) mediates iodide (I−) uptake in the thyroid gland, the first and rate-limiting step in the biosynthesis of the thyroid hormones. The expression and function of NIS in thyroid cells is mainly regulated by TSH and by the intracellular concentration of I−. High doses of I− for 1 or 2 days inhibit the synthesis of thyroid hormones, a process known as the Wolff-Chaikoff effect. The cellular mechanisms responsible for this physiological response are mediated in part by the inhibition of I− uptake through a reduction of NIS expression. Here we show that inhibition of I− uptake occurs as early as 2 hours or 5 hours after exposure to excess I− in FRTL-5 cells and the rat thyroid gland, respectively. Inhibition of I− uptake was not due to reduced NIS expression or altered localization in thyroid cells. We observed that incubation of FRTL-5 cells with excess I− for 2 hours increased H2O2 generation. Furthermore, the inhibitory effect of excess I− on NIS-mediated I− transport could be recapitulated by H2O2 and reverted by reactive derived oxygen species scavengers. The data shown here support the notion that excess I− inhibits NIS at the cell surface at early times by means of a posttranslational mechanism that involves reactive derived oxygen species.
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Cardoso, Luciene C., Denise C. L. Martins, Marcia D. L. Figueiredo, Doris Rosenthal, Mario Vaisman, Alice H. D. Violante, and Denise P. Carvalho. "Ca2+/Nicotinamide Adenine Dinucleotide Phosphate-Dependent H2O2 Generation Is Inhibited by Iodide in Human Thyroids." Journal of Clinical Endocrinology & Metabolism 86, no. 9 (September 1, 2001): 4339–43. http://dx.doi.org/10.1210/jcem.86.9.7823.
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A calcium and NAD(P)H-dependent H2O2-generating activity has been studied in paranodular thyroid tissues from four patients with cold thyroid nodules and from nine diffuse toxic goiters. H2O2 generation was detected both in the particulate (P 3,000 g) and in the microsomal (P 100,000 g) fractions of paranodular tissue surrounding cold thyroid nodules (PN), with the same biochemical properties described for NADPH oxidase found in porcine and human thyroids. In PN tissues, the particulate NADPH oxidase activity (224 ± 38 nmol H2O2·h−1·mg−1 protein) was similar to that described for the porcine thyroid enzyme. However, no NADPH oxidase activity was detectable in the particulate fractions from eight diffuse toxic goiter patients treated with iodine before surgery; all but one also received propylthiouracil or methimazole in the preoperative period. Thyroid cytochrome c reductase (diffuse toxic goiters = 438 ± 104 nmol NADP+·h−1·mg−1 protein; PN = 78 ± 10 nmol NADP+·h−1·mg−1 protein) and thyroperoxidase (diffuse toxic goiters = 621 ± 179 U·g−1 protein; PN = 232 ± 121 U·g−1 protein) activities were unaffected by iodide. Thus, the human NADPH oxidase seems to be inhibited by iodinated compounds in vivo and probably is an enzyme involved in the Wolff-Chaikoff effect. Our findings reinforce the hypothesis that thyroid NADPH oxidase is responsible for the production of H2O2 necessary for thyroid hormone biosynthesis.
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Eng, Peter H. K., Guemalli R. Cardona, Shih-Lieh Fang, Michael Previti, Sharon Alex, Nancy Carrasco, William W. Chin, and Lewis E. Braverman. "Escape from the Acute Wolff-Chaikoff Effect Is Associated with a Decrease in Thyroid Sodium/Iodide Symporter Messenger Ribonucleic Acid and Protein1." Endocrinology 140, no. 8 (August 1999): 3404–10. http://dx.doi.org/10.1210/endo.140.8.6893.
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Rump, Alexis, Stefan Eder, Andreas Lamkowski, Manabu Kinoshita, Tetsuo Yamamoto, Michael Abend, Nariyoshi Shinomiya, and Matthias Port. "Development of New Biokinetic-Dosimetric Models for the Simulation of Iodine Blockade in the Case of Radioiodine Exposure in Man." Drug Research 69, no. 11 (August 7, 2019): 583–97. http://dx.doi.org/10.1055/a-0960-5590.
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AbstractIn 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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Paz-Ibarra, José Luis. "Disfunción tiroidea inducida por amiodarona en la práctica clínica." Anales de la Facultad de Medicina 72, no. 1 (February 20, 2013): 69. http://dx.doi.org/10.15381/anales.v72i1.1105.
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La amiodarona (AMD) es una droga antiarrítmica potente (clase III) usada en la práctica clínica para la profilaxis y el tratamiento de muchos disturbios del ritmo cardiaco, desde la fibrilación auricular paroxística hasta las taquiarritmias ventriculares que amenazan la vida. Frecuentemente causa cambios en las pruebas de función tiroidea principalmente relacionados a la inhibición de la actividad de la 5'-deiodinasa, resultando en una disminución de la generación de T3 desde T4 y el consecuente incremento en la producción de T3 reversa y una disminución de su aclaramiento. En 14 a 18% de pacientes tratados con AMD hay una disfunción tiroidea manifiesta, ya sea tirotoxicosis inducida por amiodarona (TIA) o hipotiroidismo inducido por amiodarona (HIA). Tanto TIA como HIA pueden desarrollarse en glándulas aparentemente normales o en glándulas con anormalidades preexistentes clínicamente silentes. La TIA está primariamente relacionada a la síntesis de hormonas tiroideas inducida por el exceso de yodo en una glándula tiroidea anormal (TIA tipo 1) o a una tiroiditis destructiva relacionada a la amiodarona (TIA tipo 2), aunque frecuentemente ocurren formas mixtas. La tiroiditis de Hashimoto preexistente es un factor de riesgo definido para la ocurrencia de HIA. La patogenia del HIA es la falla para escapar del efecto agudo de Wolff-Chaikoff inducido por el yodo, debido a los defectos en la hormonogénesis tiroidea y, en pacientes con pruebas de autoanticuerpos tiroideos positivos, para tiroiditis de Hashimoto concomitante. La TIA es más común en zonas deficientes de yodo mientras que el HIA es usualmente visto en zonas suficientes en yodo. En contraste al HIA, la TIA es una condición difícil de diagnosticar y tratar, y usualmente se recomienda la descontinuación de la amiodarona. En esta revisión se analiza, de acuerdo a los datos actuales, las alteraciones en las pruebas de función tiroidea vistas en pacientes eutirodeos bajo tratamiento con AMD así como la epidemiología y opciones de tratamiento disponibles para ambos tipo de disfunción tiroidea inducida por amiodarona, TIA e HIA.
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Rump, A., S. Eder, C. Hermann, A. Lamkowski, M. Kinoshita, T. Yamamoto, M. Abend, N. Shinomiya, and M. Port. "A comparison of thyroidal protection by iodine and perchlorate against radioiodine exposure in Caucasians and Japanese." Archives of Toxicology 95, no. 7 (May 18, 2021): 2335–50. http://dx.doi.org/10.1007/s00204-021-03065-5.
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AbstractRadioactive iodine released in nuclear accidents may accumulate in the thyroid and by irradiation enhances the risk of cancer. Radioiodine uptake into the gland can be inhibited by large doses of stable iodine or perchlorate. Nutritional iodine daily intake may impact thyroid physiology, so that radiological doses absorbed by the thyroid as well as thyroid blocking efficacy may differ in Japanese with a very rich iodine diet compared to Caucasians. Based on established biokinetic–dosimetric models for the thyroid, we derived the parameters for Caucasians and Japanese to quantitatively compare the effects of radioiodine exposure and the protective efficacy of thyroid blocking by stable iodine at the officially recommended dosages (100 mg in Germany, 76 mg in Japan) or perchlorate. The maximum transport capacity for iodine uptake into the thyroid is lower in Japanese compared to Caucasians. For the same radioiodine exposure pattern, the radiological equivalent thyroid dose is substantially lower in Japanese in the absence of thyroid blocking treatments. In the case of acute radioiodine exposure, stable iodine is less potent in Japanese (ED50 = 41.6 mg) than in Caucasians (ED50 = 2.7 mg) and confers less thyroid protection at the recommended dosages because of a delayed responsiveness to iodine saturation of the gland (Wolff–Chaikoff effect). Perchlorate (ED50 = 10 mg in Caucasians) at a dose of 1000 mg has roughly the same thyroid blocking effect as 100 mg iodine in Caucasians, whereas it confers a much better protection than 76 mg iodine in Japanese. For prolonged exposures, a single dose of iodine offer substantially lower protection than after acute radioiodine exposure in both groups. Repetitive daily iodine administrations improve efficacy without reaching levels after acute radioiodine exposure and achieve only slightly better protection in Japanese than in Caucasians. However, in the case of continuous radioiodine exposure, daily doses of 1000 mg perchlorate achieve a high protective efficacy in Caucasians as well as Japanese (> 0.98). In Caucasians, iodine (100 mg) and perchlorate (1000 mg) at the recommended dosages seem alternatives in case of acute radioiodine exposure, whereas perchlorate has a higher protective efficacy in the case of longer lasting radioiodine exposures. In Japanese, considering protective efficacy, preference should be given to perchlorate in acute as well as prolonged radioiodine exposure scenarios.
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Kwak, Leigh, Ugis Gruntmanis, Alicia De Castro, Natasa Radovanovic, and Hima Reddy Ammana. "Iodoral-Induced Iatrogenic Hypothyroidism." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A939. http://dx.doi.org/10.1210/jendso/bvab048.1919.
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Abstract Background: Iodine is essential for the formation of thyroid hormones. Therefore, the thyroid gland is generally able to maintain normal hormone synthesis despite changes in iodine availability. When there is an increase in iodide load, the thyroid gland is able to inhibit the formation of organic iodide via the Wolff-Chaikoff effect (WCE). This prevents the formation of large quantities of thyroid hormones, thus preventing hyperthyroidism1. Continued exposure to excess iodine is also overcome by the “escape” phenomenon and hormone synthesis resumes in a normal fashion2. However, some patients may lack this autoregulation and develop hypothyroidism. Clinical Case: An 86-year-old male with a history of subclinical hypothyroidism initially presented to his PCP for evaluation of cognitive decline. Workup revealed a TSH of 10 mcIU/mL (0.34 – 5.6 mcIU/mL), a normal FT4 and a negative TPOAb. It was subsequently revealed that the patient was started on Iodoral 12.5 mg daily, an iodine/potassium iodide supplement, 1 month prior to presentation by a naturopathic doctor. Prior to all this, his TSH had always ranged between 4 – 6 mcIU/mL for many years. It was recommended that he discontinue Iodoral and repeat thyroid labs in the future. Despite this, the patient continued on varying doses of Iodoral supplementation. Repeat labs obtained 8 months later revealed an elevated TSH of 99 mcIU/mL and a low FT4 of 0.43 ng/mL (0.6 – 2.6 ng/mL). Despite these numbers, he was asymptomatic and did not exhibit any overt signs of hypothyroidism. He was referred to Endocrinology and finally stopped taking Iodoral.7 weeks post-discontinuation, his repeat labs showed a resolution of hypothyroidism and return to his baseline subclinical disease with a TSH of 8.2 mcIU/mL and a normal FT4. A urine iodine/creatinine was normal at 244.2 ug/g (35 – 540 ug/g) indicating that there was no residual iodine excess from the Iodoral. Conclusion: As far as we are aware, we present the first reported case of Iodoral-induced iatrogenic hypothyroidism. As with past cases of iodine-induced hypothyroidism, our patient had underlying thyroid disease in subclinical hypothyroidism which could explain why he was unable to escape from the WCE. The half-life of Iodoral is unknown but it is generally understood that the effects of iodide are reversed between 2 to 4 weeks after withdrawal. Our patient did not repeat his thyroid function tests until 7 weeks post-discontinuation but did demonstrate a return to baseline with no other intervention. Reference: 1. Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis AG. Iodine-Induced hypothyroidism. Thyroid. 2001 May;11(5):501-10. doi: 10.1089/105072501300176462. PMID: 11396709.2. Torti JF, Correa R. Potassium Iodide. 2020 Oct 12. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan–. PMID: 31194460.
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Blount, Sydney, and Marina Litvin. "PSAT330 Excess Iodine Intake From a Cystic Fibrosis Supplement Induces Symptomatic Hypothyroidism." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A826—A827. http://dx.doi.org/10.1210/jendso/bvac150.1710.
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Abstract A 45-year-old woman with cystic fibrosis (delF508/delF508), pancreatic exocrine insufficiency, and diet-controlled cystic fibrosis-related diabetes presented with new complaints of dry skin, hair loss, and cold intolerance. She had no personal or family history of thyroid disease. Physical exam was notable for a mildly enlarged, non-tender thyroid gland without nodules, and 2+ bicep reflexes with delayed relaxation phase. Labs revealed a TSH of 17 mcIU/mL (n 0.3-4.20 mcIU/mL), free T4 of 0.6 ng/dL (n 0.9-1.7 ng/dL), and a thyroid peroxidase antibody of 15 units/mL (n 0-34 units/mL), consistent with new onset, overt hypothyroidism. Thyroid ultrasound revealed a hypervascular, heterogeneous gland, suggestive of underlying autoimmune thyroid disease. Given such an abrupt and significant change in previously normal thyroid studies, further history was obtained. The patient disclosed taking TauriNac, a supplement discovered online that is believed to help clear heavy metals, which she believed she was exposed to via IV antibiotics, and for treatment of her cystic fibrosis. The patient was taking 3-4 packets of TauriNac per day, totaling 16,000 mcg of potassium iodide, far exceeding the Recommended Dietary Allowance of 150 mcg per day. She discontinued TauriNac and one month later, thyroid function tests normalized. The patient then resumed TauriNac, 2-3 packets per day, and within five months TSH rose to 9.66 mcIU/mL with free T4 0.9 ng/dL. She again stopped taking TauriNac and two months after discontinuation thyroid levels normalized. Later, after yet again resuming TauriNac, 5 packets per week, her TSH increased to 4.71 mcIU/mL. She subsequently discontinued TauriNac with normalization of her TSH after three months. Over one year later, she remains off TauriNac and is clinically and biochemically euthyroid. In the 1970s, development of a goiter and hypothyroidism was reported in CF patients, especially those treated with iodine-based expectorants, raising concern for underlying thyroid dysfunction in CF; however the true prevalence of underlying thyroid dysfunction in CF patients is controversial. A 2016 United States-based study of CF patients revealed abnormal thyroid function tests in 27%, however the abnormalities were mild, and overt thyroid dysfunction was rare. In our center's experience, transient subclinical hypothyroidism associated with CF exacerbations is common and may correlate with poor dietary intake leading to iodine deficiency. In this case, excessive iodide intake via TauriNAC clearly correlated with the development of symptomatic hypothyroidism, presumably due to failure to escape the Wolff-Chaikoff effect. In a 2002 survey of adult CF patients, 70% reported having taken complementary and alternative medicine (CAM) in the past. The high prevalence of CAM use in the CF population as well as prior studies demonstrating iodine induced hypothyroidism in CF patients should inform providers of the potential harmful effects of iodine supplementation in an iodine-replete population. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
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Al-Tamimi, Hosam J., Amani Al-Dawood, and Zainab Mahasneh. "The Wolff–Chaikoff effect ameliorates heat stress in rats." Animal Biotelemetry 7, no. 1 (April 8, 2019). http://dx.doi.org/10.1186/s40317-019-0170-x.
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Pitsiavas, V., P. Smerdely, and SC Boyages. "Amiodarone compared with iodine exhibits a potent and persistent inhibitory effect on TSH-stimulated cAMP production in vitro: a possible mechanism to explain amiodarone-induced hypothyroidism." European Journal of Endocrinology, March 1, 1999, 241–49. http://dx.doi.org/10.1530/eje.0.1400241.
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Amiodarone (AMD) is a powerful anti-arrhythmic drug used for the treatment of a wide variety of cardiac arrhythmias and its most striking feature is its high iodine content. Thyroid dysfunction is a limiting side-effect of the drug and both AMD-induced hypothyroidism (AIH) and AMD-induced thyrotoxicosis (AIT) are reported. To examine the hypothesis that altered bioavailability of iodine is a contributing event in the pathogenesis of AIH, we compared the effects of AMD and inorganic iodine in vitro on events involved in the process of thyroid autoregulation. FRTL-5 cells and JP26 CHO cells (transfected with the human TSH receptor) were exposed to AMD or NaI in the presence of TSH, and cAMP production was measured as an indicator of cellular function. Forskolin and cholera toxin were also used to determine the possible target sites of AMD and iodide. Our results indicated that there was a difference between the effects of AMD versus those of physiological doses of iodide. The inhibitory effects of AMD occurred at lower concentrations of iodide than those seen in the NaI-treated cells. The effects of AMD were irreversible indicating a possible persistence of the Wolff-Chaikoff effect due to a constant high intracellular iodide level. The inhibitory effects of AMD (also seen at supraphysiological doses of iodide) were partially overcome by forskolin but not by cholera toxin indicating an effect on TSH receptor interactions with the other signal transduction elements such as G proteins and adenylate cyclase. The persistence of the Wolff-Chaikoff effect through loss of autoregulation may be a mechanism of the observed hypothyroidism in some patients taking AMD. The combined effects of the constant release of iodide together with the drug toxicity may be the mechanism for the observed effects.
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Eng, PH, GR Cardona, MC Previti, WW Chin, and LE Braverman. "Regulation of the sodium iodide symporter by iodide in FRTL-5 cells." European Journal of Endocrinology, February 1, 2001, 139–44. http://dx.doi.org/10.1530/eje.0.1440139.
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OBJECTIVE: The acute decrease in iodide organification in the thyroid in response to excess iodide is termed the acute Wolff-Chaikoff effect and normal organification resumes in spite of continued high plasma iodide concentrations (escape from the acute Wolff-Chaikoff effect). We have recently reported that large doses of iodide given to rats chronically decrease the sodium/iodide symporter (NIS) mRNA and protein, suggesting that escape is due to a decrease in NIS and subsequent iodide transport. We have now studied the effect of excess iodide on NIS in FRTL-5 cells to further explore the mechanisms whereby excess iodide decreases NIS. DESIGN: FRTL-5 cells were employed and were incubated in the presence or absence of various concentrations of iodide. NIS mRNA and protein and the turnover of NIS were assessed. METHODS: NIS mRNA was measured by Northern analysis, NIS protein by Western analysis and NIS turnover by pulse-chase labeling experiments. RESULTS: Iodide (10(-) mol/l) had no effect on NIS mRNA in FRTL-5 cells at 24 and 48 h compared with cells cultured in the absence of iodide. However, excess iodide decreased NIS protein by 50% of control values at 24 h and by 70% at 48 h. This effect of iodide was dose dependent. Pulse-chase experiments demonstrated that there was no effect of iodide on new NIS protein synthesis and that the turnover of NIS protein in the presence of iodide was 27% faster than in the absence of added iodide. CONCLUSIONS: Excess iodide does not decrease NIS mRNA in FRTL-5 cells but does decrease NIS protein, suggesting that in this in vitro thyroid cell model iodide modulates NIS, at least in part, at a post-transcriptional level. This iodide-induced decrease in NIS protein appears to be due, at least partially, to an increase in NIS protein turnover.
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Akofu, Anota, Stephen A. Brietzke, Nicole Sheung, Ashraf Uddin, Nwamaka Akabogu, Siroj Dejhansathit, and Fnu Marium. "SAT488 Wolff-Chaikoff’s Revenge: There-and-Back Again Graves Thyrotoxicosis." Journal of the Endocrine Society 7, Supplement_1 (October 2023). http://dx.doi.org/10.1210/jendso/bvad114.1961.
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Abstract Disclosure: A. Akofu: None. S.A. Brietzke: None. N. Sheung: None. A. Uddin: None. N. Akabogu: None. S. Dejhansathit: None. F. marium: None. Grave’s disease is due to autoantibodies activating TSH receptors, driving downstream effects of iodine organification, iodotyrosine coupling, and release of T4 and T3 from intracellular stores. Severe thyrotoxicosis is traditionally treated with high dose thionamides to block thyroid hormone synthesis, iodides to slow iodine transport and block thyroid hormone release (collectively known as the Wolff-Chaikoff effect), and beta-blockers to slow heart rate and relieve tremulousness. We report the case of a health-conscious patient who had taken OTC iodide for years, and whose thyrotoxic condition abruptly worsened with discontinuation of his iodide supplement. A 67-year-old man was found in a delirious state wandering in the woods and was taken to the hospital ED. He had afib with RVR and evidence of high-output CHF. Diffuse goiter twice normal size was obvious on exam, and he was tremulous and diaphoretic. Serum TSH was <0.005 mcU/ml, with FT4 > 7.77 ng/dl and FT3 7.8 pg/ml. Initial treatment was metoprolol 25 mg TID, propylthiouracil (PTU) 300 mg TID, cholestyramine 4g BID and Lugol’s iodine 10 drops TID. Encephalopathy resolved after 2 days and FT4 decreased to 3.72 ng/dl after 8 days. Cholestyramine and Lugol’s iodine were thus discontinued. 2 days later, FT4 further declined to 2.75 ng/dl and he was switched from PTU to methimazole 30 mg twice daily. After 3 days, FT4 had increased to 5.17 ng/dl, and in response methimazole was increased to 40 mg TID. 3 days later FT4 increased further to 6.43 ng/dl, prompting a switch from methimazole back to PTU 300 mg TID. Because of further increase in FT4 and FT3, cholestyramine and Lugol's iodine were resumed. 3 days later, FT4 had declined from > 7.7 to 5.4 ng/dl, and he was discharged with plan to perform thyroidectomy once FT4 and FT3 reached nearly normal levels. Near the end of his hospitalization, he divulged that he had taken iodide drops for “thyroid health” for many years independent of medical advice, but hadn’t taken it for several days during the period of being lost in the woods prior to admission. Possible explanations for resistance of thyrotoxicosis to aggressive prescribed treatment include medication non-adherence, drug malabsorption, hyperaccelerated drug metabolism, anti-drug antibodies and antagonism of thionamide action by excessive intrathyroidal iodine. In this case, we hypothesize that his use of iodide serendipitously attenuated severity of Graves disease, by giving him a prolonged Wolf-Chaikoff effect. Discontinuation of iodide over a matter of days allowed reversal of this phenomenon and prevented control of his hyperthyroid condition until the deliberate restoration of the Wolf-Chaikoff effect with therapeutically prescribed Lugol’s solution. Whenever response to usual hyperthyroidism treatment is ineffective or paradoxical, as in this case patients should be specifically queried regarding use of OTC iodine preparations. Presentation Date: Saturday, June 17, 2023
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Tng, Eng-Loon, Aye Thida Aung, and Nicole Chong. "Myxedema Coma Precipitated by Iohexol: Case Report and Brief Literature Review on the Wolff–Chaikoff Effect." Thyroid, March 22, 2022. http://dx.doi.org/10.1089/thy.2022.0021.
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Rump, A., C. Hermann, A. Lamkowski, M. Abend, and M. Port. "Simulations of radioiodine exposure and protective thyroid blocking in a new biokinetic model of the mother–fetus unit at different pregnancy ages." Archives of Toxicology, August 4, 2022. http://dx.doi.org/10.1007/s00204-022-03331-0.
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AbstractIn the case of nuclear incidents, radioiodine may be released. After incorporation, it accumulates in the thyroid and enhances the risk of thyroidal dysfunctions and cancer occurrence by internal irradiation. Pregnant women and children are particularly vulnerable. Therefore, thyroidal protection by administering a large dose of stable (non-radioactive) iodine, blocking radioiodide uptake into the gland, is essential in these subpopulations. However, a quantitative estimation of the protection conferred to the maternal and fetal thyroids in the different stages of pregnancy is difficult. We departed from an established biokinetic model for radioiodine in pregnancy using first-order kinetics. As the uptake of iodide into the thyroid and several other tissues is mediated by a saturable active transport, we integrated an uptake mechanism described by a Michaelis–Menten kinetic. This permits simulating the competition between stable and radioactive iodide at the membrane carrier site, one of the protective mechanisms. The Wollf–Chaikoff effect, as the other protective mechanism, was simulated by adding a total net uptake block for iodide into the thyroid, becoming active when the gland is saturated with iodine. The model’s validity was confirmed by comparing predicted values with results from other models and sparse empirical data. According to our model, in the case of radioiodine exposure without thyroid blocking, the thyroid equivalent dose in the maternal gland increases about 45% within the first weeks of pregnancy to remain in the same range until term. Beginning in the 12th pregnancy week, the equivalent dose in the fetal thyroid disproportionately increases over time and amounts to three times the dose of the maternal gland at term. The maternal and fetal glands’ protection increases concomitantly with the amount of stable iodine administered to the mother simultaneously with acute radioiodine exposure. The dose–effect curves reflecting the combined thyroidal protection by the competition at the membrane carrier site and the Wolff–Chaikoff effect in the mother are characterized by a mean effective dose (ED50) of roughly 1.5 mg all over pregnancy. In the case of the fetal thyroid, the mean effective doses for thyroid blocking, taking into account only the competition at the carrier site are numerically lower than in the mother. Taking into account additionally the Wolff–Chaikoff effect, the dose–effect curves for thyroidal protection in the fetus show a shift to the left over time, with a mean effective dose of 12.9 mg in the 12th week of pregnancy decreasing to 0.5 mg at term. In any case, according to our model, the usually recommended dose of 100 mg stable iodine given at the time of acute radioiodine exposure confers a very high level of thyroidal protection to the maternal and fetal glands over pregnancy. For ethical reasons, the possibilities of experimental studies on thyroid blocking in pregnant women are extremely limited. Furthermore, results from animal studies are associated with the uncertainties related to the translation of the data to humans. Thus model-based simulations may be a valuable tool for better insight into the efficacy of thyroidal protection and improve preparedness planning for uncommon nuclear or radiological emergencies.
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Jing, Li, and Qiang Zhang. "Intrathyroidal feedforward and feedback network regulating thyroid hormone synthesis and secretion." Frontiers in Endocrinology 13 (September 15, 2022). http://dx.doi.org/10.3389/fendo.2022.992883.
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Thyroid hormones (THs), including T4 and T3, are produced and released by the thyroid gland under the stimulation of thyroid-stimulating hormone (TSH). The homeostasis of THs is regulated via the coordination of the hypothalamic-pituitary-thyroid axis, plasma binding proteins, and local metabolism in tissues. TH synthesis and secretion in the thyrocytes-containing thyroid follicles are exquisitely regulated by an elaborate molecular network comprising enzymes, transporters, signal transduction machineries, and transcription factors. In this article, we synthesized the relevant literature, organized and dissected the complex intrathyroidal regulatory network into structures amenable to functional interpretation and systems-level modeling. Multiple intertwined feedforward and feedback motifs were identified and described, centering around the transcriptional and posttranslational regulations involved in TH synthesis and secretion, including those underpinning the Wolff-Chaikoff and Plummer effects and thyroglobulin-mediated feedback regulation. A more thorough characterization of the intrathyroidal network from a systems biology perspective, including its topology, constituent network motifs, and nonlinear quantitative properties, can help us to better understand and predict the thyroidal dynamics in response to physiological signals, therapeutic interventions, and environmental disruptions.
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Campos, Ana de Carmo, Isabel Cruz Carvalho, Sara Sarmento, and Teresa Fonseca. "Iodine-Induced Hypothyroidism After Chemoembolization With Ethiodized Oil: A Case of Failure to Escape From Wolff-Chaikoff Effect (WCE)." Cureus, May 22, 2023. http://dx.doi.org/10.7759/cureus.39352.
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Selvathesan, Nithiakishna, Craig Jefferies, Benjamin Albert, Georgie Yonge, and Amanda Dickens. "Severe iodine‐induced hypothyroidism in an infant on peritoneal dialysis: A salient reminder of the Wolff‐Chaikoff effect of iodine." Journal of Paediatrics and Child Health, November 8, 2022. http://dx.doi.org/10.1111/jpc.16276.
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Sohn, Seo Young, Kosuke Inoue, Connie M. Rhee, and Angela M. Leung. "Risks of Iodine Excess." Endocrine Reviews, June 13, 2024. http://dx.doi.org/10.1210/endrev/bnae019.
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Abstract Iodine is a micronutrient that is required for thyroid hormone synthesis. The iodide cycle in thyroid hormone synthesis consists of a series of transport, oxidation, organification, and binding/coupling steps in thyroid follicular cells. Common sources of iodine include the consumption of an iodine-rich diet or iodine fortified foods, the administration of amiodarone, iodine-containing supplements, or iodinated contrast media, and other miscellaneous sources. Methods to assess population iodine status include the measurement of urinary iodine concentrations, blood thyroglobulin levels, prevalence of elevated neonatal TSH levels, and thyroid volume. Although excessive iodine intake or exposure is generally well tolerated, an acute iodine load may result in thyroid dysfunction (hypothyroidism or hyperthyroidism) in certain susceptible individuals due to the failure to escape from the Wolff-Chaikoff effect and to the Jod-Basedow phenomenon, respectively. In this review, we discuss the associations between excessive iodine intake or exposure, with particular focus on iodinated contrast media as a common source of excess iodine in healthcare settings, and risks of incident thyroid dysfunction. We also summarize the risks of iodine excess in vulnerable populations and review current guidelines regarding the screening and monitoring of iodinated contrast-induced thyroid dysfunction. Finally, we discuss the long-term potential nonthyroidal health risks associated with iodine excess and suggest the need for more data to define safe upper limits for iodine intake, particularly in high-risk populations.
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Vargas-Uricoechea, Hernando, and Carlos Hernán Sierra-Torres. "Thyroid hormones and the heart." Hormone Molecular Biology and Clinical Investigation 18, no. 1 (January 1, 2014). http://dx.doi.org/10.1515/hmbci-2013-0059.
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AbstractThyroid hormones have a significant impact on heart function, mediated by genomic and non-genomic effects. Consequently, thyroid hormones deficit as well as excess are expected to result in profound changes in cardiac function regulation and cardiovascular hemodynamics. Thyroid hormones upregulate the expression of the sarcoplasmic reticulum calcium-activated ATPase and downregulate the expression of phospholamban. Overall, hyperthyroidism is characterized by an increase in resting heart rate, blood volume, stroke volume, myocardial contractility, and ejection fraction. The development of “high-output heart failure” in hyperthyroidism may be due to “tachycardia-mediated cardiomyopathy.” In contrast, in the hypothyroid state, thyroid hormone deficiency results in lower heart rate and weakening of myocardial contraction and relaxation, with prolonged systolic and early diastolic times. Cardiac preload is decreased owing to impaired diastolic function, cardiac afterload is increased, and chronotropic and inotropic functions are reduced. Subclinical thyroid dysfunction is relatively common in patients >65 years of age. In general, subclinical hypothyroidism increases the risk of cardiovascular heart disease (CHD) mortality and CHD events, but not of total mortality. The risk of CHD mortality and atrial fibrillation (but not other outcomes) in subclinical hyperthyroidism is higher among patients with very low levels of thyrotropin. Finally, medications such as amiodarone may induce hypothyroidism (mediated by the Wolff-Chaikoff effect) as well as hyperthyroidism (mediated by the Jod-Basedow effect). In both instances, the underlying cause is the high concentration of iodine in this medication. The purpose of this review is to assess the effects of thyroid hormones on the heart, and their clinical repercussions.
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Rampengan, Starry H. "AMIODARON SEBAGAI OBAT ANTI ARITMIA DAN PENGARUHNYA TERHADAP FUNGSI TIROID." JURNAL BIOMEDIK (JBM) 3, no. 2 (February 6, 2013). http://dx.doi.org/10.35790/jbm.3.2.2011.863.
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Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring. Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.
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D’Ambrosio, Fabiola, Laika M. Nur, Stelios Mantis, and Carla Z. Minutti. "MON-082 The Neonatal Screen That Cried Wolff." Journal of the Endocrine Society 4, Supplement_1 (April 2020). http://dx.doi.org/10.1210/jendso/bvaa046.298.
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Abstract Introduction: Hypothyroidism is one of the major causes of preventable mental retardation. Neonatal screening aids in the prompt diagnosis of newborns with congenital hypothyroidism. There are other clinical conditions that can alter thyroid function during the newborn period, including exposure of high iodine concentrations. Case Presentation: One day old female born at 37 3/7 weeks of gestational age by C-section with imperforated anus and congenital heart disease was transferred to our children’s hospital within the first day of life for a hybrid cardiac procedure of bilateral pulmonary artery banding and PDA stenting. She had an Illinois Neonatal screen done at 36 hours of life that was normal. Her cardiac surgery was performed at 10 days of life, where she was exposed to iodine products transdermally. At 14 days of age, she had a repeat Illinois Neonatal screen that was positive for congenital hypothyroidism with a TSH of 78 mIu/mL (normal < 20 mIu/mL) and reflex total T4 of 5.4ug/dL (normal is > 8ug/dL). No family history of thyroid disease; mother was healthy during pregnancy and was not on medications that could affect baby’s thyroid function. Subsequent serum laboratory testing confirmed a TSH of 74.3mIu/mL and Free T4 of 0.6ng/dL. Patient was diagnosed with Wolff-Chaikoff effect, which is the phenomenon of transient hypothyroidism caused by exposure to high doses of iodine (iodine containing contrast agents or topical antiseptics). Pediatric Endocrinology was consulted at 2 weeks of life and she was started on 25mcg of levothyroxine PO daily. Levothyroxine dose decreased at 16 month of age to 12.5mcg due to stable thyroid function tests. The patient was last seen at 30 months of age by Pediatric Endocrinology. She is still on the low dose of levothyroxine and her thyroid labs have been within normal limits for an infant. She will likely not require lifelong thyroid supplementation. Conclusion: Risk of hypothyroidism among neonates must be considered seriously after large iodine exposure and monitoring for transient hypothyroidism should be performed. It is thus recommended that attempts should be made to reduce the amount of iodine used during procedures and to carefully monitor thyroid function in all neonates exposed to an excess of iodine. Reference: Markou, K., et al. “Iodine-Induced Hypothyroidism.” Thyroid, vol. 11, no. 5, 2001, pp. 501–510., doi:10.1089/105072501300176462. Linder N, Sela B, German B, et al. Iodine and hypothyroidism in neonates with congenital heart disease. Archives of Disease in Childhood - Fetal and Neonatal Edition 1997;77:F239-F240. Kovacikova, Lubica, et al. “Thyroid Function and Ioduria in Infants after Cardiac Surgery: Comparison of Patients with Primary and Delayed Sternal Closure.” Pediatric Critical Care Medicine, vol. 6, no. 2, 1 Mar. 2005, pp. 154–159., doi:10.1097/01.pcc.0000154960.59452.06.