Iodine-induced Hyperthyroidism Research Articles

Iodine-induced hyperthyroidism after long-term use of povidone-iodine: a report of two cases

Iodine-induced hyperthyroidism after long-term use of povidone-iodine: a report of two cases

SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption

Abstract Disclosure: M.K. Shakir: None. K.F. Brown: None. J.S. Hatfield: None. N.O. Vietor: None. T.D. Hoang: None. Introduction: In iodine-replete countries, iodine-induced thyrotoxicosis may occasionally develop after ingestion or therapy with high doses of iodine. Recently, Himalayan salt has become very popular to bridge iodine deficiency, control hypothyroidism, and improve thyroid function. We report a patient with a history of treated Graves’ disease (GD) who developed acute thyrotoxicosis following the use of Himalayan salt. Case report: A 58-year-old woman presented with symptoms of heat intolerance, and unexpected 18-lbs weight loss over 3 months. Physical examination: HR 108 bpm, BP 110/70 mm Hg, normal eye examination, thyroid 45 gms, diffusely enlarged. Examinations of the heart, lungs and abdomen were normal. Lab tests: TSH 0.01 IU/mL, free T4 3.8 ng/dL, T3 308 pg/dL, thyrotropin receptor Ab 4.2 IU/L (<1.0), and thyroid stimulating immunoglobulin 1.89 1U/L (0.06-0.55). The I131 uptake was 60% at 4 hours and the thyroid scan revealed diffuse homogenous uptake confirming GD. She was treated with methimazole (MMI) for 2 years and remission was achieved. MMI was stopped and she remained euthyroid. Twelve months later, she developed hyperthyroid symptoms with a 15-lb weight loss, palpitations, and anxiety. Examination confirmed a 50-gram diffuse goiter and other physical findings consistent with hyperthyroidism. She admitted that she had been taking Himalayan salt (approximately 10 grams daily) in place of regular salt for the past 6 months. Lab tests confirmed recurrent GD: TSH <0.01 IU/mL, FT4 4.1 ng/dL, total T3 278 pg/dL, and I131 uptake was 55% at 24 hours. A 24-hours urine iodine was 898 mcg (normal 100-199) and plasma iodine level was 484 mcg/L (normal 52-109). A diagnosis of iodine-induced recurrence of GD was made, and she was treated with MMI and low iodine diet. After 3 months, she improved significantly and was able to discontinue the MMI by 6 months. A follow- up urine iodine was 189 mcg/L with a plasma iodine level of 78 mcg/L. Subsequently she remained euthyroid for an additional 18 months of follow-up without any treatment. Conclusion: The recommended daily dietary allowance for iodine in adults is 150mcg. Himalayan rock salt may provide a rich source of iodine and consumption of large amounts can lead to iodine excess. However, the available studies do not provide the iodine content in commercially available Himalayan salt preparations. Although the Himalayan salt is advertised to have beneficial effects in patients with thyroid disorders, this food supplement may have deleterious effects in susceptible patients who do not have iodine deficiency, have GD, or are at risk for thyrotoxicosis. Indeed, Himalayan salt use exacerbated GD in our patient, as evidenced by iodine overdose during acute exacerbation and resolution of GD with iodine normalization and low dose MMI. We recommend that patients with thyroid disorders be educated regarding Himalayan salt use. Presentation Date: Saturday, June 17, 2023

Povidone-iodine-induced transient triiodothyronine thyrotoxicosis in a Japanese patient with prolonged habitual gargling: A case report and literature review.

Iodine-induced hyperthyroidism and triiodothyronine (T3) thyrotoxicosis in patients who routinely gargle with povidone-iodine (PVP-I) gargling solution are rare in Japan. A 50-year-old man presented to our hospital for a close examination of an enlarged thyroid, which was noted during a complete health checkup. The thyroid was slightly enlarged with no palpable nodules. He had an increased appetite but no weight gain. He had been routinely gargling with PVP-I gargling solution 4 times daily for >10 years. He had no history of thyroid disease. Test results revealed suppressed thyroid-stimulating hormone, normal free thyroxine, and increased free triiodothyronine levels, leading to the diagnosis of T3 thyrotoxicosis. The patient agreed to stop gargling with PVP-I gargle solution. The free triiodothyronine and thyroid-stimulating hormone levels returned to normal at 18 and 21 weeks, respectively, after discontinuation of PVP-I gargling. After an improvement in thyroid function, he gained 5 kg in 1 year. To our knowledge, this is the first case report that describes PVP-I gargle-induced T3 thyrotoxicosis in a healthy individual without thyroid disease. In Japan, which is an iodine-sufficient country, considering the possibility of high-dose iodine intake-induced thyrotoxicosis due to long-term PVP-I gargling or other causes is necessary, even in individuals with no history of thyroid disease.

Iodine-Induced Hyperthyroidism and Long-term Risks of Incident Atrial Fibrillation and Flutter.

Although iodine-induced hyperthyroidism is a potential consequence of iodinated radiologic contrast administration, its association with long-term cardiovascular outcomes has not been previously studied. To investigate the relationships between hyperthyroidism observed after iodine contrast administration and incident atrial fibrillation/flutter. Retrospective cohort study of the U.S. Veterans Health Administration (1998-2021) of patients age ≥18 years with a normal baseline serum thyrotropin (TSH) concentration, subsequent TSH <1 year, and receipt of iodine contrast <60 days before the subsequent TSH. Cox proportional hazards regression was employed to ascertain the adjusted hazard ratio (HR) with 95% CI of incident atrial fibrillation/flutter following iodine-induced hyperthyroidism, compared with iodine-induced euthyroidism. Iodine-induced hyperthyroidism was observed in 2500 (5.6%) of 44 607 Veterans (mean ± SD age, 60.9 ± 14.1 years; 88% men) and atrial fibrillation/flutter in 10.4% over a median follow-up of 3.7 years (interquartile range 1.9-7.4). Adjusted for sociodemographic and cardiovascular risk factors, iodine-induced hyperthyroidism was associated with an increased risk of atrial fibrillation/flutter compared with those who remained euthyroid after iodine exposure (adjusted HR 1.19, 95% CI 1.06-1.33). Females were at greater risk for incident atrial fibrillation/flutter than males (females, HR 1.81, 95% CI 1.12-2.92; males, HR 1.15, 95% CI 1.03-1.30; P for interaction = .04). Hyperthyroidism following a high iodine load was associated with an increased risk of incident atrial fibrillation/flutter, particularly among females. The observed sex-based differences should be confirmed in a more sex-diverse study sample, and the cost-benefit analysis of long-term monitoring for cardiac arrhythmias following iodine-induced hyperthyroidism should be evaluated.

Iodine in the Therapy of Graves' Disease: A Century After Henry S. Plummer.

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PSAT335 Histopathological changes of the thyroid may be subtle yet important in Amiodarone induced thyrotoxicosis (AIT).

Abstract Background Amiodarone is an effective antiarrhythmic for several cardiac arrhythmias. Due to its high iodine content and long half-life with direct toxic effects on the thyroid gland, it is known to cause a spectrum of thyroid dysfunction. AIT type 1, a form of iodine-induced hyperthyroidism, and AIT type 2, a drug induced destructive thyroiditis, pose a diagnostic and therapeutic challenge. Since the physical and psychological consequences of long-term therapy with either condition are too large to ignore, it is crucial to differentiate between the two types. Histopathologic findings in AIT includes disrupted follicles filled with desquamated vacuolated epithelial cells, foamy macrophages, scattered lymphocytes, involution changes and fibrosis. However, these changes may be subtle in patients who have been treated with long term high dose steroids, but helpful in establishing either AIT 1 or 2. Case A 56-year-old man with a history of cardiomyopathy with an ejection fraction of 30% and atrial flutter treated previously with six months of amiodarone, presented for a routine appointment found to be in atrial flutter with rapid ventricular rate. The patient was off amiodarone therapy for ∼ 6 months prior to current presentation. The patient was referred to the ER where initial vital signs were remarkable for heart rate in the 140s. Exam was remarkable for mild tremor of the outstretched bilateral hands. Labs were remarkable for TSH of 0.01 ulU/ml (0.27-4.20), Free T4 of 2.2 ng/dl (0.93-1.70), Free T3 of 5.9 pg/ml(2.3-4.2). Thyroid ultrasonography revealed a heterogeneously enlarged thyroid gland with no increased vascularity, and 2.4 cm isthmus nodule of a TI-RAD-3. Thyroid stimulating immunoglobulins (TSI) of 96 (&amp;lt;140%), and thyroid peroxidase (TPO) of 2IU/ml (&amp;lt;9). Thyroid radioactive iodine uptake (RAIU) revealed a severely decreased uptake in the setting of amiodarone use. Mixed AIT was suspected and patient was placed on titrated dose of Methimazole (MMI) and Prednisone. Approximately three weeks later, patient was discharged on MMI 40 mg TID and Prednisone 60 mg daily. He had a close outpatient follow up with further titration of prednisone to 80 mg daily. Due to prolonged nature of disease, he was subsequently referred for total thyroidectomy. Histological examination revealed subtle changes including desquamated follicular epithelial cells and intrafollicular foamy macrophages. The thyroid architecture was maintained and no inflammatory infiltrates of fibrosis were noted. These findings are consistent with AIT type 2. Conclusion AIT is a challenging diagnosis, and in medically refractory cases, total thyroidectomy is a curative option. The pathological findings in a patients treated with prolonged steroids may dampen inflammation of AIT2, and therefore careful histologic examination and monitoring of inflammatory markers may help to consolidate diagnosis. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

The correlation between iodine nutrition and autoimmunity among hyperthyroid goiter patients in tertiary care hospital of Tamil Nadu

Background: Iodine is a trace element that is essential for the formation of thyroid hormones. It is essential for the human life’s growth and development. The thyroid gland size and functions affected by deficient or excessive intake of iodine. Iodine excess intake was found to associating with iodine-induced hyperthyroidism (IIH) and autoimmune thyroiditis. Aims and Objectives: The present study was to find the hyperthyroid goiter patient nutritional status by urinary iodine excretion (UIE) measurement and correlate them with thyroid hormone and thyroid autoantibodies. Materials and Methods: In this study, 100 adult hyperthyroid goiter ssubjects and 100 apparently normal adult subjects were conveniently recruited in this study.Urinary iodine estimation and serum TSH, fT4, fT3, AMA, and ATG were estimated,which were estimated for case and control groups. Results: The hyperthyroid goiter patient mean UIE concentration was 278.98 μg/L and 68% of excess UIE which was found. There was significant difference in the UIE between the hyperthyroid goiter patient and control (P&lt;0.001). The following types of goiter, based on palpation, were identified among the 100 hyperthyroid patients: Grade I – 4 %, Grade II – 63%, and Grade III – 33%. There were elevated serum AMA levelswith positive correlation of excess iodine for hyperthyroid goiter patient. Conclusion: In this study, there were excess UIEs among patients; hence, these associated complications, namely, benign goiter (14%), thyroiditis (43%), cancer of thyroid (4%), and thyrotoxicosis (39%) were observed.

IODINE INTAKE AND CANCER

Objectives: Iodine is a trace element that is essential for the synthesis of thyroid hormone. Both chronic iodine deficiency or iodine excess have been associated with hypertrophy and hyperplasia of follicular cells in thyroid gland and the influence of thyroid hormone (T3, T4) and thyrotropin (TSH) secretion. Increase rates of the thyroid cancer are increasing after radiation exposure to 131I in children or aldolescents.&#x0D; Methodology: In respective published reports in literature and in combination of our previous study, dietary iodine excess goiter, iodine induced hyperthyroidism (IIH) and IIT, Iodine intake and the prevalence of papillary carcinoma (PTC), as well as the case-control and cohort studies of thyroid cancer and intake of seafood and milk products, were systematically reviewed. Relative factors that should be considered when studying the effect of dietary iodine in the development of thyroid cancer include screening programs, pathological criteria, diagnostic techniques, radioactive iodine, and standard of medical care in the studied population.&#x0D; Results and conclusion: In current surveys, papillary thyroid carcinoma forms the largest group of thyroid malignancies, after iodine intake excess or iodine prophylaxis where an increase in the papillary: follicular carcinoma ratio was uncovered. Also, there is clear temporal relationship in many countries between introduction of iodine intake excess especially as to radioactive iodine and an increase in incidence of PTC. Iodine goiter, IIH and IIT were also noted. Autoimmune hashimoto's thyroiditis are linked to dietary iodine. Dietary iodine intake is another care of environmental relevance factor in thyroid diseases and papillary carcinoma. Available evidence of oncogenic thyroid hormone receptor mutants from animal experiments and clinical investigation have been a shift toward the oncogenic function of human thyroid carcinoma, and also its target therapy.&#x0D;                    &#x0D; Peer Review History: &#x0D; Received:  May 2021; Revised:  June; Accepted:  June, Available online: 15 July 2021&#x0D; Academic Editor: Ahmad Najib, Universitas Muslim Indonesia, Makassar, Indonesia, ahmad.najib@umi.ac.id&#x0D; UJPR follows the most transparent and toughest ‘Advanced OPEN peer review’ system. The identity of the authors and, reviewers will be known to each other. This transparent process will help to eradicate any possible malicious/purposeful interference by any person (publishing staff, reviewer, editor, author, etc) during peer review. As a result of this unique system, all reviewers will get their due recognition and respect, once their names are published in the papers. We expect that, by publishing peer review reports with published papers, will be helpful to many authors for drafting their article according to the specifications. Auhors will remove any error of their article and they will improve their article(s) according to the previous reports displayed with published article(s). The main purpose of it is ‘to improve the quality of a candidate manuscript’. Our reviewers check the ‘strength and weakness of a manuscript honestly’. There will increase in the perfection, and transparency. &#x0D; Received file:                Reviewer's Comments:&#x0D; Average Peer review marks at initial stage: 5.0/10&#x0D; Average Peer review marks at publication stage: 7.0/10&#x0D; Reviewer(s) detail:&#x0D; Prof. Dr. A. Hakan AKTAŞ, Süleyman Demirel University, Faculty of Science and Art, Department of Chemistry, Isparta-Turkey, hakanaktas@sdu.edu.tr&#x0D; Dr. Vladimir Zaichick, Radionuclide Diagnostics Department, Medical Radiological Research Centre, Obninsk, 249036, Russia. vzaichick@gmail.com &#x0D; Dr. U. S. Mahadeva Rao, Universiti Sultan Zainal Abidin, Terengganu Malaysia, raousm@gmail.com&#x0D;  &#x0D; Similar Articles:&#x0D; TREATMENT OF PATIENTS WITH ADVANCED CANCER FOLLOWING CHEMOTHERAPY AND TRADITIONAL MEDICINE - LONG TERM FOLLOW UP OF 75 CASES &#x0D; EpCAM- AN OLD CANCER ANTIGEN, TURNED ONCOGENIC RECEPTOR AND ITS TARGETING IMMUNOTHERAPY

Severe Thyrotoxicosis Following Topical Iodine Application

Background: Exposure to iodine can lead to iodine-induced hyperthyroidism in patients with underlying thyroid disease. Clinical Case: A 67 year-old woman with a history of nontoxic multinodular goiter and atrial fibrillation presented with fatigue, palpitations, weight loss, and tremor. Laboratory evaluation demonstrated new-onset profound biochemical hyperthyroidism (FT4 > 7.77 ng/dL, n 0.8 – 1.8 ng/dL; FT3 >27.0 pg/mL, n 2.0-4.4 pg/mL). She was treated with beta-blocker, high doses of methimazole, and cholestyramine while further evaluation was pursued. She declined SSKI due to reported iodine allergy and steroids due to concerns about impact on wound healing following recent hip arthroplasty. TSI and TRAb were negative, and thyroid ultrasound showed stable nodules at 1.7cm. Pelvic ultrasound and MRI were obtained due to concern for non-thyroidal etiology, and revealed a 3.7cm septated cystic ovarian lesion, raising suspicion for struma ovarii. Whole body scan to localize site of thyroid hormone production could not be obtained due to high risk of clinical deterioration off methimazole, as she had persistent clinical and biochemical thyrotoxicosis on high doses (up to 90mg/day). She ultimately required 3 sessions of plasma exchange to lower her thyroid hormone levels, and then underwent bilateral salpingo-oophorectomy. Final pathology revealed mucinous cystadenoma without ectopic thyroid tissue. Post-operatively, her thyroid hormone levels were persistently elevated but improved compared to pre-operative levels, allowing for brief cessation of methimazole and completion of whole body scan. Imaging demonstrated a single focus of radioactive iodine uptake in the lower right thyroid lobe, correlating with the dominant 1.7 cm nodule on prior ultrasound, consistent with a toxic adenoma. Additionally, she was found to have an elevated urine iodine level (1200 mcg/24 hours, n 75 – 851 mcg/24 hours). Patient endorsed low iodine diet due to allergy history, and denied recent contrasted imaging study, dietary supplements, or amiodarone use. Upon further inquiry, she recalled using povidone-iodine solution to care for her surgical site post-arthroplasty, approximately a week before the onset of her initial symptoms. Her clinical presentation was ultimately attributed to toxic adenoma, with severe thyrotoxicosis exacerbated by iodine load. She underwent total thyroidectomy and is doing well on levothyroxine post-operatively. Conclusions: Topical iodine administration can contribute to iodine-induced hyperthyroidism in patients with underlying thyroid disease, and its use should be carefully considered in these patients. When evaluating a patient with new thyrotoxicosis, a detailed history of oral, IV, and topical iodine use should be obtained.

Prevention of Iodinated Contrast Media-Induced Hyperthyroidism in Patients with Euthyroid Goiter

Introduction: Iodinated contrast media (ICM)-induced hyperthyroidism is an underestimated, potentially severe condition; however, its prevention has not been sufficiently investigated. The aim of this study was to evaluate the influence of ICM on thyroid status, the advantages of prophylactic therapy for iodine-induced hyperthyroidism (IIH) in patients with euthyroid goiter and cardiovascular comorbidities, and the association between the incidence of IIH and thyroid volume. Methods: Thirty-six euthyroid patients undergoing procedures involving ICM administration were divided into 2 groups: the first group (n = 13) received prophylactic treatment with thiamazole or thiamazole combined with sodium perchlorate during ICM exposure; the second group (n = 23) did not receive prophylaxis. Thyroid-stimulating hormone levels were evaluated before and after ICM, and thyroid hormone levels were assessed after ICM at different points in time. The morphology of the thyroid was evaluated by ultrasonography. Results: Twenty-one patients (58%) developed hyperthyroidism after ICM. Hyperthyroidism was observed more frequently in the group without prophylactic treatment than in the group with prophylaxis (65 vs. 15%, respectively; p = 0.006). No cases of overt hyperthyroidism were observed in the group receiving thiamazole with sodium perchlorate. IIH persisted for a median time of 52.5 days. Larger thyroid volume was associated with a significantly higher occurrence of ICM-induced hyperthyroidism (p = 0.04). Conclusions: Patients with euthyroid goiter receiving ICM are at risk of developing hyperthyroidism. The occurrence of hyperthyroidism after ICM in euthyroid patients with goiter is higher in those with larger thyroid volume. The frequency of ICM-induced hyperthyroidism in euthyroid patients with goiter is lower in those receiving prophylactic therapy with thiamazole in monotherapy or in combination with sodium perchlorate than in those not receiving prophylactic treatment.

Jod-Basedow fenomen - fenomenalna tirotoksikoza?

A Deucalione iodine is an essential mineral vital for the optimal function of the thyroid gland in human beings. Apart from being found in a variety of foods, it is a component of various medications, amiodarone and expectorants, iodine-based swabs used for skin cleaning before interventional and surgical procedures, and iodinated contrast media in medical settings. Jod-Basedow Phenomenon, also known as Jod-Basedow Syndrome or iodine-induced thyrotoxicosis, is a rare cause of thyrotoxicosis that characteristically refers to a paradoxical phenomenon in which large loads of exogenous iodine can cause hyperthyroidism. This phenomenon is mainly seen in populations already at risk for thyroid diseases, such as autoimmune thyroid diseases, prior thyroid surgical history, latent Graves' disease, and prior non-toxic diffuse or nodular goiter formation, or those with underlying kidney disease, such as chronic kidney disease and end-stage renal disorders, which can impact iodine excretion. Typically, it is recognized in those with the administration of a large iodine load, dietary supplement, iodinated contrast media used in conjunction with computed tomography scans, angiography, and various other imaging studies, iodinated antiseptic solutions and oral supplements, or a medication, mainly amiodarone, class III antiarrhythmic drug used in the treatment of recurrent severe ventricular arrhythmias, paroxysmal atrial tachycardia, atrial fibrillation and maintenance of sinus rhythm after cardioversion of atrial fibrillation. Prophylactic medical management of the phenomenon may include antithyroid drugs, methimazole, or perchlorate, to be considered for patients at risk for developing iodine-induced thyrotoxicosis that is scheduled for imaging modalities by using iodinated contrast media. Moreover, the preliminary management modality comprises cessation of iodine administration, avoiding further exposure, administration of beta-adrenergic antagonists, thionamides, corticosteroids, and rarely lithium. Prognosis is usually favorable, although a small percentage of cases could suffer permanent sequelae from iodine-induced thyrotoxicosis. Nevertheless, complications are remarkable including thyroid storm, permanent hyperthyroidism, atrial fibrillation, and fetal hypothyroidism with goiter development, in terms of ordering iodinated contrast media in pregnants. Jod-Basedow Phenomenon should not be overlooked and should be managed by an interprofessional healthcare team serving and officiating not only to treat it but also to concern themselves, actively in the relevant prophylaxis.

Prevalence of Iodine-Induced Hyperthyroidism After Administration of Iodinated Contrast During Radiographic Procedures: A Systematic Review and Meta-Analysis of the Literature.

Background: Iodine-induced hyperthyroidism (IIH) was a common issue in the early twentieth century after introduction of iodine supplementation in dietary salt. Currently, IIH is mostly encountered in Western countries as a consequence of radiographic procedures involving the administration of iodinated contrast media (ICM). However, little is known about the magnitude and clinical relevance of this issue. To assess the incidence of hyperthyroidism after ICM exposure, we performed a systematic review and meta-analysis of the literature. Methods: MEDLINE, Embase, and the Cochrane Library were systematically searched for studies published between 1946 and May 2018. Studies were considered eligible if they investigated the association between hyperthyroidism and iodinated contrast. Data on study design, baseline characteristics, and outcomes were extracted independently by two reviewers. Results: Thirty out of 1493 retrieved studies were included in the analysis. The time endpoint to assess thyroid hormone levels after ICM exposure varied between 1 and 541 days among studies, with most studies having a time endpoint between 7 and 56 days. The overall estimated prevalence of overt hyperthyroidism after ICM exposure was extremely low (0.1% [confidence interval, CI 0-0.6%]), and did not change after adjustments for baseline thyroid function status (0.3% in euthyroid patients at baseline [CI 0-1.7%]). There were no cases with overt hyperthyroidism at 7 days after ICM exposure, and the incidence was very low at 30 days (0.2% [CI 0-0.8%]). Conclusion: The incidence of IIH after ICM administration during radiographic procedures is extremely low.

Thyrotoxicosis. Clinical guidelines for diagnosis and treatment. Part ІІ

Background. Recently they have reported an increased rate of thyrotoxicosis, which is characterized by polyetiology, a variety of clinical manifestations and potential treatment. Appropriate treatment requires an accurate diagnosis and depends on the comorbidities and preferences of the patient.&#x0D; Purpose. To highlight the key points of clinical guidelines for diagnosis and treatment of thyrotpxicosis provided by the American Thyroid Association and the American Association of Clinical Endocrinologists, US Endocrine Society dealing with diagnosis and treatment of thyroid diseases as well as the local clinical protocols of SO «Grigoriev Institute for Medical Radiology and Oncology of the National Academy of Medical Sciences of Ukraine».&#x0D; Materials and methods. Based on the search of contributions in the electronic databases over the last 5 years, which are included in the Cochrane Library, PUBMED and MEDLINE databases. Clinical guidelines are based on expert consensus and assessing the significance according to the international guidelines for thyrotoxicosis.&#x0D; Results and discussion. The paper deals with up-to-date guidelines on diagnosis, management and treatment of patients with different forms of thyrotoxicosis. It presents a detailed strategy for those patients depending on etiology of the disease. The therapeutic approaches to treating Graves’ disease, autoimmune ophthalmopathy, thyrotoxic crisis, gravidae as well as the peculiarities of treating patients with subclinical hyperthyroidism and iodine-induced thyrotoxicosis have been substantiated.&#x0D; Conclusions. The treatment of thyrotoxicosis remains a challenging issue of modern internal medicine. Despite the existing numerous clinically proven protocols for the treatment of this pathology, the comorbid background of patients complicates following them. The implementation of the provided protocol elements will make it possible to introduce the principles of a customized approach in thyrotoxicosis patients.

[Iodine-induced thyroid dysfunction].

Iodine-induced thyroid dysfunctions are, despite their rare occurrence, important clinical syndromes. Their immediate recognition can avoid serious consequences. Important triggers can be iodine-containing contrast agents, amiodarone or iodine-containing disinfectants. Iodine-induced hypothyroidism and hyperthyroidism need to be distinguished, whereby the former is usually self-limiting. The aim of this article is to present current knowledge on the pathogenesis, therapy, and prophylaxis of iodine-induced thyroid dysfunction. We performed aliterature search of current publications and linked them to daily clinical experience. In iodine-induced hyperthyroidism, antithyroid drugs and perchlorate are primarily used to decrease thyroid hormone synthesis and further iodine uptake into the thyroid. For the prophylaxis of x‑ray contrast agent-induced hyperthyroidism, perchlorate can be administered in high-risk settings in combination with antithyroid drugs, if possible starting one day before the iodine exposure.

Awareness of the population in Russian Federation about iodine deficiency, its effects and methods for prevention of iodine deficiency disorders.

Background: Throughout all territory of Russian Federation has been confirmed absence of iodine deficiency of varying severity. Chronic iodine deficiency leads to irreversible defects in the intellectual and physical development of children, thyroid gland diseases, including such severe manifestations as functional autonomy and iodine-induced thyrotoxicosis and reproductive disorders.&#x0D; Aims: To assess the awareness of Russians about the effect of iodine deficiency on health and the need to use iodized salt in food.&#x0D; Materials and methods: During November 2019 we conducted an anonymous online survey about iodine deficiency and methods of its prevention. The participants of this survey were 9309 Russians of different age categories. Weasked each respondent six questions regarding their knowledge about the importance of iodine for the body and its supply sources. This study is one-staged, uncontrolled, full-designed, and conducted using Google Forms (Google LLC, 2019). As a result, we summarized data on the awareness of Russians about iodine deficiency disorders and methods for its prevention.&#x0D; Results: 60.4% of respondents is using iodized salt, while the number of respondents who consider prevention with iodized salt to be unhealthy (or have lack knowledge of its effects) is related to the number of respondents who do not use iodized salt. We get that in Volga region only 50% of population is using iodized salt (the lowest level), while 62.83% of the European South inhabitants is using iodized salt. In the rest of Russian Federation, this indicator varies from 52 to 57%. There is a low awareness of the population about prevention of iodine deficiency disorders and as a result myth about the dangers of universal salt iodization are widespread in Russian Federation.&#x0D; Conclusions: Awareness of Russians about prevention of iodine deficiency disorders still remains at a low level, and it is directly affecting the success of ongoing prevention programs.

Jodom-izazvan hipertireoidizam - da li ste?

Iodine can be obtained by consumption of the foods that include it or to which it is added. Iodine-induced hyperthyroidism, also known as Jod-Basedow Syndrome, usually rise in the cases of underlying thyroid disease, such as autoimmune thyroid disease, latent Graves disease, non-toxic diffuse or nodular goiter or previous thyroid surgery. Iodine-induced hyperthyroidism is frequently self-limited with a period of 1-18 months after the discontinuanceation of iodine supply/replation. The prognosis is frequently favorable, the majority returns to the baseline hormonal status. The long-term outcomes of Jod-Basedow effects remain unknown due to the scarcity of phenomenon. Nonetheless, it is remarkable that treatment, devoted to the underlying thyroid diseases, should be addressed after resolution of the acute episode. Furthermore, an interprofessional health care team must serve and officiate not only to treat iodine-induced hyperthyroidism, but also to concern themselves actively in prophylaxis.

Effect of iodine status on nutritional status of school-age children in artisanal and small scale gold mining area

Background: Nutritional status of school-age children is influenced by several factors, e.g., nutrition intake, hormone, and underlying disease. Mercury, as a pollutant from artisanal and small scale gold mining (ASGM), inhibits thyroxin production-metabolism regulating hormone. The objective of this study was to evaluate the effect of iodine status and nutritional intake on nutritional status of school-age children in ASGM area.Methods: Study design was cross sectional. There were two groups; case group was school-age children exposed by mercury from ASGM area from Sekotong subdistrict, and control group was school-age children in Narmada subdistrict. Sixty two children from ASGM were enrolled, and fifty two children from the Narmada subdistrict. Iodine status was assessed by measured urine iodine excretion using acid digestion method; nutrition intake assessed by using recall 24 hours; nutritional status by measured anthropometry. Correlation between nutritional and iodine status was examined by using Spearman’ test.Results: Nutritional status of case group found 45.1 % were stunted and 27.4 % were underweight. Control group found 13.4 %  stunted and 9.6 % underweight. Iodine status of case group: 3.9 %  deficient and 68.6 % at risk of iodine-induced hyperthyroidism, the control group was found that 3.8 % inadequate and 72.8 % at risk of iodine-induced hyperthyroidism. Iodine intake both groups were under RDA value that of the case group was 8.3 µg/day, and the control group was 11.5 µg/day. All nutrition supporting growth did not meet the RDA value.  Spearman’s test result was p=0.56.Conclusion: Iodine status did not correlate with the nutritional status of children in ASGM area.

EANM practice guideline/SNMMI procedure standard for RAIU and thyroid scintigraphy.

Scintigraphic evaluation of the thyroid gland enables determination of the iodine-123 iodide or the 99mTc-pertechnetate uptake and distribution and remains the most accurate method for the diagnosis and quantification of thyroid autonomy and the detection of ectopic thyroid tissue. In addition, thyroid scintigraphy and radioiodine uptake test are useful to discriminate hyperthyroidism from destructive thyrotoxicosis and iodine-induced hyperthyroidism, respectively. Several radiopharmaceuticals are available to help in differentiating benign from malignant cytologically indeterminate thyroid nodules and for supporting clinical decision-making. This joint practice guideline/procedure standard from the European Association of Nuclear Medicine (EANM) and the Society of Nuclear Medicine and Molecular Imaging (SNMMI) provides recommendations based on the available evidence in the literature. The purpose of this practice guideline/procedure standard is to assist imaging specialists and clinicians in recommending, performing, and interpreting the results of thyroid scintigraphy (including positron emission tomography) with various radiopharmaceuticals and radioiodine uptake test in patients with different thyroid diseases.

SAT-609 Plasmapheresis as Salvage Treatment in a Patient with Amiodarone-Associated Thyroid Dysfunction

Introduction: Treatment with amiodarone is associated with thyroid dysfunction. Thyrotoxicosis is a possible consequence and 3 types of amiodarone-induced thyrotoxicosis (AIT) are commonly defined: AIT1 (Iodine-induced hyperthyroidism), AIT2 (hyperthyroidism resulting from destructive thyroiditis) and mixed/indefinite forms resulting from a mixture of types 1 and 2. Treatment consists of thionamides or glucocorticoids, depending on the AIT type. Subsequently, thyroidectomy should be considered. Plasmapheresis has been mentioned as a "life-saving" treatment, although its use is not yet a standard practice in the resolution of thyrotoxicosis. Case report: 61-year-old man, with history of NYHA class II/III ischemic heart failure, submitted to cardiac resynchronization therapy defibrillator in 2014, permanent atrial fibrillation, dyslipidaemia, ex-smoker and COPD. No history of thyroid pathology. His usual medication included amiodarone 200mg od. On February of 2018, the patient entered the emergency room due to anginal pain that developed for cardiorespiratory arrest (CRA) and reverted after cardioversion. He was admitted to the Coronary Unit where an analytical study showed TSH - 0.01 μUI/mL, FT4-4.21ng/dL. Endocrinology evaluation was requested. The patient presented with digital tremor, without exophthalmia and a nodule was perceptible on palpation. It was prescribed thiamazole 30mg/day because of the suspicion of AIT 1. He performed thyroid ultrasonography with doppler that showed isoechoic nodule of 14mm in the right lobe, aspects suggestive of thyroiditis and preserved vascularization of the gland. Anti-thyroid and anti-TSH receptor antibodies were absent. Thus, the hypothesis of AIT 2 was more likely to occur and prednisolone 20mg/day was added, aiming to achieve euthyroidism that would provide the necessary conditions for the patient to undergo total thyroidectomy. From this moment on, FT4 and TSH assays were repeated every 3 days and prednisolone and thiamazole doses were increased to a maximum of 70mg and 40mg, respectively. Approximately 50 days after the onset of hospitalization, due to the inability to achieve euthyroidism and also to the progression of the heart disease that motivated a new CRA during the admission, total thyroidectomy was mandatory and therefore it was decided to proceed to plasmapheresis. The procedure went without any harm and a FT4 of 1,82 ng/dL was reached. This value was above the reference range, however with a marked improvement compared to the value prior to the procedure. The patient was then submitted to total thyroidectomy but died 2 days later due to multiorganic dysfunction. Conclusion: This case shows the difficulties that are often found in the treatment of AIT. Still, it makes clear that in urgent cases, plasmapheresis can be a viable and effective alternative in the restoration of euthyroidism, with the potential to save lifes.

[Iodinated contrast medium in patients with thyroid disorders].

Adequate intake of iodine is essential for normal thyroid function. However, sudden exposure to high amounts of iodine may cause thyroid dysfunction. The aims of this paper are to summarize the literature on the effects of iodinated contrast medium (CM) on thyroid function, the risk to develop CM-induced hyper- and hypothyroidism, and to describe procedures for clinical practice regarding diagnosis, prevention, and treatment of CM-induced hyperthyroidism. The occurrence of CM-induced hyperthyroidism is very rare (<0.5%). In Germany, thyroid function is commonly assessed with laboratory tests (TSH determination) before the use of iodinated CM. Older patients (>60years) with autonomous thyroid and concomitant cardiac diseases are at particular risk of developing hyperthyroidism. The main focus of prevention is to identify patients at risk of developing iodine-induced hyperthyroidism and carry out further thyroid diagnostic procedures prior to CM use. In these patients, prophylaxis with perchlorate and/or thionamides is recommended or alternatively careful monitoring of the patients after use of CM. In patients with overt hyperthyroidism, the use of CM is contraindicated. Iodine-induced hypothyroidism is predominantly found in regions with sufficient iodine supply and in patients with autoimmune thyroiditis. Free iodide influences iodide uptake into the thyroid and therefore interferes with nuclear diagnostic procedures like thyroid scintigraphy as well as radioactive iodine treatment which may be hampered for 2months or longer after use of CM.