Types Of Amiodarone-induced Thyrotoxicosis Research Articles

Monitoring thyroid function during amiodarone use.

Amiodarone is an antiarrhythmic drug used to treat cardiac tachyarrhythmias. It has many adverse effects, with thyroid dysfunction one of the most notable. Through various mechanisms, both thyrotoxicosis and hypothyroidism can occur secondary to amiodarone therapy. There are two types of amiodarone-induced thyrotoxicosis: type 1 occurs in those with pre-existing thyroid disease and is treated with thionamide, whereas type 2 occurs in those without and is treated with glucocorticoids. Patients with amiodarone-induced hypothyroidism may be given levothyroxine to replace thyroid hormone, but in some cases, the appropriate management may be cessation of amiodarone.

Abstract #1382972: Between a Rock and a Hard Place: A Case of Amiodarone Induced Thyrotoxicosis Presenting with Methimazole Induced Agranulocytosis

Amiodarone is a frequently used anti-arrhythmic drug which may often cause thyroid dysfunction. Management of amiodarone induced thyrotoxicosis (AIT) often hinges on distinguishing between type I and II AIT which is not often possible. When antithyroid drugs (ATD) are used, higher than average doses are often needed, increasing risk for complications. We report a case of a 67-year-old man who presented with palpitations, tremors, hyperdefecation and weight loss, consistent with thyrotoxicosis. He had been treated with amiodarone for paroxysmal atrial fibrillation (a-fib) for several years. Admission labs showed TSH < 0.01 uIU/ml (0.36-3.74 uIU/ml), free T4 3.32 ng/dL (0.76-1.46), total T3 237 ng/dL (86-192), negative thyrotropin receptor blocking antibodies < 1.10 IU/L (0.0-1.75), thyroglobulin antibodies < 20 IU/mL (0.0-40.0) and thyroid peroxidase antibodies < 10.0 IU/mL (0.0-35.0). Thyroid ultrasound showed a mildly enlarged, heterogeneous thyroid without discrete nodules and normal vascularity. He was treated empirically for both type I and type II AIT with methimazole 40 mg and prednisone 40 mg. Despite treatment, he returned with similar complaints one month later. EKG showed a-fib with a heart rate of 120 bpm. Repeat labs showed TSH < 0.01 uIU/ml, free T4 4.01 ng/dL and total T3 146 ng/dL. His overall evaluation was consistent with impending thyroid storm. CBC was notable for a WBC and ANC of 4.0 10ˆ3 cells/μL and 520 cells/μL respectively, which decreased further to a nadir of 2.6 10ˆ3 cells/μL and 62 cells/μL the following day. The inability to use ATDs in the setting of severe agranulocytosis made thyroidectomy an attractive option. His WBC improved with discontinuation of methimazole and resolved completely a day after administration of G-CSF. He was treated with potassium Iodide, prednisone, cholestyramine and metoprolol in preparation for surgery. He did well after surgery and was discharged home in stable condition on postoperative day two. AIT types I and II are distinct clinical entities. First line treatment consists of ATDs for AIT type I, and steroids for AIT type II. In the acute setting it may be difficult to distinguish between both types and some patients may have features of both. Importantly, a 10-fold increased risk for ATD associated agranulocytosis has been reported in patients with AIT compared to thyrotoxicosis due to other etiologies. Higher doses of ATDs are often required in AIT and the risk for agranulocytosis from ATDs is likely dose dependent. Although neutropenia resolves in most patient in 1-3 weeks after cessation of ATDs, use of G-CSF may shorten recovery times, decrease risk for infections and shorten hospital stays.

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.

Draft of the federal clinical recommendations for diagnosisi and treatment of amiodarone-induced thyroid dysfunction

Amiodarone is an antiarrhythmic drug that is commonly used for treatment of various supraventricular and ventricular arrhythmias. Amiodarone and its main active metabolite desethylamiodarone have a direct dose-dependent cytotoxic effect on thyroid follicular cells. Consequently, some patients receiving amiodarone may develop thyroid dysfunction: amiodarone-induced hypothyroidism (AIH) or amiodarone-induced thyrotoxicosis (AIT). The diagnosis, classification, and treatment of amiodarone-induced thyroid dysfunction remain to be a challenge to all clinicians deal with this problem. This draft of clinical recommendations was developed by a group of specialists experienced in the diagnosis and treatment of amiodarone-induced thyroid dysfunction. AIH does not require amiodarone withdrawal. Thyroxine treatment is recommended for all patients with manifest AIH, subclinical forms of AIH do not always need its prescription. There are two main types of amiodarone-induced thyrotoxicosis: AIT type 1 (is a hyperthyroidism that develops due to excessive iodine intake in autonomous thyroid nodules or latent Graves ‘ disease) and AIT type 2 (develops due to destructive thyroiditis because of the cytotoxic effect of amiodarone). In addition, there is a mixed form, which has features of both types of AIT. Autonomous AIT 1 is characterized by the presence of one or more «hot» nodules in the thyroid. Elevated TSH receptor antibodies or typical clinical manifestations confirm the diagnosis of diffuse toxic goiter and, consequently, AIT1. Colour-flow Doppler sonography (CFDS) is proposed as the basic method of differential diagnosis of AIT 1 and AIT 2. CFDS «pattern 0», usually indicates AIT 2, the presence of «patterns I-III» mostly typical for AIT 1. The thyreostatics are recommended for AIT 1, oral glucocorticoids for AIT 2 and their combination for a mixed AIT. Emergency thyroidectomy should be applied to patients with deteriorating cardiovascular pathology and ineffective drug therapy. In the absence of clinical suspicion on thyroid dysfunction, thyroid hormones assessment should be done 3 months after the start of amiodarone treatment, thereafter every 6 months.

Abstract #794867: A Case of Surgical Management of Refractory Amiodarone Induced Thyrotoxicosis Type 2

Abstract #794867: A Case of Surgical Management of Refractory Amiodarone Induced Thyrotoxicosis Type 2

Amiodarone-induced thyroid dysfunction in the developmental period: prenatally, in childhood, and adolescence - case reports and a review of the literature.

Amiodarone is an important antiarrhythmic drug used in paediatric practice, mainly in children with complex congenital cardiac diseases and/or severe arrhythmias. One of the side effects of amiodarone therapy is thyroid dysfunction, which is observed in about 20% of patients. The thyroid dysfunction may present with various forms: from subclinical changes in hormone levels to amiodaroneinduced thyrotoxicosis (AIT) and amiodarone-induced hypothyroidism (AIH). We reported six patients in the age range from two weeks to 14 years, with complex congenital cardiac diseases and severe arrhythmias, who developed amiodarone-induced thyroid dysfunctions: thyrotoxicosis or hypothyroidism or both together. The clinical signs and symptoms of all thyroid dysfunctions were atypical, most patients presented with an aggravation of heart insufficiency. Our patients with thyrotoxicosis were treated with combined therapy including thionamides and corticosteroids due to the presentation of mixed-identified type of AIT. Currently, five patients (one patient's status is unknown) are in biochemical and clinical euthyreosis; however, in one of them it was impossible to discharge amiodarone treatment. Three of them are still treated with levothyroxine, and two do not need thyroid treatment. Amiodarone-induced thyroid dysfunction is usually atypical; therefore, monitoring of thyroid status before, during, and after amiodarone is demanded. AIH could significantly influence the development of the child, while AIT could significantly deteriorate the clinical status of children with complex cardiac diseases. Early and proper diagnose of AIT and AIH allows the introduction of immediate and appropriate treatment considering the cardiac condition of the young patient.

Амиодарон-индуцированный тиреотоксикоз 1 типа: особенности ведения пациентов

Амиодарон-индуцированный тиреотоксикоз 1 типа: особенности ведения пациентов

Plasma Beta-Glucuronidase Activity: A Novel Tool to Distinguish Type 1 from Type 2 Amiodarone-Induced Thyrotoxicosis?

Background: Amiodarone-induced thyrotoxicosis (AIT) is a common and deleterious side effect of amiodarone use. There are two types of AIT, characterized by distinct pathogenic mechanisms and, hence, different treatments. Discriminating between type 1 (AIT1) and type 2 (AIT2) AIT is often very challenging. Beta-glucuronidase (β-G) is a lysosomal enzyme released into the extracellular fluid during inflammation. Objectives: To examine whether the determination of the plasma activity of β-G is useful in distinguishing AIT1 from AIT2. Methods: The study included 67 subjects: 9 with AIT1, 9 with AIT2, 14 with hyperthyroidism due to Grave’s disease or toxic multinodular goiter, 14 with subacute thyroiditis, and 21 euthyroid controls. Thyroid function tests and plasma β-G activity were determined in all participants, while thyrotoxic patients also underwent thyroid ultrasound/scintigraphy and urine iodine excretion assessment. Results: Plasma β-G activity (expressed as mean ± SD in nmol 4-methylumbelliferone [4-MU]/mL plasma/h) in AIT2 was higher compared to AIT1 (2,263.6 ± 771 vs. 1,101.8 ± 201.9, p < 0.05) and similar to subacute thyroiditis (2,263.6 ± 771 vs. 2,083.2 ± 987.5, p = ns). β-G activity did not differ significantly between AIT1 and controls (1,101.8 ± 201.9 vs. 954.6 ± 248.6, p = ns). ROC curve analysis revealed that β-G activity had a high predictive value for destructive processes, namely AIT2 and subacute thyroiditis (AUC 0.846, 95% CI 0.748–0.943) and a cut-off value of 1,480.5 nmol 4-MU/mL plasma/h was able to discriminate between destructive and non-destructive thyroid conditions with 74% sensitivity and 82% specificity. Conclusion: In our study, plasma β-G activity performed well in distinguishing AIT1 from AIT2. Further studies are warranted to establish its usefulness as a discriminator between the two AIT types.

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.

Amiodarone-induced thyrotoxicosis type 2: predictors and treatment options

Amiodarone-induced type 2 thyrotoxicosis remains a  significant problem of modern endocrinology and cardiology. The unique pharmacological character and multifaceted properties of amiodarone explain its high prescription frequency and the leading position among antiarrhythmic drugs. In its turn, cytotoxicity and supra-physiological iodine content in the drug increase the risk of drug-induced destructive thyroiditis. The development of thyrotoxicosis leads to recurrence of cardiac arrhythmias, increased left ventricular dysfunction and manifestations of chronic heart failure. Correct identification of the type of thyrotoxicosis determines the subsequent patient management strategy. Glucocorticoids have been recognized as the first-line treatment among the possible therapy options. Rapid correction of thyrotoxicosis is crucial, especially in elderly patients with severe heart disease. Of interest for practical medicine is the search for specific predictors (deep understanding of the pathogenetic mechanisms) and new possibilities of therapy for amiodarone-induced thyrotoxicosis type 2.

Frequent ventricular extrasystoles after heart transplantation: a late presentation of amiodarone-induced thyrotoxicosis: a case report.

BackgroundThere is a lack of information about a mixed type of amiodarone-induced thyrotoxicosis (AIT) after heart transplantation (HTx) with no amiodarone treatment in almost 1 year. Frequent ventricular extrasystoles (VES) associated with a mixed type of AIT can often be treated using thiamazole and prednisolone, without the need for specific antiarrhythmic treatment.Case summaryWe present a clinical case of a 65-year-old heart transplanted male patient with frequent VES associated with mixed type of AIT. Recipient had managed with amiodarone prior to HTx but there were no indications for it after the surgery. One year after antiarrhythmic treatment was discontinued, monomorphic VES (total amount: 27 472/day) were diagnosed. In addition, our investigation revealed that thyrotoxicosis developed. Prednisolone and thiamazole were added to the treatment with positive outcomes. The antithyroid treatment had been discontinued after 9 months and results of the 24-h Holter electrocardiogram monitoring showed only two VES/24 h.DiscussionThe case highlights the association of amiodarone, thyroid disorders, and VES. In mixed type AIT or if diagnosis is uncertain, it is reasonable to use mixed therapy. Next is to decide whether you need special treatment for VES. There was no evidence of ventricular tachycardia. Thyroid function tests remained normal off antithyroid medications and the total amount of VES significantly decreased. There were no indications for any antiarrhythmic treatment or ablation.

Free thyroid hormons ration in patients with amiodaron-induced thyrotoxicosis type 1 and type 2

Differentiation between amiodarone-induced thyrotoxicosis type 1 (AmIT1) and type 2 (AmIT2) is a diagnostic challenge. The current diagnostic tests are often unable to differentiate these two types of thyrotoxic syndrome. Several studies had shown that the serum T4 level and T3/T4 ratio are significantly different in patients with destructive thyroiditis, and those with Graves` disease. These studies showed that the serum T4 concentration is significantly higher, and the T3/T4 ratio is significantly lower in patients with destructive forms of thyroiditis compared to their values  in Graves’ disease. Since AmIT1 is known to develop in patients with latent Graves` disease, and AmIT2 is a destructive thyroiditis, the purpose of our study was to evaluate the serum FТ4 level and FT4/FT3 ratio in AmIT1 and AmIT2 as an additional diagnostic test for differentiating these types of thyrotoxicosis. 45 patients with thyrotoxicosis (33 with AmIT1 and 12 AmIT2) were included in the study. The diagnosis of thyrotoxicosis type (AmIT1 or AmIT2) was established on the basis of clinical data, color flow Doppler sonography (CFDS), the presence of TSH receptor autoantibody in patients with AmIT1, as well as the effect of treatment. There was no difference in FT3 levels in patients with AmIT1 and AmIT2, while the FT4 values were significantly higher in patients with AmIT2 (36,2±19,1 mmol/L) than in those with AmIT1 (17,8±3,7 mmol/L, p= 0,002). Also, a difference in the FT4/FT3 ratio was found between AmIT1 (2,7±0,8) and AmIT2 (6,1±5,7, p=0,048). Moreover, 75% of patients with AmIT1 had FT4/FT3ratio &lt; 3,10, while 75% of patients with AmIT2 had FT4/FT3 ratio &gt; 3,65. The FT4/FT3 ratio can be used as an additional test in the differential diagnosis AmIT1 and AmIT2.

Issues in amiodarone-induced thyrotoxicosis: Update and review of the literature

Amiodarone, a benzofuranic iodine-rich pan-anti-arrhythmic drug, induces amiodarone-induced thyrotoxicosis (AIT) in 7–15% of patients. AIT is a major issue due to its typical severity and resistance to anti-thyroid measures, and to its negative impact on cardiac status. Classically, AIT is either an iodine-induced thyrotoxicosis in patients with abnormal thyroid (type 1), or due to acute thyroiditis in a “healthy” thyroid (type 2). Determination of the type of AIT is a diagnostic dilemma, as characteristics of both types may be present in some patients. As it is the main etiological factor in AIT, it is recommended that amiodarone treatment should be stopped; however, it may be the only anti-arrhythmic option, needing to be either continued or re-introduced to improve cardiovascular survival. Recently, a few studies demonstrated that amiodarone could be continued or re-introduced in patients with history of type-2 AIT. However, in the other patients, it is recommended that amiodarone treatment be interrupted, to improve response to thioamides and to alleviate the risk of AIT recurrence. In such patients, thyroidectomy is recommended once AIT is under control, allowing safe re-introduction of amiodarone.

Enjeux liés à l’hyperthyroïdie induite par l’amiodarone

Amiodarone, a benzofuranic iodine-rich pan antiarrhythmic drug, is frequently associated with thyroid dysfunction. This side effect is heterogeneous and unpredicted, motivating regular evaluation of thyroid function tests. In contrary to hypothyroidism, amiodarone-induced thyrotoxicosis (AIT) is a challenging situation owing to the risk of deterioration of the general and cardiac status of such debilitating patients. Classically, AIT is either an iodine-induced thyrotoxicosis in patients with an abnormal thyroid (type I), or due to a subacute thyroiditis on a "healthy" thyroid (type II). Even if many studies tried to better identify the types of AIT, the diagnostic dilemma of type of AIT could be present, and many patients are treated by an association of antithyroid drugs (useful for type I AIT) with corticoids (useful for type II AIT). Being the main etiological factor in AIT, amiodarone is supposed to be stopped, but it could remain the only anti-arrhythmic option that is needed to be either continued or reintroduced to improve the cardiovascular survival. Recently, many studies demonstrated that amiodarone could be continued or reintroduced in patients with history of type II AIT. Nevertheless, in the other patients, amiodarone maintenance complicates the therapeutic response to the antithyroid drugs and increases the risk of AIT recurrence. Thus, amiodarone therapy is preferred to be interrupted. In such patients, thyroid ablation is recommended once AIT is under control.

"White Thyroid" on Unenhanced Computed Tomography in Amiodarone-Induced Thyrotoxicosis Type 2.

Amiodarone-induced thyrotoxicosis is a common complication of long-term amiodarone treatment. In a patient with amiodarone-induced lung toxicity and amiodarone-induced thyrotoxicosis type 2 (AIT2), a "white thyroid" was incidentally observed on an unenhanced chest computed tomography (CT) scan. This "white thyroid" resembled a thyroid image on a contrast-enhanced CT scan. Therefore, the thyroid density was prospectively evaluated on unenhanced CT scans in cases of AIT2, in euthyroid patients on amiodarone (AEuth), and in unexposed controls. The aim was to test the hypothesis of a higher thyroid density in AIT2 compared to AEuth. The thyroid density, as measured in Hounsfield Units on unenhanced CT scans, is higher in AIT2 compared to AEuth and much higher than in controls. The causality of this association and its potential diagnostic use require further study.

Amiodarone-induced thyrotoxicosis: state of the art

В обзоре представлены данные литературы последних лет о патогенезе, диагностике, лечении амиодарон-индуцированного тиреотоксикоза (АИТ), который является частым осложнением терапии амиодароном (Ам). Описаны изменения секреции и метаболизма тиреоидныхгомонов под влиянием кратковременной и длительной терапии Ам. Развитие АИТ всегда приводит к ухудшению течения аритмии, усугублению недостаточности кровообращения, утяжелению состояния пациента. Выделяют АИТ 1 типа и АИТ 2 типа, а также смешанную форму. Описаны диагностические критерии АИТ 1 и 2 типа. Наиболее информативным тестом для дифференциальной диагностики АИТ 1, 2 типов и смешанных форм является сонография щитовидной железы с допплеровским исследованием кровотока и сканирование с 99mTc-sestaMIBI. Тактика лечения определяется типом АИТ, состоянием сердечно-сосудистой системы, риском повторных аритмий. Консервативное лечение зависит от типа АИТ и осуществляется тиреостатиками или глюкокортикоидами. Обсуждается возможность продолжения антиаритмической терапии Ам у пациентов, перенесших АИТ. При АИТ 1 типа и смешанной форме требуется отмена препарата, если это невозможно – радикальное лечение тиреотоксикоза (радиойодтерапия, тиреоидэктомия). АИТ 2 типа является самолимитирующимся процессом, при жизненно угрожающих аритмиях прием Ам может быть продолжен. Показана эффективность радиойодтерапии для радикального лечения тиреотоксикоза при АИТ 1 и 2 типа, несмотря на низкий захват радиойода. Однако этот вопрос требует дальнейшего изучения и обсуждения. Для быстрого восстановления эутиреоза у тяжелых больных применяют плазмаферез и тиреоидэктомию.

Evaluation of 99mTc-MIBI in thyroid gland imaging for the diagnosis of amiodarone-induced thyrotoxicosis.

Amiodarone-induced thyrotoxicosis (AIT) is caused by amiodarone as a side effect of cardiovascular disease treatment. Based on the differences in their pathological and physiological mechanisms, many methods have been developed so far to differentiate AIT subtypes such as colour flow Doppler sonography (CFDS) and 24-h radioiodine uptake (RAIU). However, these methods suffer from inadequate accuracy in distinguishing different types of AITs and sometimes lead to misdiagnosis and delayed treatments. Therefore, there is an unmet demand for an efficient method for accurate classification of AIT. Technetium-99 methoxyisobutylisonitrile (99mTc-MIBI) thyroid imaging was performed on 15 patients for AIT classification, and the results were compared with other conventional methods such as CFDS, RAIU and 99mTcO4 imaging. High uptake and retention of MIBI in thyroid tissue is characteristic in Type I AIT, while in sharp contrast, low uptake of MIBI in the thyroid tissue was observed in Type II AIT. Mixed-type AIT shows uptake value between Types I and II. MIBI imaging outperforms other methods with a lower misdiagnosis rate. Among the methods evaluated, MIBI imaging enables an accurate identification of Type I, II and mixed-type AITs by showing distinct images for different types of AITs. The results obtained from our selected subjects revealed that MIBI imaging is a reliable method for diagnosis and classification of AITs and MIBI imaging has potential in the treatment of thyroid diseases. Advances in knowledge: 99mTc-MIBI imaging is a useful method for the diagnosis of AIT. It can distinguish different types of AITs especially for mixed-type AIT, which is usually difficult to treat. 99mTc-MIBI has potential advantages over conventional methods in the efficient treatment of AIT.

A clinical case of cardiac arrhythmia and amiodarone-induced thyrotoxicosis in a patient with coronary heart disease

The article analyzes a clinical cases of cardiac arrhythmia and amiodarone-induced thyrotoxicosis (AIT) in a patient with coronary artery disease (CAD). The article discussed the causes of cardiac arrhythmia and the treatment approach for CAD based on coronary angiography (CAG), as well as the efficacy of revascularization by coronary artery bypass grafting. The importance of hormonal tests and thyroid ultrasound before routine CAG is considered, and at least once in 6 months during amiodarone therapy. Differential diagnosis to clarify the type of AIT is carried out, as type I AIT is treated with tireostatics, and type II AIT with glucocorticosteroids. Comorbidity of somatic diseases in cardiological practice is one of the most crucial prognostic factors defining the outcome of the underlying disease. The article considers the choice of treatment approach for patients with CAD based on clinical tests.

Amiodarone-Induced Thyrotoxicosis Recurrence After Amiodarone Reintroduction

Reintroduction of amiodarone in patients with a history of amiodarone-induced thyrotoxicosis (AIT) is rarely used. To date, the risk of AIT recurrence after amiodarone reintroduction is unpredicted. The aim of the study was to evaluate the risk of AIT recurrence. Retrospectively, from 2000 to 2011, all euthyroid patients with a history of AIT with amiodarone reintroduction were included. Type and severity of the first AIT, amiodarone chronology, and thyroid function evolution after reintroduction of amiodarone were investigated: 46 of 172 patients with AIT history needed amiodarone reintroduction. At first AIT episode, the mean age was 62.2 ± 16 years with male gender predominance; 65% of patients were classified as type 1 AIT. AIT recurred in 14 patients (30%), 12 patients developed hypothyroidism (26%), and 20 patients remained euthyroid (44%). Characteristics of type 1 AIT during the first episode, namely briefer exposure period to amiodarone and longer duration of treatment to normalize thyroid hormones, were predictive of AIT recurrence; 73% of patients (8 of 11) with previous episode of type 1 AIT, who did not receive a preventive thioamide treatment, developed a second episode of AIT. Thioamide preventive treatment could be useful to prevent type 1 AIT recurrence. In conclusion, AIT recurrence after amiodarone reintroduction is 4 times more frequent in patients with type 1 AIT history. Thyroid ablation before amiodarone reintroduction in patients with a history of type 1 AIT is preferred. Preventive thioamide treatment could be suggested in patients with type 1 AIT history pending for surgery.

Quantitative assessment of thyroid-to-background ratio improves the interobserver reliability of technetium-99m sestamibi thyroid scintigraphy for investigation of amiodarone-induced thyrotoxicosis

Amiodarone-induced thyrotoxicosis (AIT) is caused by excessive hormone synthesis and release (AIT I), a destructive thyroiditis (AIT II), or a combination of both (AIT Ind). Although no gold-standard diagnostic test is available, technetium-99m sestamibi thyroid scintigraphy (99mTc-STS) has been previously reported to be an accurate tool for differentiating subtypes with important therapeutic implications. However, the information to guide reporting of 99mTc-STS is qualitative and highly subjective. This study aims to compare the interobserver reliability of 99mTc-STS before and after the use of quantitative thyroid-to-background ratios (TBRs) displayed on a time-activity curve for differentiation of AIT subtypes. A retrospective audit of Nuclear Medicine Departments at Royal Melbourne Hospital (Parkville, Victoria, Australia) and Cabrini Hospital (Malvern, Victoria, Australia) identified 15 consecutive 99mTc-STS studies performed for AIT. Four nuclear medicine physicians reported the studies according to previously established criteria (series 1). Quantitative TBR and estimated 'normal' range TBR were subsequently provided before the studies were reordered and reported again (series 2). Interobserver reliability was calculated using Fleiss' κ statistic for each assessment. The overall percentage of agreement (PoA) and κ statistics for use of conventional 99mTc-STS for diagnosis of AIT improved from 47 to 80% and from 0.30 to 0.67 following the use of quantitative TBR displayed on a time-activity curve with reference to a normal population. Interobserver reliability improved substantially under all diagnostic comparisons, particularly for differentiation of either AIT I (PoA 80% to 94%, κ: 0.48 to 0.84) or AIT Ind (PoA 47% to 82%, κ: -0.05 to 0.51) from other types of AIT. Use of quantitative TBR improves the interobserver reliability of reporting 99mTc-STS for investigation of different types of AIT. There is 'almost perfect' agreement upon differentiation of AIT I from AIT II and AIT Ind, with important implications for rationalizing the use of corticosteroid therapy. Prospective identification of AIT Ind is improved from 'poor' to a 'moderate' level of agreement to facilitate rational use of combination therapy at diagnosis.