Amiodarone-induced Thyroid Dysfunction Research Articles

Cardiac evaluation in amiodarone-induced thyroid dysfunction with suspected cardiac ischemia?: a case report and review of the literature

BackgroundAmiodarone-induced thyroid dysfunction (AIT) is a side-effect associated with the use of Amiodarone for the treatment of refractory arrythmias. Resulting hyperthyroidism can precipitate cardiac complications, including cardiac ischemia and myocardial infarction, although this has only been described in a few case reports.Case presentationWe present here a clinical scenario involving a 66-year-old male Caucasian patient under Amiodarone for atrial fibrillation, who developed AIT. In the presence of dyspnea, multiple cardiovascular risk factors and ECG abnormalities, a transthoracic echocardiogram was performed, showing inferobasal hypokinesia. This led to further investigations through a cardiac PET-CT, where cardiac ischemia was suspected. Ultimately, the coronary angiography revealed no abnormalities. Nonetheless, these extensive cardiologic investigations led to a delay in initiating an emergency endovascular revascularization for acute-on-chronic left limb ischemia. Although initial treatment using Carbimazole was not successful after three weeks, the patient reached euthyroidism after completion of the treatment with Prednisone so that eventually thyroidectomy was not performed. Endovascular revascularization was finally performed after more than one month.ConclusionsWe discuss here cardiac abnormalities in patients with AIT, which may be due to relative ischemia secondary to increased metabolic demand during hyperthyroidism. Improvement of cardiac complications is expected through an optimal AIT therapy including medical therapy as the primary approach and, when necessary, thyroidectomy. Cardiac investigations in the context of AIT should be carefully considered and may not justify delaying other crucial interventions. If considered mandatory, diagnostic procedures such as coronary angiography should be preferred to functional testing.

Amiodarone induced thyroid dysfunction

Abstract Introduction Amiodarone causes hypothyroidism in 12-25% of treated patients, depending on the classification of hypothyroidism. Amiodarone induced thyrotoxicosis is seen in 1.2%-12%. It is recommended to taper thyroid supplementation after discontinuing amiodarone. Purpose To investigate the prevalence of amiodarone induced thyroid dysfunction in Iceland and the effects of dosage and treatment duration. Design The study population comprised of all patients that were subscribed amiodarone in Iceland during the calendar year of 2014, a total of 1054 patients. Ten patients that never took amiodarone were excluded and there was missing data in 22. Hypothyroidism had been diagnosed in 91 patients before starting amiodarone and 59 took amiodarone for less than 90 days and were excluded from further analysis, leaving 871 patients. Follow up data was obtained from the national health care records both retrospectively and prospectively for first prescription of amiodarone and signs of thyroid related problems. Amiodarone induced hypothyroidism was defined as a raised TSH more than 90 days after starting treatment and further classified into subclinical (with normal T4) and overt (low T4). Amiodarone induced thyrotoxicosis was defined as low TSH with an elevated T4. Results Amiodarone induced hypothyroidism was seen in 22.2% of patients at a mean age of 74 years. 10.7% had overt AIH and 11.6% had subclinical hypothyroidism. Hypothyroidism occurred on average after 3.3 ±0.4 years of treatment. The incidence increased with treatment duration and peaked at 41.8% after 15 years of treatment. The risk did not change with dosage. Only 4.6% on thyroid supplementation therapy had stopped treatment after a mean follow-up of 4.5 years after discontinuing amiodarone. Amiodarone induced thyrotoxicosis was seen in 10.0% with a mean age of 65.6 years. The mean duration of treatment at diagnosis of thyrotoxicosis was 3.9 ±0.6 years. The cumulative risk of thyrotoxicosis was highest (9.9%) during years 3 to 5 but persisted with ongoing treatment and peaked at 17.6% after 13 years of treatment. Higher dosage of amiodarone increased the risk in a dose dependent manner. It was 5% with <200 mg, 11.8% with 200 mg and 14.1% with >200mg (p<0.01). Hospital admission due to thyrotoxicosis was required in 35.3% of patients, 8.8% had thyroidectomies, 2.0% died and 26.5% had hypothyroidism following thyrotoxicosis. 48% were treated with carbimazole, of them 2.0% suffered agranulocytosis, 4.1% had hepatitis and 4.1% had pancreatitis. Conclusion In this nationwide study we found that long term users of amiodarone are at a higher risk of amiodarone induced hypothyroidism or thyrotoxicosis than previously described. Thyroid supplementation treatment is rarely stopped despite the pro-arrhythmic risk of overtreating hypothyroid patients. The high incidence of thyroid related adverse effects is a reminder of the serious side effects of amiodarone treatment.Amiodarone induced hypothyroidismAmiodarone induced Thyrotoxicosis

Type 2 amiodarone-induced thyrotoxicosis: prevalence, time and predictors of development

BACKGROUND: Amiodarone takes a leading position in arrhythmological practice in the prevention and relief of various cardiac arrhythmias. Type 2 amiodarone-induced thyrotoxicosis is a frequent side effect of the drug. It is the most complex type of thyroid dysfunction both in terms of the severity of clinical manifestations, and in terms of understanding the mechanisms of pathogenesis, possibility of differential diagnosis and providing effective treatment. Due to the increasing life expectancy of the population, corresponding increase in the frequency of cardiac arrhythmias, the problem does not lose its relevance. Identification of predictors, assessment and prediction of the individual risk of developing this thyroid pathology is a necessity in daily clinical practice for making a reasonable decision when prescribing the drug, determining the algorithm for further dynamic monitoring of the patient.AIM: To evaluate the structure of amiodarone-induced thyroid dysfunction, prevalence, time and predictors of development type 2 amiodarone-induced thyrotoxicosis in a prospective cohort study. MATERIALS AND METHODS: The study involved 124 patients without thyroid dysfunction who received amiodarone therapy for the first time. Evaluation of the functional state of the thyroid gland was performed initially, after prescribing the drug for the first 3 months 1 time per month, in the future – every 3 months. The follow-up period averaged 12-24 months. The end of the observation occurred with the development of amiodaron-induced thyroid dysfunction or patient's refusal to further participate in the study. For the differential diagnosis of the type of amiodarone-induced thyrotoxicosis, the level of anti-TSH receptor antibodies and thyroid scintigraphy with technetium pertechnetate were determined. The type and frequency of thyroid dysfunction, time and predictors of development type 2 amiodarone-induced thyrotoxicosis were evaluated.RESULTS: The structure of amiodarone-induced thyroid dysfunction was represented by hypothyroidism in 19,3% (n=24), type 1 thyrotoxicosis in 1,6% (n=2), type 2 thyrotoxicosis in 23,4% (n=29). The median time of its development was 92,0 [69,0;116,0] weeks; the average period of common survival – 150,2±12,6 weeks (95% CI: 125,5–175,0), median – 144±21,7 weeks (95% CI: 101,4–186,6). The main predictors of type 2 amiodarone-induced thyrotoxicosis were: age (OR=0,931; 95% CI: 0,895–0,968; p<0.001), BMI (OR=0,859; 95% CI: 0,762–0,967; p=0,012), time from the start of amiodarone therapy (OR=1,023; 95% CI: 1,008–1,038; p=0,003). Age ≤60 years was associated with increased risk of the dysfunction by 2.4 times (OR=2,352; 95% CI: 1,053–5,253; p=0,037), BMI≤26,6 kg/m2 – 2,3 times (OR=2,301; 95% CI: 1,025–5,165; p=0,043). CONCLUSION: The results allow to personalized estimate the risk of type 2 amiodarone-induced thyrotoxicosis and determine the patient's management tactic.

Explainable Machine Learning Techniques To Predict Amiodarone-Induced Thyroid Dysfunction Risk: Multicenter, Retrospective Study With External Validation

Machine learning offers new solutions for predicting life-threatening, unpredictable amiodarone-induced thyroid dysfunction. Traditional regression approaches for adverse-effect prediction without time-series consideration of features have yielded suboptimal predictions. Machine learning algorithms with multiple data sets at different time points may generate better performance in predicting adverse effects. We aimed to develop and validate machine learning models for forecasting individualized amiodarone-induced thyroid dysfunction risk and to optimize a machine learning-based risk stratification scheme with a resampling method and readjustment of the clinically derived decision thresholds. This study developed machine learning models using multicenter, delinked electronic health records. It included patients receiving amiodarone from January 2013 to December 2017. The training set was composed of data from Taipei Medical University Hospital and Wan Fang Hospital, while data from Taipei Medical University Shuang Ho Hospital were used as the external test set. The study collected stationary features at baseline and dynamic features at the first, second, third, sixth, ninth, 12th, 15th, 18th, and 21st months after amiodarone initiation. We used 16 machine learning models, including extreme gradient boosting, adaptive boosting, k-nearest neighbor, and logistic regression models, along with an original resampling method and 3 other resampling methods, including oversampling with the borderline-synthesized minority oversampling technique, undersampling-edited nearest neighbor, and over- and undersampling hybrid methods. The model performance was compared based on accuracy; Precision, recall, F1-score, geometric mean, area under the curve of the receiver operating characteristic curve (AUROC), and the area under the precision-recall curve (AUPRC). Feature importance was determined by the best model. The decision threshold was readjusted to identify the best cutoff value and a Kaplan-Meier survival analysis was performed. The training set contained 4075 patients from Taipei Medical University Hospital and Wan Fang Hospital, of whom 583 (14.3%) developed amiodarone-induced thyroid dysfunction, while the external test set included 2422 patients from Taipei Medical University Shuang Ho Hospital, of whom 275 (11.4%) developed amiodarone-induced thyroid dysfunction. The extreme gradient boosting oversampling machine learning model demonstrated the best predictive outcomes among all 16 models. The accuracy; Precision, recall, F1-score, G-mean, AUPRC, and AUROC were 0.923, 0.632, 0.756, 0.688, 0.845, 0.751, and 0.934, respectively. After readjusting the cutoff, the best value was 0.627, and the F1-score reached 0.699. The best threshold was able to classify 286 of 2422 patients (11.8%) as high-risk subjects, among which 275 were true-positive patients in the testing set. A shorter treatment duration; higher levels of thyroid-stimulating hormone and high-density lipoprotein cholesterol; and lower levels of free thyroxin, alkaline phosphatase, and low-density lipoprotein were the most important features. Machine learning models combined with resampling methods can predict amiodarone-induced thyroid dysfunction and serve as a support tool for individualized risk prediction and clinical decision support.

PSUN38 Incidence and prognosis of amiodarone induced thyroid dysfunction: a nationwide cohort study in Korea

Abstract Background Amiodarone is commonly associated with thyroid dysfunction. Incidence of amiodarone induced thyroid dysfunction is variable in the literature and prognosis of patients who developed amiodarone induced thyroid dysfunction compared to euthyroid patients is still unclear. Results During a mean follow up of 7.4 years, 777 (3.9%) developed thyrotoxicosis (incidence rate 3.96 per 1000 person years) and 2,225 (11.3%) developed hypothyroidism (incidence rate 11.93 per 1000 person years). Patients with thyrotoxicosis or hypothyroidism had a lower MACE rate compared to euthyroid patients (45.2% vs. 50.2% and 48.5% vs. 50.2%). Multivariate analysis revealed that older age (>65 years), chronic kidney, ischemic heart disease and chronic obstructive lung disease were independent risk factors of MACE. Patients who developed thyrotoxicosis or hypothyroidism had a lower risk of MACE than euthyroid patients (HR=0.75 [95% CI: 0.68-0.83] and HR=0.73 [95% CI: 0.69-0.77]). Conclusion The incidence of amiodarone-induced thyrotoxicosis was higher compared to hypothyroidism. The patients with thyrotoxicosis or hypothyroidism had lower cardiovascular events in patients treated with amiodarone. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Case report: Amiodarone-induced thyroid dysfunction

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

The effects of amiodarone on thyroid function in pediatric and adolescent patients.

Amiodarone-induced thyroid dysfunction is well established. The present review discusses recent literature related to the effects of amiodarone on the thyroid gland and thyroid function in pediatrics. Current guidelines in adults treated with amiodarone recommend baseline thyroid function testing followed by initiation of thyroid hormone monitoring after 3 months on therapy. Two retrospective studies to evaluate amiodarone-induced thyroid dysfunction in children and young adults reveal thyroid dysfunction as soon as 2 weeks after amiodarone initiation with a greater percentage of pediatric patients developing amiodarone-induced hypothyroidism rather than thyrotoxicosis. Although additional studies are needed to determine if AIH is associated with negative impact on growth and neurocognitive development, what is clear is that in both adults and pediatrics, there is low compliance with recommended side effect-monitoring guidelines. Pediatric patients are at similarly high risk to develop amiodarone-induced thyroid dysfunction as are adults. It is hoped that through improved education of providers and patients further research into the incidence, the potential risks of amiodarone therapy and the potential benefits of thyroid hormone replacement therapy in patients with AIH will be investigated and reported.

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.

Amiodarone-induced thyroid dysfunction in children: insights from the THYRAMIO study.

Background:Amiodarone treatment is effective against various types of arrhythmias but is associated with adverse effects affecting, among other organs, thyroid function. Amiodarone-induced thyroid dysfunction was not thoroughly evaluated in children as it was in adults, yet this affection may lead to irreversible neurodevelopmental complications. Our study aimed to define the incidence and risk factors of amiodarone-induced thyroid dysfunction in children.Methods:The study was designed as an observational study with a retrospective clinical series of 152 children treated by amiodarone in the Pediatric Cardiology Unit of our center from 1990 to 2019. All patients were divided into three groups according to their thyroid status: euthyroid, AIH (amiodarone-induced hypothyroidism) or AIT (amiodarone-induced thyrotoxicosis). Patients from these three groups were compared in terms of key clinical and therapeutic features.Results:Amiodarone-induced thyroid dysfunction was present in 23% of patients. AIT (5.3%) was three times less common than AIH (17.7%), and its occurrence increased with older age (p < 0.05), treatment dosage (p < 0.05), treatment duration (p < 0.05) and the number of loading doses administered (p < 0.05). There were no distinctive clinical features between euthyroid and AIH groups. A multivariable prediction model of AIT was built, with a yield of 66.7% as positive predictive value and 96.7% as negative predictive value.Conclusion:We observed that one in five children developed amiodarone-induced thyroid dysfunction. Special attention is required for older children with a high dosage and long-term therapy and who received a large number of loading doses, since these children are at risk to develop AIT, which is more delicate to manage than AIH.

The effects of amiodarone on thyroid function in pediatric and young adult patients

Context Amiodarone is used in patients with arrhythmias, but thyroid dysfunction [amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH)] is a common adverse effect. As the onset of AIT and AIH has not been studied in children, the timing of dysfunction and long-term monitoring are not known in this population. Objective To describe the incidence and timing of amiodarone-induced thyroid dysfunction in children and adolescents, with a secondary aim to identify risk factors for amiodarone-induced thyroid dysfunction, and to identify variance in thyroid hormone surveillance and treatment. Design Retrospective review of thyroid dysfunction in children and young adults treated with amiodarone between 2007 and 2018. Setting Children's Hospital of Philadelphia. Patients Children and young adults treated with amiodarone. Main outcome measures Prevalence of amiodarone-induced thyroid dysfunction. Results Of 484 patients, 190 had thyroid-function testing; 17.3% were found to have subclinical hypothyroidism, and 13.7% testing developed hypothyroidism. Hyperthyroidism occurred in 2.1%. In patients with subclinical hypothyroidism, 63% returned to normal thyroid function without thyroid hormone replacement. Only 26% of patients with hypothyroidism had spontaneous normalization of thyroid function. Twenty-five percent of AIT patients had spontaneous normalization of thyroid function. Conclusions This study looks at a pediatric and young-adult population in an effort to describe the natural history of amiodarone-induced thyroid dysfunction. Based on our data, we recommend that a complete thyroid-function panel be obtained within the first week and then at weekly intervals for the first 5 weeks after initiation. The majority of thyroid dysfunction was noted within the first 35 days of treatment.

The Role of Nuclear Medicine in the Clinical Management of Benign Thyroid Disorders, Part 1: Hyperthyroidism.

Benign thyroid disorders, especially hyper- and hypothyroidism, are the most prevalent endocrine disorders. The most common etiologies of hyperthyroidism are autoimmune hyperthyroidism (Graves disease, GD), toxic multinodular goiter (TMNG), and toxic thyroid adenoma (TA). Less common etiologies include destructive thyroiditis (e.g., amiodarone-induced thyroid dysfunction) and factitious hyperthyroidism. GD is caused by autoantibodies against the thyroid-stimulating hormone (TSH) receptor. TMNG and TA are caused by a somatic activating gain-of-function mutation. Typical laboratory findings in patients with hyperthyroidism are low TSH, elevated free-thyroxine and free-triiodothyronine levels, and TSH-receptor autoantibodies in patients with GD. Ultrasound imaging is used to determine the size and vascularity of the thyroid gland and the location, size, number, and characteristics of thyroid nodules. Combined with lab tests, these features constitute the first-line diagnostic approach to distinguishing different forms of hyperthyroidism. Thyroid scintigraphy with either radioiodine or 99mTc-pertechnetate is useful to characterize different forms of hyperthyroidism and provides information for planning radioiodine therapy. There are specific scintigraphic patterns for GD, TMNG, TA, and destructive thyroiditis. Scintigraphy with 99mTc-sestamibi allows differentiation of type 1 from type 2 amiodarone-induced hyperthyroidism. The radioiodine uptake test provides information for planning radioiodine therapy of hyperthyroidism. Hyperthyroidism can be treated with oral antithyroid drugs, surgical thyroidectomy, or 131I-iodide. Radioiodine therapy is generally considered after failure of treatment with antithyroid drugs, or when surgery is contraindicated or refused by the patient. In patients with TA or TMNG, the goal of radioiodine therapy is to achieve euthyroid status. In GD, the goal of radioiodine therapy is to induce hypothyroidism, a status that is readily treatable with oral thyroid hormone replacement therapy. Dosimetric estimates based on the thyroid volume to be treated and on radioiodine uptake should guide selection of the 131I-activity to be administered. Early side effects of radioiodine therapy (typically mild pain in the thyroid) can be handled by nonsteroidal antiinflammatory drugs. Delayed side effects after radioiodine therapy for hyperthyroidism are hypothyroidism and a minimal risk of radiation-induced malignancies.

Thyroid effects of amiodarone: clinical update.

Amiodarone-induced thyroid dysfunction is well established and commonly encountered but is associated with several diagnostic and management challenges. The present review discusses recent evidence published related to the effects of amiodarone on the thyroid gland and thyroid function. Retrospective studies to evaluate amiodarone-induced thyroid dysfunction in children show the occurrence of potential clinically significant changes within 2 weeks of amiodarone initiation that may not be detected if standard adult guidelines for thyroid hormone monitoring are followed. A small study evaluating beta-glucuronidase activity in amiodarone-induced thyrotoxicosis (AIT) demonstrated higher levels in patients with AIT type 2 compared to type 1. New data have suggested the incidence of agranulocytosis may be higher in patients on thionamides with AIT compared to hyperthyroidism because of other causes. In a small study, investigators demonstrated the use of a combination of intravenous and oral steroids to treat refractory AIT which needs to be evaluated in further controlled trials. Finally, recent data demonstrated a possible mortality benefit of surgery over medical therapy for AIT in patients with moderate to severe reduction in left ventricular ejection fraction. Recent research regarding the prevalence, diagnosis, and management of amiodarone-induced thyroid dysfunction were reviewed.

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.

The Effects of Amiodarone on Thyroid Function in Pediatric and Young Adult Patients

Amiodarone is used in patients with arrhythmias, but thyroid dysfunction [amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH)] is a common adverse effect. As the onset of AIT and AIH has not been studied in children, the timing of dysfunction and long-term monitoring are not known in this population. To describe the incidence and timing of amiodarone-induced thyroid dysfunction in children and adolescents, with a secondary aim to identify risk factors for amiodarone-induced thyroid dysfunction, and to identify variance in thyroid hormone surveillance and treatment. Retrospective review of thyroid dysfunction in children and young adults treated with amiodarone between 2007 and 2018. Children's Hospital of Philadelphia. Children and young adults treated with amiodarone. Prevalence of amiodarone-induced thyroid dysfunction. Of 484 patients, 190 had thyroid-function testing; 17.3% were found to have subclinical hypothyroidism, and 13.7% testing developed hypothyroidism. Hyperthyroidism occurred in 2.1%. In patients with subclinical hypothyroidism, 63% returned to normal thyroid function without thyroid hormone replacement. Only 26% of patients with hypothyroidism had spontaneous normalization of thyroid function. Twenty-five percent of AIT patients had spontaneous normalization of thyroid function. This study looks at a pediatric and young-adult population in an effort to describe the natural history of amiodarone-induced thyroid dysfunction. Based on our data, we recommend that a complete thyroid-function panel be obtained within the first week and then at weekly intervals for the first 5 weeks after initiation. The majority of thyroid dysfunction was noted within the first 35 days of treatment.

Pre-operative embolization of thyroid arteries in a case of refractory amiodarone-induced thyrotoxicosis. Case report

Introduction: Amiodarone has become one of the main antiarrhythmic drugs. However, it may cause a wide variety of adverse effects, sometimes severe. Amiodarone-induced thyroid dysfunction is one of the best known problems, resulting in either thyrotoxicosis or hypothyroidism. Case presentation: A patient who, after 2 years of using amiodarone for the control of atrial fibrillation, developed thyrotoxicosis, refractory to conventional medical treatment. To optimize the patient's clinical condition before total thyroidectomy, embolization of thyroid arteries was performed. Conclusion: Embolization of the thyroid arteries as bridge therapy to thyroidectomy is an uncommon alternative in patients with amiodarone-induced hyperthiroidism. However, this treatment was useful to improve our patient's symptoms and to optimize the anesthetic/surgical procedure.

Amiodarone induced thyroid dysfunction

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Patterns of amiodarone-induced thyroid dysfunction in infants and children

Heart Rhythm Society guidelines recommend obtaining thyroid function tests (TFTs) at amiodarone initiation and every 6 months thereafter in adults, with no specific pediatric recommendations. Untreated hypothyroidism in young children negatively affects brain development and somatic growth, yet the optimal screening frequency for pediatric patients remains unclear, and limited data exist on pediatric amiodarone-induced thyroid dysfunction. The purpose of this study was to describe the patterns of amiodarone-induced thyroid dysfunction in pediatric patients. We established a retrospective cohort of 527 pediatric patients who received amiodarone between 1997 and 2017. We defined amiodarone therapy lasting 3-30 days as "short term" and >30 days as "long term." The final cohort (n = 150) consisted of 27 neonates (18%), 25 infants (16%), 27 young children (18%), and 71 children (47%). Of the children in whom TFTs were checked, half (50.8%) developed a thyroid-stimulating hormone (TSH) value above the reference for age. Neonates had the highest median peak TSH values in both short- and long-term groups: 23.5 mIU/L (interquartile range 11.4-63.1) and 28.8 mIU/L (interquartile range 11.4-34.4), respectively. Although concurrent use of inotropic support was significantly associated with lower initial TSH values, no variable related to cardiac illness or type of heart disease was associated with peak TSH values. Neonates and infants receiving amiodarone had more thyroid dysfunction with greater degrees of TSH elevation than older children. TSH elevations occurred early, even with short-term exposure. Given the concern for brain development and growth in hypothyroid children, our results suggest the need for more rigorous pediatric-specific thyroid monitoring guidelines.

Diagnosis and Clinical Course of Three Adolescents with Amiodarone-Induced Hyperthyroidism

Amiodarone-induced hyperthyroidism is a known side effect of amiodarone treatment. In the pediatric population, long-term amiodarone treatment is rarely indicated because of its severe side effects including thyroid function impairment. Treatment is therefore restricted to therapy-resistant arrhythmias. In the literature, scarce data are available on the management and therapy of amiodarone-induced thyroid dysfunction at a young age. We present three adolescent patients developing amiodarone-induced thyrotoxicosis in the months after amiodarone therapy. A latency period for thyroid dysfunction has been described in adulthood but was not previously reported in pediatric patients. The gap between amiodarone treatment and the development of symptoms and the diagnosis of hyperthyroidism was between 3 and 10months. In two patients, hyperthyroidism was transient and resolved without treatment. These two patients, one boy and on girl, were almost asymptomatic. In contrast, in one male patient overt and severe hyperthyroidism developed. We began treatment with thiamazole without benefit. Control of hyperthyroidism was achieved under prednisone treatment, which was continued for 9months. Clinical evaluation proved an amiodarone-induced destructive thyroiditis in this patient. Amiodarone-induced thyroid dysfunction is frequent also in pediatric patients with long-term amiodarone treatment. Patients and clinicians should be aware of the impact of amiodarone on thyroid function during and also in the months and maybe years after treatment. Careful follow-up is needed, as symptoms might be associated with the underlying cardiac disease in these patients. Amiodarone-induced thyrotoxicosis often resolves without treatment but can be challenging in some cases.

Correction: Amiodarone-Induced Thyroid Dysfunction: A Clinical Update.

Correction: Amiodarone-Induced Thyroid Dysfunction: A Clinical Update.

Amiodarone-induced thyrotoxicosis

Amiodarone-induced thyroid dysfunction occurs in about 15-20% of patients under amiodarone therapy. Amiodarone-induced hypothyroidism (AIH) can develop in patients with an apparently normal thyroid gland or in those with an underlying chronic autoimmune thyroiditis. On a clinical ground, AIH is not challenging and can be easily treated with L-thyroxine therapy. Amiodarone-induced thyrotoxicosis (AIT) can occur in patients with (AIT 1) or without (AIT 2) an underlying thyroid disease. AIT 1 is a true iodine-induced hyperthyroidism occurring in patients with an underlying thyroid autonomy while AIT 2 is a drug-induced destructive thyroiditis. According to the different pathogenetic mechanism, AIT 2 is treated with glucocorticoids while AIT 1 usually responds to thionamides. Thyroidectomy should be considered when AIT represents an imminent risk for cardiac conditions, when patients require a prompt resolution of thyrotoxicosis or when they do not respond to the medical therapy. An effective collaboration between cardiologists and endocrinologists is crucial in each part of the management of AIT patients, including the evaluation of cardiological conditions with regard to thyroid hormone excess and whether, or not, it is necessary to continue amiodarone therapy.