Amiodarone-induced Thyrotoxicosis Research Articles

Is there a familial predisposition to severe amiodarone-induced thyrotoxicosis? Report of two cases

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

What you choose makes the difference: the first medical therapy for amiodarone-induced thyrotoxicosis has significant implications on cardiovascular events and hospitalizations

What you choose makes the difference: the first medical therapy for amiodarone-induced thyrotoxicosis has significant implications on cardiovascular events and hospitalizations

Amiodarone-induced thyrotoxicosis refractory to medical therapy: A case report

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

Role of plasmapheresis in the management of severe amiodarone-induced hyperthyroidism refractory to conventional medical treatment

Role of plasmapheresis in the management of severe amiodarone-induced hyperthyroidism refractory to conventional medical treatment

Heart Mate 3 Pump Thrombosis After Ventricular Tachycardia Ablation: Pushing the Boundaries of Hemocompatibility

<h3>Introduction</h3> The risk for pump thrombosis (PT) following ventricular tachycardia (VT) ablation in HeartMate II and HeartWare HVAD left ventricular assist devices (LVADs) has been described previously; however, it is unknown whether Heart Mate 3 (HM3) LVADs are also at increased risk of PT following VT ablation. <h3>Case Report</h3> A 51-year-old male with non-ischemic cardiomyopathy status post HM3 LVAD as destination therapy, VT on mexiletine and quinidine with previous VT ablation, and amiodarone-induced thyrotoxicosis presented to the emergency room in VT storm after multiple defibrillator shocks. He underwent successful endocardial/epicardial VT ablation of seven VT morphologies, ethanol ablation of the coronary sinus branch, as well as coil embolization of two left circumflex branches that fed the culprit territory. Target ACT was achieved throughout the procedure and he was bridged to warfarin with a therapeutic INR upon discharge. Two weeks later, he presented with low flow LVAD alarms, a subtherapeutic INR, and an elevated lactate dehydrogenase concerning for PT. Despite volume resuscitation and pressors, he required initiation of venoarterial extracorporeal membrane oxygenation (VA-ECMO), intra-aortic balloon pump, and underwent a LV outflow tract aortogram. Thrombus was noted in the LVAD outflow graft and the LVAD flow was 0 liters per minute. Thrombolytics were not given due to the patient's tenuous status and need for emergent pump exchange, so decision was made to turn off the LVAD to prevent a cardioembolic event while he was supported by VA-ECMO. Transthoracic echocardiogram confirmed PT with a large thrombus extending out of the inflow cannula. The patient was deemed not to be a surgical candidate given a high operative mortality after worsening shock, liver failure, and bacteremia. His family proceeded with comfort care and support was withdrawn. <h3>Summary</h3> While PT is rare with HM3 LVADs even with lower intensity anticoagulation, there may be a higher risk of PT after VT ablation.

Salvage total thyroidectomy for amiodarone-induced thyrotoxicosis in a SARS-CoV-2 positive patient: results of the viral genome research on the pathology sample of this destructive thyroiditis

Salvage total thyroidectomy for amiodarone-induced thyrotoxicosis in a SARS-CoV-2 positive patient: results of the viral genome research on the pathology sample of this destructive thyroiditis

Invasive Heart Rate Control as a Salvage Therapy in Amiodarone-induced Thyroid Storm.

Atrial fibrillation (AF) is the most common arrhythmia, and amiodarone is one of the most commonly used drugs for medical cardioversion of AF, which should be used carefully due to its toxic effects. Amiodaroneinduced thyrotoxicosis (AIT) may develop in amiodarone-treated patients. In contrast, the most common rhythm disturbance accompanying a thyroid storm is AF. This association may put both AF and thyrotoxicosis treatment into a vicious circle, leading to AI cardiomyopathy. Herein, we aimed to present atrioventricular node ablation as a salvage therapy in a patient with AIT who had AF-causing hemodynamic impairment, resistance to medical therapy, and cardioversion.

AMIODARONE AND THYROID DYSFUNCTION.

Thyroid gland has a key role in maintaining the body homeostasis. Thyroxine is the main hormone secreted from the thyroid gland, its effect being predominantly achieved after the intracellular conversion of thyroxine to triiodothyronine, which exhibits a higher affinity for the receptor complex, thus modifying gene expression of the target cells. Amiodarone is one of the most commonly used antiarrhythmics in the treatment of a broad spectrum of arrhythmias, usually tachyarrhythmias. Amiodarone contains a large proportion of iodine, which is, in addition to the intrinsic effect of the medication, the basis of the impact on thyroid function. It is believed that 15%-20% of patients treated with amiodarone develop some form of thyroid dysfunction. Amiodarone may cause amiodarone-induced hypothyroidism (AIH) or amiodarone-induced thyrotoxicosis (AIT). AIT is usually developed in the areas with too low uptake of iodine, while AIH is developed in the areas where there is a sufficient iodine uptake. Type 1 AIT is more common among patients with an underlying thyroid pathology, such as nodular goiter or Graves' (Basedow's) disease, while type 2 mostly develops in a previously healthy thyroid. AIH is more common in patients with previously diagnosed Hashimoto's thyroiditis. Combined types of the diseases have also been described. Patients treated with amiodarone should be monitored regularly, including laboratory testing and clinical examinations, to early detect any deviations in the functioning of the thyroid gland. Supplementary levothyroxine therapy is the basis of AIH treatment. In such cases, amiodarone therapy quite often need not be discontinued. Type 1 AIT is treated with thyrostatic agents, like any other type of thyrotoxicosis. If possible, the underlying amiodarone therapy should be discontinued. In contrast to type 1 AIT, the basic pathophysiological substrate of which is the increased synthesis and release of thyroid hormones, the basis of type 2 AIT is destructive thyroiditis caused by amiodarone, desethylamiodarone as its main metabolite, and an increased iodine uptake. Glucocorticoid therapy is the basis of treatment for this type of disease.

Pulse methylprednisolone as preparation for thyroidectomy for drug-resistant amiodarone-induced thyrotoxicosis

Pulse methylprednisolone as preparation for thyroidectomy for drug-resistant amiodarone-induced thyrotoxicosis

Increasing use of amiodarone in Norway

Abstract Background Amiodarone may be used against ventricular arrhythmias to reduce ICD-shocks, and for rhythm control in patients with atrial fibrillation. The 2020 ESC atrial fibrillation guidelines upgraded the recommendation for amiodarone in rhythm control to class I, level of evidence A, although still with a caution to consider other antiarrhythmic drugs first. Amiodarone is the most potent antiarrhythmic drug in clinical use, but it has frequent and potentially severe side effects affecting several organ systems. We have seen an increasing number of patients with amiodarone-induced thyrotoxicosis. Purpose We wanted to study the prescription rate of amiodarone in Norway, which indications were most prevalent, and whether there had been any changes over time. Methods From the Norwegian Prescription Registry, we have collected data on how many patients had received amiodarone, and the number of defined daily doses delivered (DDDs), related to various reimbursement categories. Results From 2010 to 2019, the number of individuals receiving amiodarone from a pharmacy in Norway increased from 5359 to 7789 (45% increase), and the number of DDDs delivered from 994905 to 1412796 (42% increase) (Figure). With an atrial fibrillation-related reimbursement code, we found during the same period an increase of individuals from 3616 to 5776 (60% increase) and number of DDDs from 661531 to 1061601 (60% increase). The dispenses for ventricular arrhythmia-related reimbursement codes were close to unchanged during the same period of years (Figure). The fraction of amiodarone use related to atrial fibrillation increased from 66% in 2009 to 75% in 2019. Conclusion We observed a 42–45% increase in the total use of amiodarone over 10 years, and almost the whole increase was related to atrial fibrillation. In 2019, atrial fibrillation-related diagnoses accounted for 75% of the total amount of amiodarone dispensed in Norway. Due to the several side effects of amiodarone, we are concerned if the threshold for use of amiodarone diminishes. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Norwegian Institute of Public HealthOslo University Hospital, Rikshospitalet Number of patientsNumber of DDDs

Surgical treatment of patient with combination of amiodaron-induced thyrotoxic and esophagesl cancer

The article presents the successful experience of surgical treatment of a patient with a malignant tumor of the esophagus, which was detected in a patient with amiodarone-induced thyrotoxicosis. Thyroidectomy made it possible to quickly eliminate thyrotoxicosis and timely perform radical surgery for esophageal cancer.

Thyrotropin-Receptor Antibody Positivity Does Not Correlate with Type 1 or Type 2 Amiodarone-Induced Thyrotoxicosis Phenotype

Thyrotropin-Receptor Antibody Positivity Does Not Correlate with Type 1 or Type 2 Amiodarone-Induced Thyrotoxicosis Phenotype

Identification of Two Different Phenotypes of Patients with Amiodarone-Induced Thyrotoxicosis and Positive Thyrotropin Receptor Antibody Tests.

Introduction: Serum thyrotropin (TSH) receptor antibodies (TRAbs) are occasionally found in patients with amiodarone-induced thyrotoxicosis (AIT), and usually point to a diagnosis of type 1 AIT (AIT1) due to Graves' disease (GD). However, the TRAb role and function in AIT have not been clarified. Methods: A retrospective cohort study of 309 AIT patients followed at a single academic center over a 30-year period. AIT TRAb-positive patients (n = 21, 7% of all cases) constituted the study group; control groups consisted of type 2 AIT (AIT2) TRAb-negative patients (n = 233), and 100 non-AIT patients with GD. Clinical and biochemical data at diagnosis and during the course of disease were compared. Histological samples of patients who had total thyroidectomy were reviewed. Stored serum samples were used for a functional assay of TRAb class G immunoglobulins (IgGs) in Chinese hamster ovary (CHO) cells stably transfected with complementary DNA encoding for the TSH receptor. Results: TRAb-positive patients were grouped according to color flow Doppler sonography, radioactive iodine thyroid uptake, and duration of amiodarone therapy before thyrotoxicosis in type 1 (n = 9, 43%; TRAb1) or type 2 (n = 12, 57%; TRAb2) AIT. TRAb1 patients had clinical and biochemical features indistinguishable from GD controls, and were responsive to methimazole. Conversely, TRAb2 patients had clinical features similar to AIT2 controls, and were responsive to glucocorticoids, but not to methimazole. The CHO cell functional assay demonstrated that TRAb1 IgGs had a stimulatory effect on cyclic AMP production, which was absent in TRAb2 IgGs. Pathology in TRAb1 showed hyperplastic thyroid follicles and mild lymphocyte infiltration, reflecting thyroid stimulation. On the contrary, TRAb2 samples revealed follicle destruction, macrophage infiltration, and sometimes fibrosis, consistent with a destructive process. Conclusions: Almost 60% of TRAb-positive AIT patients had a destructive thyroiditis. TRAb-positive tests in AIT patients do thus not necessarily imply a diagnosis of GD and AIT1, and should be evaluated in the clinical and biochemical setting of each AIT patient and confirmed by measuring thyroid-stimulating immunoglobulins.

Thyroidectomy in patients with amiodarone-induced thyrotoxicosis

The OBJECTIVE of the study was to analyze the experience of performing thyroidectomy (TE) in patients with amiodarone-induced thyrotoxicosis (AmIT) at our centre.METHODS AND MATERIALS. The study included 12 patients with AmIT who underwent TE. Medical records were analyzed to assess the features of the AmIT and indications for TE. We also studied the operation protocols and postoperative follow-up data. Intraoperative, early and long-term postoperative complications were recorded. The long-term TE results were evaluated by the dynamics of the left ventricular ejection fraction (LVEF) based on the echocardiography data.RESULTS. The main indications for TE included the resistance of thyrotoxicosis to medication and worsening of the cardiac pathology. No cases of thyrotoxicosis progression or thyrotoxic crisis were registered during the operation. The vocal cord paresis developed in one case, completely restored in a year. Blood loss was minimal in all cases. Other intraoperative complications were absent. Not a single death was registered in the early postoperative period. At this period, a short paroxysm of atrial fibrillation resolved on its own was registered in patient with arrhythmogenic right ventricular dysplasia. A patient with biventricular chronic heart failure of a high functional class died 39 days after the operation due to a massive pulmonary thromboembolism. The long-term results of TE were evaluated in eight patients. In four out of five patients with initially reduced LVEF, it increased. In three patients with initially normal LVEF, it did not change.CONCLUSION. Thyroidectomy is an effective and safe treatment in patients with AmIT, including those with the persistent thyrotoxicosis and severe cardiac pathology. The success is possible when the preparation of patients for the intervention is carried out by a team of specialists experienced in treating of such patients.

Role of amiodarone in the management of atrial arrhythmias in adult Fontan patients

BackgroundPatients with Fontan circulation are known to be at high risk for developing atrial tachyarrhythmias (AAs). Our objective was to examine the efficacy and safety of amiodarone in the management...

Abstract #997062: Methimazole Induced Agranulocytosis in a Patient with Amiodarone Induced Thyrotoxicosis

Methimazole induced agranulocytosis is a rare (0.1-0.5 %) but serious complication, with approximately 10 times increased risk in patients with Amiodarone induced thyrotoxicosis (AIT). We report such a case.

Amiodarone-induced thyrotoxicosis in children: a clinical case

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

Amiodarone-induced hyperthyroidism

Amiodarone-induced hyperthyroidism

Amiodarone Induced Thyrotoxicosis in the Setting of End Stage Cardiomyopathy

Amiodarone is a class III antiarrhythmic agent which has effects of myocardial depolarization and repolarization. Due to its many side effects including thyroid dysfunction, its use is limited to life-threatening arrhythmias. The thyrotoxicosis can be from the iodine content of amiodarone or its direct toxicity on the thyroid gland. Because of the long half-life, causing amiodarone to have effects for months, medical management can be challenging, and thyroidectomy may be indicated. This is a 76-year-old man with a history of systolic heart failure with reduced ejection fraction (15%), on milrinone after cardiac resynchronization therapy, and recurrent ventricular tachycardia on amiodarone. He was admitted after his ICD device fired. During initial admission, his TSH was <0.015mcunit/mL and FT4 was 2.34ng/dL. Due to concern for amiodarone induced thyrotoxicosis (AIT), he was started on methimazole, prednisone, and cholestyramine. FT4 decreased from 2.34ng/dL to 2.23ng/dL and he discharged on methimazole 30mg daily and prednisone 20mg daily with plans to taper. He was seen outpatient with continued improvement in his FT4 to 2.09ng/dL. He was then seen again and found to have a rising FT4 to 2.22ng/dL and his regimen of prednisone was reinitiated at 10mg daily and methimazole increased to 40mg daily. Despite the medication changes, he continued to have an elevation in his FT4 up to 3.00ng/dL at which point he returned to the hospital for further evaluation and was given methimazole 60mg TID, prednisone 20mg daily, and restarted cholestyramine. With his significant cardiovascular risk, aggressive medical management was attempted prior to surgical evaluation. After his thyroid function failed to respond to medical intervention, multidisciplinary discussion was had with patient, family, and physician teams regarding surgical intervention versus continued long-term monitoring. Family elected to pursue surgery. Thyroidectomy was performed by an experienced endocrine surgeon successfully and his FT4 and T3 decreased appropriately requiring him to be initiated on levothyroxine supplementation. AIT can be separated into Type I, in which there is an increase in synthesis of T4 and T3 with amiodarone providing increasing substrate, and Type II in which there is destructive thyroiditis, releasing excess T4 and T3. In the United States, approximately 5% of individuals who are on amiodarone therapy develop hyperthyroidism, majority being Type II. If possible, amiodarone should be discontinued in Type I AIT, but there is no clear evidence for discontinuation in Type II. Medical management includes thionamides for Type I AIT and glucocorticoids for Type II AIT. Patients who are refractory to drug therapy should be treated with thyroidectomy. The advantages of a surgical procedurewith careful cardiovascular monitoring overall outweigh the morbidity and mortality of uncontrolled thyrotoxicosis.

Amiodarone Induced Thyrotoxicosis: A Case of Refractory Disease Treated With Thyroidectomy

Amiodarone induced thyrotoxicosis (AIT) is a challenging diagnosis that affects 3-5% of patients taking amiodarone in the United States. Type I AIT is seen in patients with preexisting thyroid disease and is generally treated with thionamides while type II AIT represents a destructive thyroiditis that responds to glucocorticoids. A mixed type exists and is associated with higher mortality, especially in older adults with cardiovascular disease. Thyroidectomy is considered a last resort option for patients intolerant or refractory to medical treatment.A 70 year-old male with a history of coronary artery disease, ventricular tachycardia (VT), and heart failure was referred to the endocrine clinic for abnormal thyroid function tests that showed TSH <0.0023 uIU/mL (0.4-4.7), Free T4 2.51 ng/dL (0.7-1.48) and Free T3 5.37 pg/mL (1.71-3.71). He endorsed palpitations, excessive sweating, tremors, and reported taking amiodarone for 3 years prior to presentation. Vitals showed normal pulse and blood pressure. Thyroid autoantibodies including TSI and TBII were within normal limits. Thyroid ultrasound showed mild thyromegaly with normal vascularity and no nodules. AIT was suspected and he was started on methimazole 20 mg daily, prednisone 30 mg daily and continued on his home metoprolol 100 mg daily. Methimazole and prednisone were both up titrated in a week because his labs did not improve. One month later, he presented to the hospital with acute exacerbation of heart failure. His TFTs showed (TSH <0.0021 uIU/mL, FT4 >5.0 ng/dL, FT3 4.61 pg/mL). Thyroid RAIU showed severely decreased uptake secondary to the high iodine content of amiodarone. He remained thyrotoxic despite using higher doses of prednisone (60 mg daily) and methimazole (90 mg daily). He was changed to PTU (900 mg daily) and started on cholestyramine, with no improvement in overall status. Several weeks after admission, a total thyroidectomy was performed. His postoperative course was unremarkable except for hypoparathyroidism. He was clinically and biochemically euthyroid one week after his procedure. At 6 months follow up, he remained stable on levothyroxine 100 mcg/day but continued to require calcitriol and calcium supplementation.We present an interesting case of mixed type AIT refractory to medical therapy associated with cardiovascular compromise. This case highlights the challenges in the diagnosis and management of such patients. Thyroid autoantibodies, thyroid ultrasound and RAIU were more indicative of Type II AIT, however, lack of response to high dose steroids was inconsistent with the diagnosis. While receiving the treatment for both Type I and II AIT, our patient had persistent clinical and biochemical thyrotoxicosis and required thyroidectomy. Although most AIT patients are treated medically, thyroidectomy is reserved for those most severe and refractory cases and is considered a viable option in such patients.