Imaging evaluation of amiodarone-induced thyroid dysfunction: ultrasonographic and radionuclide findings with clinical correlation

Introduction

Amiodarone is a widely used antiarrhythmic medication in clinical practice (1). As an iodinated benzofuran derivative, it exerts its electrophysiological effects by prolonging the action potential and the effective refractory period of myocardial tissues at various sites. The typical maintenance dose is 200 mg per day, which includes 75 mg of iodine; this dosage is metabolized in vivo to yield 6 mg of inorganic iodine, an amount of 50–100 times greater than the recommended daily intake. Amiodarone has a long half-life, typically around 40 to 60 days, and in some cases, even up to 100 days. Moreover, amiodarone remains in fat tissues and organs for weeks to months, continuing to affect thyroid metabolism even after withdrawal, and full recovery of thyroid function may take 6 months or more, and the thyroid function sometimes never normalizes. The primary mechanism by which amiodarone induces thyroid dysfunction is high iodine exposure, which can result in amiodarone-induced hypothyroidism (AIH) and/or two distinct types of thyrotoxicosis (2). The mechanisms include (I) inhibition of peripheral conversion of T4 to T3; (II) destructive thyroiditis or iodine-induced thyrotoxicosis; and (III) the molecular formula (C₂₅H₂₉I₂NO₃) showing the two iodine atoms (https://pubchem.ncbi.nlm.nih.gov/compound/2157#section=2D-Structure), which can disrupt thyroid function by either causing hypothyroidism (due to inhibition of thyroid hormone production) or hyperthyroidism through iodine-induced hormone release or thyroid inflammation.

Amiodarone’s high iodine load persistently inhibits thyroid hormone synthesis (Wolff-Chaikoff effect), triggers autoimmune thyroiditis, and directly suppresses thyroid peroxidase (TPO) and 5’-deiodinase, leading to hypothyroidism (AIH). Type I amiodarone-induced thyrotoxicosis (AIT1) typically occurs in patients with pre-existing nodular goiter or latent Graves’ disease. In these patients, excessive iodine exposure leads to increased synthesis and release of thyroid hormones, similar to patients with iodine-induced hyperthyroidism caused by other sources of excessive iodine. Type II amiodarone-induced thyrotoxicosis (AIT2) is characterized by destructive thyroiditis induced by the drug. Differentiating between these two types of AIT is crucial due to their distinct therapeutic approaches. In this study, the pathogenetic characteristics and imaging manifestations (assessed via thyroid ultrasonography and scintigraphy) of amiodarone-induced thyroid disorders were examined from a clinical perspective, and relevant influencing factors were analyzed to provide robust evidence for clinical diagnosis and treatment decisions. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1247/rc).

Methods

Clinical data

A total of 628 patients admitted to the hospital from December 2018 to October 2023, who had been treated with amiodarone for arrhythmia and had no prior thyroid-related conditions (normal thyroid function and no significant abnormalities detected by thyroid ultrasound), were selected for this study. The group included 389 females and 239 males, aged 38 to 79 years. Additionally, 80 healthy individuals who visited the hospital during the same period were included in the control group. The study group, all local residents aged 30 to 77 years, were selected while excluding those with thyroid disorders, a family history of thyroid disorders, or patients whose thyroid levels could be influenced by factors like iodine-rich medications and foods, sex hormones, glucocorticoids, bromocriptine, dopamine, phenytoin sodium, lithium, and so on after they had gotten the approval of medical ethics. All patients in the study group had no family history of thyroid diseases (biological association) before enrollment, and the thyroid function test (TFT) results before the initiation of amiodarone treatment were all within the normal range. This study was approved by the Ethics Committee of Tianjin Fourth Central Hospital (No. SZXLL-2018-K037). This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from all participants.

Test method

Free thyroxine (FT4), free triiodothyronine (FT3), thyroid-stimulating hormone (TSH), TPO antibody (TPOab), thyroglobulin antibody (Tgab), and TSH receptor antibody (TRab) levels in serum were measured using LIAISON chemiluminescence immunoassay, with test kits purchased from DiaSorin, Saluggia, Italy. The detection ranges for the assays were as follows: FT3: 1.54–30.8 pmol/L, with a normal reference range of 3.4–6.5 pmol/L; FT4: 1.287–128.7 pmol/L, with a normal reference range of 10.2–21.8 pmol/L; TSH: 0.004–100 mIU/L, with a normal reference range of 0.3–5.25 mIU/L; TPOab: 1–2,000 IU/mL; and Tgab: 5–5,000 IU/mL. TRab levels were measured using the Roche Cobas E411 system (Mannheim, Germany), with the range of TRab being 0.8–1.75 IU/L.

The clinical symptoms of AIH are no different from those caused by other reasons. Laboratory tests show that the FT4 level is decreased and the TSH level is increased. Elevated thyroid hormone concentration and decreased TSH level can be used to diagnose AIT. The diagnostic criteria for AIT1: ultrasound examination shows an increase in thyroid volume or nodules; color flow Doppler sonography (CFDS) shows increased vascular supply; increased uptake of technetium-99m pertechnetate thyroid scintigraphy tracer. The diagnostic criteria for AIT2: normal or slightly enlarged thyroid volume without nodules; no high blood supply on CFDS (type 0); no imaging of the thyroid gland on technetium-99m pertechnetate thyroid scintigraphy.

Examination methods

Ultrasound examinations were performed on all participants, and thyroid radionuclide imaging was conducted on the study group regardless of the results of TFT. Single-photon emission computed tomography (SPECT) examination was conducted using ^99mTcO4 (sodium pertechnetate) from Beijing Senke Medicine Co., Ltd., Beijing, China. The tracer was administered via the median cubital vein at a dose of 74–185 MBq (2–5 mCi) in a volume of 0.5–1 mL. We used the static acquisition sequence to acquire images of the neck 20–30 minutes after injection by using a low-energy universal collimator. The anterior-posterior position was routinely used, with an acquisition count of 300–500K.

Ultrasound examinations were performed using a Vivid E9 CFDS machine from GE (Horten, Norway), with the probe frequency set between 7 and 12 MHz. Patients were arranged in the supine position, with the anterior neck fully exposed. Pillows were placed behind the shoulders and neck, positioning the head lower and the neck higher. Anteroposterior and transverse diameters were measured, and key areas were examined using longitudinal, transverse, and oblique sections. Color Doppler blood flow imaging was subsequently used to assess the blood flow distribution within the gland. We used the spectral Doppler to measure blood flow parameters in the superior thyroid artery (STA) and inferior thyroid artery (ITA) and in the lesion. The ultrasound images and radionuclide imaging results were reviewed jointly by two experienced radiologists, who made the diagnosis by consensus. The “double-blind” principle was strictly adhered to while selecting radiologists.

Administration method and TFT

Dosage and administration of amiodarone: Patients were prescribed oral amiodarone tablets, initially at a dosage of 200 mg three times a day (TID) for 7 days, followed by 200 mg twice a day (BID) for another 7 days. Maintenance doses were then set at either 200 mg every day (QD), 200 mg every other day (QOD), or 100 mg QD, depending on the individual case. The tablets, manufactured by Sanofi Pharmaceutical Factory (Antony, France), were to be taken with warm boiled water, and the treatment duration ranged from 3 months to 6 years. Thyroid function was tested before the treatment, and re-evaluated 1 month after initiating amiodarone treatment and subsequently monitored on a monthly basis.

Statistical methods

Statistical analyses were performed using SPSS 24.0 software. Measurement data that followed a normal distribution were expressed as mean and standard deviation (SD). Differences between groups were assessed using analysis of variance (ANOVA), and multiple comparisons were conducted using the SNK-q test. Enumeration data were presented as absolute values (percentages), and differences between groups were assessed using the χ² test or Fisher’s exact probability test.

Results

Amiodarone administration and thyroid function changes

Among the 628 patients, 476 (75.80%) maintained normal thyroid function, while 152 (24.20%) exhibited abnormal thyroid function. Among those with abnormal thyroid function, 32 (5.10%) had subclinical hyperthyroidism, 48 (7.64%) had subclinical hypothyroidism, 80 (12.74%) had thyrotoxicosis [including 32 patients with AIT1, 40 patients with AIT2, and 8 patients with mixed type (AIT3)], and 16 (2.55%) had hypothyroidism. Radionuclide imaging revealed increased thyroid uptake in 21 cases (3.34%) and decreased uptake in 14 cases (2.23%).

Following administration, significant differences in FT3, FT4, and TSH levels were observed in the hyperthyroidism, hypothyroidism, and thyroiditis groups compared to the control group (t value range, 5.07–20.63; P<0.01). In the subclinical hyperthyroidism and subclinical hypothyroidism groups, there were no significant differences in FT3 and FT4 levels compared to the control group (t value range: 5.07–20.63; P<0.01), but significant differences in TSH levels were observed (t value range, 5.21–20.49; P<0.01). The differences in Tgab and TPOab levels between the hyperthyroidism and hypothyroidism groups and the control group were statistically significant after administration (χ² value range, 8.4–21.16; P<0.01). In the thyroiditis group, the difference in Tgab levels was not statistically significant compared to the control group (χ²=5.10; P>0.05), whereas the difference in TPOab levels was statistically significant (χ²=10.59; P<0.01). See Table 1 for details.

Changes in TRab levels after drug administration

For TRab levels after administration, a statistically significant difference was observed between the hyperthyroidism group and the control group (χ²=11.72; P<0.05). No significant differences in TRab levels were found between the other groups and the control group (P>0.05).

Relationship between thyroid ultrasound results and thyroid function

From the ultrasound examination, we could ascertain that following administration, 16 cases (2.55%) in the hyperthyroidism group exhibited enlarged thyroid lobes and increased blood flow, as depicted in Figure 1. Additionally, 18 cases (2.87%) of thyroiditis were diagnosed by ultrasound. The images indicated an increase in thyroid volume, decreased internal echo, and an indistinct boundary between the hypoechoic area and surrounding normal tissues. Color Doppler imaging revealed a reduced blood supply in the hypoechoic region of the thyroid, with a rich blood supply in the surrounding tissues, as depicted in Figure 2.

Figure 1 Hyperthyroidism. From the ultrasound examination, the hyperthyroidism group exhibited enlarged thyroid lobes and increased blood flow.

Figure 2 Thyroiditis. The images indicated an increase in thyroid volume, decreased internal echo, and an indistinct boundary between the hypoechoic area and surrounding normal tissues. Color Doppler imaging revealed a reduced blood supply in the hypoechoic region of the thyroid, with a rich blood supply in the surrounding tissues.

Comparison of thyroid SPECT findings

Although technetium is not involved in iodine metabolism, it reflects the thyroid’s uptake function of iodide ions, because, as a member of the same group of elements, it is also absorbed by thyroid tissue. The radioactive nuclide imaging of the thyroid showed that there were 24 cases (3.82%) with a significant increase in thyroid uptake and 38 cases (6.05%) with a significant decrease in thyroid uptake. See Figures 3-5.

Figure 3 Significantly enhanced nuclide uptake ability of thyroid. The location of the right thyroid gland has been indicated by red arrows. The corresponding position on the opposite side is that of the left lobe of the thyroid gland. ANT, anterior phase.

Figure 4 Approximately normal uptake ability of thyroid. The location of the right thyroid gland has been indicated by red arrows. The corresponding position on the opposite side is that of the left lobe of the thyroid gland. ANT, anterior phase; SE, serial.

Figure 5 Significantly reduced uptake ability of thyroid. The location of the right thyroid gland has been indicated by red arrows. The corresponding position on the opposite side is that of the left lobe of the thyroid gland. ANT, anterior phase; SE, serial.

Radionuclide imaging is valuable for assessing thyroid function and distinguishing between AIT1 and AIT2 in patients with thyrotoxicosis.

Diagnosis and differential diagnosis

CFDS is an important tool for differentiating AIT1 and AIT2. During the assessment, it is necessary to pay attention to the overall blood flow distribution of the thyroid gland (the ‘inferno’ sign is a typical manifestation of AIT1). AIT1—thyroid ultrasound image of hyperthyroidism (Figure 6): it shows the high uptake image from the thyroid scintigraphy and the “inferno” sign image with abundant blood flow on the CFDS. AIT2—hypothyroidism or normal thyroid image—AIT2 typical case (Figures 7,8): it shows the low uptake image from the thyroid scintigraphy and the image with basically normal blood flow signal on the CFDS. At the same time, pulse Doppler spectral analysis can be used to quantitatively evaluate the hemodynamics of the thyroid arteries. The most commonly measured arteries are the STA and ITA. Although both can provide valuable information, the STA is preferred in clinical practice and research because of its more superficial location, greater ease of repeated detection, and less dependence on the operator. The current consensus usually takes peak systolic velocity (PSV) as the key indicator. A PSV greater than 100 cm/s typically suggests extremely rich thyroid blood flow, strongly supporting the diagnosis of AIT1; while a PSV less than 45–50 cm/s is more likely to indicate AIT2 or a normal thyroid. It is worth noting that these values are the recognized thresholds for STA, and the absolute values of ITA may vary slightly, but their trend is consistent with STA (that is the PSV of ITA also significantly increases during AIT1).

Figure 6 AIT1—thyroid ultrasound image of hyperthyroidism: it shows the high uptake image from the thyroid scintigraphy and the “inferno” sign image with abundant blood flow on the CFDS. AIT1, type I amiodarone-induced thyrotoxicosis; CFDS, color flow Doppler sonography.

Figure 7 Hypothyroidism.

Figure 8 Normal thyroid image.

Discussion

Amiodarone, a crucial iodine-rich medication used in the treatment of arrhythmia, is commonly administered at a dose of 200 mg per day. This dosage results in an estimated daily iodine intake of approximately 7 mg, leading to a forty-fold increase in blood iodine concentration and a corresponding urinary iodine concentration of up to 15,000 µg/day (3). The incidence of amiodarone-induced thyroid disorders is reported to be 15–20% (4). Thyroid dysfunction may arise from both excessive iodine and amiodarone itself (or its metabolite, desethylamiodarone) due to direct cytotoxic effects on thyroid cells (5). Previous studies on the clinical correlation of these effects have been limited. In this study, clinical data of patients with amiodarone-induced thyroid disorders were analyzed along with ultrasound and SPECT findings to accurately classify the different types of thyroid disorders and subsequently provide tailored treatment for each tissue type.

Radioactive iodine (RAI) therapy is a safe and effective treatment for hyperthyroidism and certain thyroid cancers. One study showed that RAI is an effective treatment strategy for AIT2 if the patient cannot tolerate steroids and is not a candidate for thyroidectomy (6). When RAI or other elements from the iodine group are introduced into the body, they are absorbed by functioning thyroid tissue. SPECT imaging can detect the gamma rays emitted by these elements, allowing for the visualization of the location, size, and functional status of the thyroid. This enables the identification of typical AIT types AIT1 and AIT2. Additionally, ultrasound can assess blood flow distribution and hemodynamics within the thyroid, thereby enhancing the diagnostic assessment of thyroid function. According to the recommendations of the 2018 European Thyroid Association (ETA) guidelines (3), for patients with suspected AIT, thyroid ultrasound (to assess blood flow) should be combined with radionuclide uptake scanning (to assess function) to distinguish between AIT1 and AIT2, which is crucial for guiding treatment. The results of this study are highly consistent with this recommended strategy.

For patients receiving amiodarone, regular monitoring of thyroid function is essential. A comprehensive assessment using both radionuclide imaging and ultrasound should be conducted to accurately determine the type of thyrotoxicosis and to guide appropriate diagnosis and treatment. This approach helps prevent delays in diagnosis and treatment and provides further evidence to support subsequent therapeutic strategies.

In our study, we observed that the hyperthyroidism group exhibited enhanced radionuclide uptake, while the hypothyroidism group showed reduced uptake. In cases where diagnostic typing was ambiguous, symptoms were atypical, and serological tests indicated thyrotoxicosis without significant blood flow changes or typical radionuclide uptake changes, symptomatic treatment combined with hormonal therapy was administered.

In the later stages of treatment, AIH can generally be managed effectively with timely thyroid hormone supplementation and regular monitoring of thyroid function. Conversely, AIT presents significant diagnostic and therapeutic challenges. Patients with AIT2 (destructive thyroiditis) often respond well to glucocorticoid therapy and may not require discontinuation of amiodarone. In contrast, AIT1 (and mixed/indeterminate types) is more complex to treat due to the resistance of iodine-sufficient thyroid tissue to antithyroid medications. Given the diagnostic difficulties in distinguishing between AIT1 and mixed/indeterminate types, a combination of pharmacological treatments is frequently used. Definitive treatment may involve RAI therapy or thyroidectomy, especially if the thyrotoxic phase persists and there is a rapidly deteriorating cardiac condition. Prolonged thyrotoxicosis has been associated with increased left ventricular ejection fraction (LVEF) and increased mortality, whereas early thyroidectomy might reduce LVEF (7). Currently, there is limited research evidence on treating amiodarone-related thyroid dysfunction, contributing to the overall difficulty in its management.

In our follow-up study, which excluded the confounding factors of underlying thyroid dysfunction, amiodarone-induced thyroid disorders were correlated with initial levels of Tgab and TPOab. Elevated initial antibody levels were found to potentially induce a stress response within the thyroid.

Our study did not find a significant association between amiodarone-induced thyroid disorders and gender. It was observed that the prevalence of AIT was higher than that of AIH. Regardless of the duration of treatment or the time elapsed since discontinuation of amiodarone, maintaining a high level of clinical suspicion for AIT is crucial, as significant changes in thyroid function can occur not only during the acute phase but also in the chronic phase (8). A study conducted at the Children’s Hospital of Philadelphia examined the effects of amiodarone on thyroid function in pediatric and young patients. The study recommended obtaining a complete assessment of thyroid function during the first week of treatment and then monitoring thyroid function weekly for the first 5 weeks. Most cases of thyroid dysfunction occurred within the first 35 days of treatment (9). Routine monthly monitoring of thyroid function at least in the early treatment course.

Currently, a study is being conducted to investigate the use of a nanodrug delivery system in a rat model to achieve sustained delivery of amiodarone to the myocardium to reduce adverse reactions (10). For long-term treatment with amiodarone, it is recommended to use the minimal effective dose to achieve satisfactory control of arrhythmia while regularly screening for thyroid, hepatic, and pulmonary toxicity (11). In cases of iodine-induced hyperthyroidism, antithyroid drugs and perchlorate are primarily used to reduce thyroid hormone synthesis and inhibit further iodine uptake by the thyroid (12). For patients with AIT who experience severe systolic dysfunction, total thyroidectomy may be considered as a therapeutic option. However, in patients with normal or only mildly reduced LVEF, total thyroidectomy does not demonstrate superiority over drug therapy (13).

Conclusions

In this study, thyroid function was assessed both before and after amiodarone treatment. This assessment was complemented by thyroid ultrasound and radionuclide imaging, allowing for a comprehensive analysis of the changes in thyroid function. The combined assessment, particularly the application of radionuclide imaging, enabled the differentiation of AIT1 and AIT2, thereby informing therapeutic regimens and prognosis assessment. In patients with underlying thyroid disorders or positive initial antibody levels, the use of amiodarone requires careful consideration and thorough assessment. It is recommended to combine ultrasound with SPECT as this has an impact on treatment. Patients with positive TPOab and/or Tgab require closer monitoring. However, the limitations of the study include a relatively small sample size and limited follow-up regarding the duration of amiodarone administration and clinical outcomes. Consequently, larger, multicenter randomized clinical trials are necessary to enhance the management of these diseases.

Acknowledgments

We would like to acknowledge the hard and dedicated work of all the staff who implemented the intervention and evaluation components of the study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1247/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1247/dss

Funding: This work was supported by Tianjin Health Science and Technology Project (No. TJWJ2022MS023) and the Foundation for the Outstanding Youth Training of 2021 in Tianjin Fourth Central Hospital (Nos. tjdszxyy20210012 and tjdszxyy20220022).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1247/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted with approval from the Ethics Committee of Tianjin Fourth Central Hospital (No. SZXLL-2018-K037). This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from all participants.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Middeldorp ME, Elliott AD, Gallagher C, Linz D, Hendriks JML, Mahajan R, Lau DH, Sanders P. Late-onset thyrotoxicosis after the cessation of amiodarone. Indian Pacing Electrophysiol J 2020;20:265-8. [Crossref] [PubMed]
2. Iyama K, Kawano H, Ando T, Ikeda S, Maemura K. Sudden onset of thyrotoxicosis induced by amiodarone mimicking low cardiac output syndrome in a patient with dilated cardiomyopathy. J Cardiol Cases 2020;22:81-4. [Crossref] [PubMed]
3. Bartalena L, Bogazzi F, Chiovato L, Hubalewska-Dydejczyk A, Links TP, Vanderpump M. 2018 European Thyroid Association (ETA) Guidelines for the Management of Amiodarone-Associated Thyroid Dysfunction. Eur Thyroid J 2018;7:55-66. [Crossref] [PubMed]
4. Jabrocka-Hybel A, Bednarczuk T, Bartalena L, Pach D, Ruchała M, Kamiński G, Kostecka-Matyja M, Hubalewska-Dydejczyk A. Amiodarone and the thyroid. Endokrynol Pol 2015;66:176-86. [Crossref] [PubMed]
5. Ylli D, Wartofsky L, Burman KD. Evaluation and Treatment of Amiodarone-Induced Thyroid Disorders. J Clin Endocrinol Metab 2021;106:226-36. [Crossref] [PubMed]
6. Rodrigues S, Yu R. Use of Radioactive Iodine in Type 2 Amiodarone-Induced Thyrotoxicosis. AACE Endocrinol Diabetes 2025;12:121-4. [Crossref] [PubMed]
7. Cappellani D, Papini P, Di Certo AM, Morganti R, Urbani C, Manetti L, Tanda ML, Cosentino G, Marconcini G, Materazzi G, Martino E, Bartalena L, Bogazzi F. Duration of Exposure to Thyrotoxicosis Increases Mortality of Compromised AIT Patients: the Role of Early Thyroidectomy. J Clin Endocrinol Metab 2020;105:dgaa464. [Crossref] [PubMed]
8. Sugiyama K, Kobayashi S, Kurihara I, Miyashita K, Yokota K, Kohno T, Yoshimura Noh J, Itoh H. Effect of long-term amiodarone treatment on thyroid function in euthyroid Japanese patients: a 12-month retrospective analysis. Endocr J 2020;67:1247-52. [Crossref] [PubMed]
9. Barrett B, Hawkes CP, Isaza A, Bauer AJ. The Effects of Amiodarone on Thyroid Function in Pediatric and Young Adult Patients. J Clin Endocrinol Metab 2019;104:5540-6. [Crossref] [PubMed]
10. Motawea A, Ahmed DAM, Eladl AS, El-Mansy AAE, Saleh NM. Appraisal of amiodarone-loaded PLGA nanoparticles for prospective safety and toxicity in a rat model. Life Sci 2021;274:119344. [Crossref] [PubMed]
11. Mujović N, Dobrev D, Marinković M, Russo V, Potpara TS. The role of amiodarone in contemporary management of complex cardiac arrhythmias. Pharmacol Res 2020;151:104521. [Crossref] [PubMed]
12. Eilsberger F, Luster M, Feldkamp J. Iodine-induced thyroid dysfunction. Med Klin Intensivmed Notfmed 2021;116:307-11. [Crossref] [PubMed]
13. Cappellani D, Papini P, Pingitore A, Tomisti L, Mantuano M, Di Certo AM, Manetti L, Marconcini G, Scattina I, Urbani C, Morganti R, Marcocci C, Materazzi G, Iervasi G, Martino E, Bartalena L, Bogazzi F. Comparison Between Total Thyroidectomy and Medical Therapy for Amiodarone-Induced Thyrotoxicosis. J Clin Endocrinol Metab 2020;105:dgz041. [Crossref] [PubMed]