Amiodarone-induced Thyrotoxicosis Research Articles

“It’s a Psychiatric Patient”: Misdiagnosing of Somatic Symptoms in Patients with Mental Disorders Due to Stigma and Inadequate Diagnostic Treatment

Aim: People with mental illness have more somatic comorbidities and are frequently mistreated. Misdiagnosis occurs for a variety of reasons, including stigma, poor communication, lack of knowledge of psychiatric pathology, and a tendency to attribute physical symptoms to a mental disorder. Case report: The factors listed above, as well as the unique circumstances of the COVID-19 pandemic led to the misdiagnosis in the case discussed in this paper. The patient was a middle-aged man diagnosed with an ICD-10 diagnosis of a chronic mental disorder in the F2 category and multiple somatic comorbidities in whom amiodarone-induced thyrotoxicosis was undiagnosed and somatic symptoms were attributed to antipsychotic-induced parkinsonism. The mechanism of amiodarone-induced thyrotoxicosis and antipsychotic-induced extrapyramidal symptoms will be described, together with the factors that caused our patient to be misdiagnosed. Conclusion: Psychiatric patients are often specific in their communication and behaviour, therefore interaction must be adapted, with a focus on destigmatizing and educating health workers.

[Type 2 amiodarone-induced thyrotoxicosis: efficacy of glucocorticoid therapy, a retrospective analysis].

Type 2 amiodarone-induced thyrotoxicosis remains a significant problem of endocrinology and cardiology. Due to the increase a life expectancy of the population, the prevalence of cardiac arrhythmias and prescribing of amiodarone are increasing. Thyrotoxicosis aggravates the existing cardiovascular disease in patients, leads to the progression of left ventricular dysfunction, relapses of arrhythmias, increasing the risk of adverse outcomes. The tactic of further management of patients is complicated: it is necessary to resolve the issue of canceling or continuing the use of antiarrhythmic drugs necessary for a patient with a history of cardiac arrhythmia, as well as competent therapy of the thyroid pathology that has arisen. Oral glucocorticoids are the first-line drugs for the treatment of patients with moderate and severe type 2 amiodarone-induced thyrotoxicosis. Despite the appearance of clinical recommendations, opinions on the management of patients are differ, both among cardiologists and among endocrinologists. Often thyrostatics are prescribed to patients simultaneously with glucocorticoids, although it doesn't have pathogenetic basis. To evaluate the efficacy of various therapy options in patients with type 2 amiodarone-induced thyrotoxicosis. The retrospective study included 38 patients (20 men and 18 women aged 35 to 85 years) with type 2 amiodarone-induced thyrotoxicosis. All patients underwent an analysis of anamnestic, anthropometric data, complex laboratory and instrumental diagnostics. According to the treatment options, 3 groups were retrospectively formed: without therapy (n=19), taking glucocorticoids (n=11) and combination of glucocorticoids and thyrostatics (n=8). The follow-up period was 6-18 months, including the treatment. The efficacy of treatment in the groups was evaluated by the time of reaching euthyroidism on the background of glucocorticoid therapy and duration of thyrotoxicosis; the search was conducted for potential predictors of delayed response to glucocorticoid therapy and long-term course of thyrotoxicosis. The average age was 62.0 [52.9; 66.3] years. The level of free thyroxine was significantly decreased after 1 month from the start of therapy in both groups: from 38.1 [32.1; 58.4] to 23.4 [19.6; 29.3] pmol/l (p<0.001) in the group taking glucocorticoids; from 73.9 [42.2; 75.6] to 39.3 [22.4; 47.2] pmol/l (p<0.001) in the combination therapy group. The time of reaching euthyroidism was longer in the combination therapy group (p=0.047), didn't depend on the dose (p=0.338) and duration of taking thiamazole (p=0.911), the delayed response to therapy correlated with age (p=-0.857; p=0.007) and time interval from the appearance of clinical symptoms of thyrotoxicosis to the start of glucocorticoid therapy (p=0.881; p<0.001). The results demonstrate the dependence of glucocorticoid response on the age of the patient and start time of therapy relative to the duration of thyrotoxicosis, inexpediency of additional prescribing thyrostatics in type 2 amiodarone-induced thyrotoxicosis.

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.

An uncommon side effect: amiodarone-related hypothyroidism in a patient with negative thyroid autoantibodies.

Amiodarone is an antiarrhythmic drug frequently used in cardiac dysrhythmias. One of the most important side effects of amiodarone is thyroid dysfunction. Amiodarone-induced thyrotoxicosis (AIT) and amiodarone-induced hypothyroidism (AIH) can occur depending on individuals' iodine status and previous thyroid disease. In this case, we aimed to present the hypothyroidism that developed in a patient with negative thyroid autoantibodies after amiodarone use.

Severe and protracted Type 2 Amiodarone Induced Thyrotoxicosis (AIT) presenting 6 months following discontinuation of Amiodarone

Severe and protracted Type 2 Amiodarone Induced Thyrotoxicosis (AIT) presenting 6 months following discontinuation of Amiodarone

Rebound worsening of amiodarone-induced thyrotoxicosis after discontinuation of pulse methylprednisolone despite treatment with oral steroids and thiamazole

Rebound worsening of amiodarone-induced thyrotoxicosis after discontinuation of pulse methylprednisolone despite treatment with oral steroids and thiamazole

Therapeutic Management and Long-Term Outcome of Hyperthyroidism in Patients with Antithyroid-Induced Agranulocytosis: A Retrospective, Multicenter Study.

Antithyroid drug-induced agranulocytosis (AIA) (neutrophils <500/µL) is a rare but serious complication in the treatment of hyperthyroidism. Adult patients with AIA who were followed up at 12 hospitals in Spain were retrospectively studied. A total of 29 patients were studied. The etiology of hyperthyroidism was distributed as follows: Graves' disease (n = 21), amiodarone-induced thyrotoxicosis (n = 7), and hyperfunctioning multinodular goiter (n = 1). Twenty-one patients were treated with methimazole, as well as six patients with carbimazole and two patients with propylthiouracil. The median (IQR) time to development of agranulocytosis was 6.0 (4.0-11.5) weeks. The most common presenting sign was fever accompanied by odynophagia. All of the patients required admission, reverse isolation, and broad-spectrum antibiotics; moreover, G-CSF was administered to 26 patients (89.7%). Twenty-one patients received definitive treatment, thirteen patients received surgery, nine patients received radioiodine, and one of the patients required both treatments. Spontaneous normalization of thyroid hormone values occurred in six patients (four patients with amiodarone-induced thyrotoxicosis and two patients with Graves' disease), and two patients died of septic shock secondary to AIA. AIA is a potentially lethal complication that usually appears around 6 weeks after the initiation of antithyroid therapy. Multiple drugs are required to control hyperthyroidism before definitive treatment; additionally, in a significant percentage of patients (mainly in those treated with amiodarone), hyperthyroidism resolved spontaneously.

THU659 Plasmapheresis As A Therapy For Amiodarone-induced Thyrotoxicosis: A Case Report And Literature Review

Abstract Disclosure: C.L. Loughner: None. P.L. Bononi: None. Introduction: Amiodarone-induced thyrotoxicosis (AIT) is a common cause of hyperthyroidism. Treatment consists of stabilizing the thyroid followed by thyroidectomy1. Plasmapheresis has been suggested as a temporary measure when illness severity precludes standard therapy. Here, we review current literature and provide a case of AIT treated with plasmapheresis. Clinical Case: A 71-year-old male was seen for progressive subclinical hyperthyroidism, diagnosed several years prior. Three years ago, he started taking amiodarone for paroxysmal ventricular tachycardia. One month prior to admission, he was admitted for decompensated heart failure and had TSH 0.02 mcU/mL (n 0.4-4.4 mcU/mL), free T4 4.48 ng/dL (n 0.7-1.9 ng/dL), and free T3 2.58 pg/mL (n 2.0-4.4 pg/mL). Amiodarone was halved after being diagnosed with AIT. Methimazole and prednisone were started. He was readmitted one month later. TSH was undetectable at admission and free T4 was 4.04 ng/dL. Amiodarone was discontinued. His hepatic enzymes were elevated, necessitating the discontinuation of methimazole. His heart failure precluded thyroidectomy. Due to the limitation of treatment options, the patient was given three rounds of plasmapheresis to reduce thyroid hormone levels. His free T4 dropped to 2.81 ng/dL. The patient underwent total thyroidectomy once stable. His free T4 was 1.73 after and was started on levothyroxine. Clinical Lesson: When patients are unable to have standard treatment of AIT, other options must be considered. While there are some case reports3,4, there are currently no RCTs for plasmapheresis for AIT. In the case of this patient with cardiac complications from AIT and concurrent hepatic impairment, plasmapheresis provided stability of thyroid hormones until surgical correction could be achieved.

THU662 Poor Response To Medical Treatment In A Patient With Amiodarone-induced Hyperthyroidism: A Therapeutic Dilemma

Abstract Disclosure: A.A. Asiri: None. R. Sulimani: None. W. Alkhidady: None. Introduction: Hyperthyroidism is a well-known complication of amiodarone therapy. An incidence of 3% is reported in North America1, and even higher percentages in amiodarone deplete areas of about 10%.2 Treatment of amiodarone-induced hyperthyroidism (AIH) is challenging, it depends on various factors including the type of AIH, dependence of the patient’s cardiac condition on amiodarone therapy, other complications or comorbidities of the patient such as hepatic injury or dysfunction and the response of the patient to antithyroid therapy. Clinical Case: We present a case of a 32-year-old lady with a therapeutic dilemma in treating type I AIH, resistant to medical therapy. Our patient first had acquired COVID-19-induced myocarditis in 2020 and subsequently developed sustained ventricular tachycardia and was treated with amiodarone and placed on an implantable cardioverter-defibrillators (ICD) device. Two years later in 2022, the patient developed type I amiodarone-induced hyperthyroidism, with a free T4 reaching 100 pmol/L (Reference range 15-22 pmol/L) and complicated with transaminitis. She was unresponsive to medical therapy including: anti-thyroid medications, IV high-dose hydrocortisone, potassium iodide drops, and cholestyramine. She also developed adverse events with two of the antithyroid medications, Carbimazole and PTU; where she had elevated liver enzymes more than five time upper limit of normal and a generalized skin rash with PTU. Plasmapheresis was not an option as some of her cardiac medications drug levels could be affected. She underwent an emergent total thyroidectomy with dual beta blockade (Propranolol and Sotalol) successfully without any post op events. Her T4 level normalized within 8 days of her operation and her liver enzymes normalized within 2 weeks. Conclusion: We report the success and safety of surgical management in a patient with a cardiac arrhythmia and uncontrolled severe amiodarone-induced hyperthyroidism in the setting of adequate beta blockade.

SAT483 Role of Cholestyramine in Refractory Amiodarone-induced Thyrotoxicosis

Abstract Disclosure: H. Zhao: None. J. Leung: None. Role of Cholestyramine in Refractory Amiodarone-Induced Thyrotoxicosis. Background: Amiodarone-induced thyrotoxicosis (AIT) is divided into type 1 (AIT1; treated with thioamides) and type 2 (AIT2; treated with glucocorticoids). Combined therapy is utilized in mixed or indefinite forms. When medical treatment is unsuccessful, radioiodine ablation or thyroidectomy are considered. Clinical Case: A 76-year-old gentleman, with a history of atrial fibrillation treated with amiodarone, presented with recurrent atrial fibrillation refractory to cardioversion. Investigations revealed TSH &amp;lt;0.01, FT4 58.1 (ref 10.0-20.0 pmol/L), FT3 16.0 (ref 3.5-6.5 pmol/L), TPO negative and TRAB negative. As thyroid ultrasound revealed absence of focal nodules or hypervascularity and technetium pertechnetate scan demonstrated no thyroid activity, AIT2 was suspected. Prednisone was initiated and amiodarone discontinued. Due to minimal response after a month, a mixed type was suggested and methimazole added. Despite intensification of the antithyroid regimen, FT4 increased to 59.5. Methimazole was discontinued for radioiodine ablation assessment. Given low thyroid uptake (&amp;lt;3%), ablation was deemed unlikely beneficial. After patient refused thyroidectomy, cholestyramine was initiated, resulting in significant improvement, with FT4 declining from 46.0 to 29.0 in 2 weeks. Euthyroidism was achieved after 2 months of cholestyramine treatment and medications were stopped. At 6 months post presentation, he developed amiodarone-related hypothyroidism and began levothyroxine. Conclusion: Previous reports propose that cholestyramine, an ion exchange resin, interrupts enterohepatic circulation of thyroid hormone and demonstrated the use of cholestyramine in refractory Grave’s hyperthyroidism. This is one of the first few reports demonstrating the possible role of cholestyramine in AIT refractory to first line medical therapy. Presentation Date: Saturday, June 17, 2023

THU654 The Use Of Plasmapheresis In A Severe Case Of Amiodarone Induced Thyrotoxicosis

Abstract Disclosure: T. Moazezi: None. C. Koh: None. Thyroid storm is an endocrine emergency that results in a hypermetabolic state due to excess levels of circulating thyroid hormone and carries a high mortality rate. Therapeutic plasma exchange (TPE) can be used in cases of thyrotoxicosis refractory to medical management to achieve hemodynamic and clinical stability. We present a case of a 74-year-old male with severe amiodarone-induced thyrotoxicosis who presented with altered mentation and ultimately required intubation and intensive care for management of thyroid storm. Standard medical therapy for treatment was initiated immediately with antithyroid drugs, beta blockers, glucocorticoids, potassium iodide solution, and cholestyramine. However, the patient remained unresponsive and intubated with worsening biochemical parameters with increased total T3 levels and sustained elevated levels of free T4 even after five days of maximal medical therapy. Due to the lack of a clinical and biochemical response to conventional medical therapy, the patient was started on plasmapheresis and underwent a total of seven cycles of plasmapheresis over a period of ten days. He significantly improved with TPE and was successfully bridged to a total thyroidectomy, which was completed without complications. Our case demonstrated a decrease in total T3 concentration of roughly 45% after one session of plasmapheresis and roughly 76% with seven sessions of plasmapheresis by the time of thyroidectomy. Free T4 levels remained elevated above reference range until the day after the fifth session of plasmapheresis. This case is important because the literature surrounding the use of TPE in thyroid storm is sparse, and there have only been case reports and retrospective studies published on the subject. Ultimately, while TPE is not conventionally used as part of routine treatment for thyroid storm, endocrinologists should keep this tool at the forefront of their management strategies to deliver quicker treatment to critically ill patients and prevent complications of thyroid storm. Nonetheless, more research is needed to delineate concrete guidelines and specific protocols for use of TPE in thyroid storm. Presentation: Thursday, June 15, 2023

Appropriate Treatment of Amiodarone-Induced Thyrotoxicosis Improves Cardiac Outcomes

Appropriate Treatment of Amiodarone-Induced Thyrotoxicosis Improves Cardiac Outcomes

How do I diagnose and treat my patient's amiodarone-induced thyrotoxicosis?

How do I diagnose and treat my patient's amiodarone-induced thyrotoxicosis?

Prevalence of Amiodarone Induced Hypothyroidism and Hyperthyroidism in Patients with Heart Diseases: A Systematic Review and Meta-Analysis.

Due to the importance of amiodarone-induced hyperthyroidism in patients with heart failure, the purpose of the present systematic review and metaanalysis was to determine the prevalence of thyroid dysfunction (hypothyroidism and hyperthyroidism) in patients with heart disease who received amiodarone. Electronic databases including Scopus, PubMed, Web of Science, and Science Direct were searched by two investigators. To assess the heterogeneity between the included studies, the chi-square χ2 test (α=0.05) and I2 index were used. Additionally, a random-effects model with 95% CI was used to estimate the pooled prevalence of thyroid dysfunction due to the heterogeneity of the studies. To identify the cause of heterogeneity, a meta-regression analysis was employed. All analyses were performed using Stata ver13 (Stata Corporation, College Station, TX, USA). The pooled prevalence of hypothyroidism was 23.43% (95% CI: 11.54-35.33) and hyperthyroidism was 11.61% (95% CI: 7.20-16.02). There was no significant association between the prevalence of hypothyroidism and the year of the study (p=0.152), sample size (p=0.805), and mean age of subjects in the sample groups (p=0.623). However, there was a significant association between the prevalence of hyperthyroidism and the year of the study (p=0.037), but no statistically significant association between either the prevalence of hyperthyroidism and sample size (p=0.425), or the prevalence of hyperthyroidism and the mean age of subjects in the sample groups (p=0.447). The prevalence of thyroid dysfunction in patients with cardiac arrhythmias receiving amiodarone was considerable. Extreme care should be exercised to improve the monitoring of any thyroid abnormalities that may arise in patients receiving amiodarone.

Mortality After Total Thyroidectomy for Amiodarone-Induced Thyrotoxicosis According to Left Ventricular Ejection Fraction.

To report cardiac outcomes after total thyroidectomy for amiodarone-induced thyrotoxicosis according to the baseline left ventricular ejection fraction in a tertiary referral center. Retrospective, monocentric. The tertiary health care system. Patients who underwent total thyroidectomy for amiodarone-induced thyrotoxicosis between 2010 and 2020 with age >18 and available preoperative left ventricular ejection fraction were included in this study. Patients were dichotomized into: group 1 with left ventricular ejection fraction ≥40% (mildly reduced/normal ejection fraction), and group 2 with left ventricular ejection fraction <40% (reduced ejection fraction). There were 34 patients in group 1 and 17 to group 2. The latter were younger (median 58.4 [Q1-Q3 48.0-64.9] vs. 69.8 years in group 1 [59.8-78.3], p = .0035) and they presented more cardiomyopathy (58.8 vs. 26.5%, p = .030). Overall, the median time until surgery referral was 3.1 [1.9-7.1] months and 47.1% underwent surgery after restoration of euthyroidism. Surgical complications accounted for 7.8%. In group 2, the median left ventricular ejection fraction was significantly improved after surgery (22.5 [20.0-25.0] vs. 29.0% [25.3-45.5], p = .0078). Five-year cardiac mortality was significantly higher in group 2 (p < .0001): 47.0% died of cardiac causes versus 2.9% in group 1. A baseline left ventricular ejection fraction <40% and a longer time until surgery referral were significantly associated with cardiac mortality (multivariable Cox regression analysis, p = .015 and .020, respectively). These results reinforce the idea that surgery, if chosen, should be performed quickly in patients with left ventricular ejection fraction <40%.

Part II: Interactive case: Drug‐induced endocrine disorders

JACCP: JOURNAL OF THE AMERICAN COLLEGE OF CLINICAL PHARMACYVolume 6, Issue 6 p. 663-668 PSAP IN JACCP Part II: Interactive case: Drug-induced endocrine disorders Amy C. Donihi Pharm.D., FCCP, Amy C. Donihi Pharm.D., FCCP orcid.org/0000-0002-5105-9323 Search for more papers by this author Amy C. Donihi Pharm.D., FCCP, Amy C. Donihi Pharm.D., FCCP orcid.org/0000-0002-5105-9323 Search for more papers by this author First published: 07 June 2023 https://doi.org/10.1002/jac5.1813Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. 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