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Electrical storm is a challenging diagnosis for the clinician and requires detailed evaluation of the patient. Amiodarone is frequently used for the cessation of ventricular tachycardia attacks. Within antiarrhythmic effects of amiodarone, there are some harmful effects of the recent drug. Thyroid gland toxicity is one of the most important adverse effects of amiodarone and is called amiodarone-induced thyrotoxicosis. Thyrotoxicosis may alter arrhythmia and lead to frequent ventricular tachycardia attacks. Herein, we report a case of electrical storm caused by amiodarone-induced thyrotoxicosis.

Amiodarone is a potent class III anti-arrhythmic drug used in clinical practice for the prophylaxis and treatment of many cardiac rhythm disturbances, ranging from paroxismal atrial fibrillation to life threatening ventricular tachyarrhythmias. Amiodarone often causes changes in thyroid function tests mainly related to inhibition of 5'-deiodinase activity resulting in decrease in the generation of T3 from T4 with consequent increase in rT3 production and decrease in its clearance. In 14-18% of amiodarone-treated patients, there is overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). Both AIT and AIH may develop either in apparently normal thyroid glands or in glands with preexisting clinically silent abnormalities. AIT is primarily related to excess iodine-induced thyroid hormone synthesis in an abnormal thyroid gland (type I AIT) or to amiodarone-related destructive thyroiditis (type II AIT). AIH pathogenesis is related to escape failure from the acute Wolff-Chaikoff effect due to defects in thyroid hormonogenesis or, in patients with positive thyroid autoantibody test, to concomitant Hashimoto's thyroiditis. AIT is more common in iodine-deficient regions of the world, whereas AIH is usually seen in iodine-sufficient areas. In contrast to AIH, AIT is a condition difficult to diagnose and treat, and discontinuation of amiodarone is usually recommended. In this review discusses, according to data from current literature, alterations in thyroid laboratory tests seen in euthyroid patients under treatment with amiodarone and the epidemiology and treatment options available of amiodarone-induced thyroid dysfunctions (AIT and AIH)., La amiodarona (AMD) es una droga antiarrítmica potente (clase III) usada en la práctica clínica para la profilaxis y el tratamiento de muchos disturbios del ritmo cardiaco, desde la fibrilación auricular paroxística hasta las taquiarritmias ventriculares que amenazan la vida. Frecuentemente causa cambios en las pruebas de función tiroidea principalmente relacionados a la inhibición de la actividad de la 5'-deiodinasa, resultando en una disminución de la generación de T3 desde T4 y el consecuente incremento en la producción de T3 reversa y una disminución de su aclaramiento. En 14 a 18% de pacientes tratados con AMD hay una disfunción tiroidea manifiesta, ya sea tirotoxicosis inducida por amiodarona (TIA) o hipotiroidismo inducido por amiodarona (HIA). Tanto TIA como HIA pueden desarrollarse en glándulas aparentemente normales o en glándulas con anormalidades preexistentes clínicamente silentes. La TIA está primariamente relacionada a la síntesis de hormonas tiroideas inducida por el exceso de yodo en una glándula tiroidea anormal (TIA tipo 1) o a una tiroiditis destructiva relacionada a la amiodarona (TIA tipo 2), aunque frecuentemente ocurren formas mixtas. La tiroiditis de Hashimoto preexistente es un factor de riesgo definido para la ocurrencia de HIA. La patogenia del HIA es la falla para escapar del efecto agudo de Wolff-Chaikoff inducido por el yodo, debido a los defectos en la hormonogénesis tiroidea y, en pacientes con pruebas de autoanticuerpos tiroideos positivos, para tiroiditis de Hashimoto concomitante. La TIA es más común en zonas deficientes de yodo mientras que el HIA es usualmente visto en zonas suficientes en yodo. En contraste al HIA, la TIA es una condición difícil de diagnosticar y tratar, y usualmente se recomienda la descontinuación de la amiodarona. En esta revisión se analiza, de acuerdo a los datos actuales, las alteraciones en las pruebas de función tiroidea vistas en pacientes eutirodeos bajo tratamiento con AMD así como la epidemiología y opciones de tratamiento disponibles para ambos tipo de disfunción tiroidea inducida por amiodarona, TIA e HIA.

La amiodarona (AMD) es una droga antiarrítmica potente (clase III) usada en la práctica clínica para la profilaxis y el tratamiento de muchos disturbios del ritmo cardiaco, desde la fibrilación auricular paroxística hasta las taquiarritmias ventriculares que amenazan la vida. Frecuentemente causa cambios en las pruebas de función tiroidea principalmente relacionados a la inhibición de la actividad de la 5'-deiodinasa, resultando en una disminución de la generación de T3 desde T4 y el consecuente incremento en la producción de T3 reversa y una disminución de su aclaramiento. En 14 a 18% de pacientes tratados con AMD hay una disfunción tiroidea manifiesta, ya sea tirotoxicosis inducida por amiodarona (TIA) o hipotiroidismo inducido por amiodarona (HIA). Tanto TIA como HIA pueden desarrollarse en glándulas aparentemente normales o en glándulas con anormalidades preexistentes clínicamente silentes. La TIA está primariamente relacionada a la síntesis de hormonas tiroideas inducida por el exceso de yodo en una glándula tiroidea anormal (TIA tipo 1) o a una tiroiditis destructiva relacionada a la amiodarona (TIA tipo 2), aunque frecuentemente ocurren formas mixtas. La tiroiditis de Hashimoto preexistente es un factor de riesgo definido para la ocurrencia de HIA. La patogenia del HIA es la falla para escapar del efecto agudo de Wolff-Chaikoff inducido por el yodo, debido a los defectos en la hormonogénesis tiroidea y, en pacientes con pruebas de autoanticuerpos tiroideos positivos, para tiroiditis de Hashimoto concomitante. La TIA es más común en zonas deficientes de yodo mientras que el HIA es usualmente visto en zonas suficientes en yodo. En contraste al HIA, la TIA es una condición difícil de diagnosticar y tratar, y usualmente se recomienda la descontinuación de la amiodarona. En esta revisión se analiza, de acuerdo a los datos actuales, las alteraciones en las pruebas de función tiroidea vistas en pacientes eutirodeos bajo tratamiento con AMD así como la epidemiología y opciones de tratamiento disponibles para ambos tipo de disfunción tiroidea inducida por amiodarona, TIA e HIA. Amiodarone is a potent class III anti-arrhythmic drug used in clinical practice for the prophylaxis and treatment of many cardiac rhythm disturbances, ranging from paroxismal atrial fibrillation to life threatening ventricular tachyarrhythmias. Amiodarone often causes changes in thyroid function tests mainly related to inhibition of 5'-deiodinase activity resulting in decrease in the generation of T3 from T4 with consequent increase in rT3 production and decrease in its clearance. In 14-18% of amiodarone-treated patients, there is overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). Both AIT and AIH may develop either in apparently normal thyroid glands or in glands with preexisting clinically silent abnormalities. AIT is primarily related to excess iodine-induced thyroid hormone synthesis in an abnormal thyroid gland (type I AIT) or to amiodarone-related destructive thyroiditis (type II AIT). AIH pathogenesis is related to escape failure from the acute Wolff-Chaikoff effect due to defects in thyroid hormonogenesis or, in patients with positive thyroid autoantibody test, to concomitant Hashimoto's thyroiditis. AIT is more common in iodine-deficient regions of the world, whereas AIH is usually seen in iodine-sufficient areas. In contrast to AIH, AIT is a condition difficult to diagnose and treat, and discontinuation of amiodarone is usually recommended. In this review discusses, according to data from current literature, alterations in thyroid laboratory tests seen in euthyroid patients under treatment with amiodarone and the epidemiology and treatment options available of amiodarone-induced thyroid dysfunctions (AIT and AIH).

Amiodarone-induced thryrotoxicosis (AIT) is a rare but serious complication of amiodarone use, especially in patients with severe cardiac disease. We present a patient who developed AIT, following administration of amiodarone for life-threatening ventricular arrhythmias. We discuss the medical management of AIT and anesthetic considerations for management of patients with thyrotoxicosis and severe cardiac disease who require surgery including thyroidectomy.

Objective:We present a patient with a rare combination of amiodarone-induced thyrotoxicosis and Eisenmenger's syndrome.Method:Case report and review of the world literature regarding the morbidity and mortality of surgical management of amiodarone-induced thyrotoxicosis and the potential hazards of non-cardiac surgery in patients with Eisenmenger's syndrome.Results:Failure of maximal medical therapy necessitated surgical management to treat amiodarone-induced thyrotoxicosis which, in this particular patient, carried significant risks. Total thyroidectomy was performed leading to rapid resolution of thyrotoxicosis, and the patient made an uncomplicated recovery. We present this case because of its rarity and the potentially hazardous nature of surgical intervention in patients with Eisenmenger's syndrome. The pathogenesis of amiodarone-induced thyrotoxicosis and the differing approaches of medical and surgical management are discussed.Conclusion:Based on our findings, we propose that surgical management should be considered earlier in the treatment algorithm (or possibly as first-line therapy) for amiodarone-induced thyrotoxicosis.

BackgroundAmiodarone-induced thyrotoxicosis (AIT) is caused by excessive hormone synthesis and release (AIT I) or a destructive process (AIT II). This differentiation has important therapeutic implications.PurposeTo evaluate 99mTc-sestaMIBI (MIBI) thyroid scintigraphy in addition to other diagnostic tools in the diagnosis and management of AIT.Subjects and methodsThyroid and 99mTc-MIBI scintigraphies were performed in 20 consecutive AIT patients, along with a series of biochemical and instrumental investigations (measurement of thyrotrophin, free thyroid hormones and thyroid autoantibodies; thyroid colour-flow Doppler sonography (CFDS) and thyroid radioiodine uptake (RAIU)).ResultsOn the basis of instrumental and laboratory data (excluding thyroid 99mTc-MIBI scintigraphy) and follow-up, AIT patients could be subdivided into six with AIT I, ten with AIT II and four with indefinite forms of AIT (AIT Ind). 99mTc-MIBI uptake results were normal/increased in all the six patients with AIT I and absent in all the ten patients with AIT II. The remaining four patients with AIT Ind showed low, patchy and persistent uptake in two cases and in the other two evident MIBI uptake followed by a rapid washout. MIBI scintigraphy was superior to all other diagnostic tools, including CFDS (suggestive of AIT I in three patients with AIT II and of AIT II in three with AIT Ind) and RAIU, which was measurable in all patients with AIT I, and also in four out of the ten with AIT II.ConclusionThyroid MIBI scintigraphy may be proposed as an easy and highly effective tool for the differential diagnosis of different forms of AIT.

Summary Objective To investigate how North American thyroidologists assess and treat amiodarone-induced thyrotoxicosis (AIT) and to compare the results with those of the same questionnaire-based survey previously carried out among European thyroidologists. Design Members of the American Thyroid Association (ATA) with clinical interests were sent by e-mail a questionnaire on the diagnosis and management of AIT, 115 responses were received from the United States and Canada, representing about one-third of ATA members with clinical interests. Results The majority of respondents (91%vs. 68% in Europe, P

Thyrotoxicosis, a life-threatening condition characterized by an excess of thyroid hormones with typical clinical manifestations and high mortality, is a well-known amiodarone side effect. Amiodarone is a highly effective antiarrhythmic drug that contains 37% iodine by weight and has a structural resemblance to thyroid hormones. The average prevalence of amiodarone-induced thyrotoxicosis is about 5%. Because of long terminal half-life amiodarone-induced thyroid dysfunction is very difficult to treat by discontinuation of amiodarone and antithyroid drugs.4, 9-11 Plasmapheresis is already known as a very effective therapeutic method for patients with thyrotoxicosis.12 Here we report on a patient with thyrotoxicosis who was successfully treated with plasmapheresis.

Introduction: Amiodarone is commonlyused in the advanced heart failure population for treatment of arrhythmias. Three to five percent of patients treatedwith amiodarone develop hyperthyroidism, most commonly Type II Amiodarone Induced Thyrotoxicosis (AIT) from destructive thyroiditis. There is little data available evaluating the prevalence of AIT in the transplant population or relatedmorbidity andmortality.Case Series: Approximately half of the patients transplanted at our center are treated with amiodarone prior to cardiac transplant. In the last 20 years, 87 patients received amiodarone prior to or immediately post transplant, and 5 patients developed thyroiditis following transplant (5.7 %). Four patients were treated with amiodarone for an average of 1.6 years prior to transplant, then discontinued at the time of transplant. One patient started amiodarone 5 days after transplant for atrial fibrillation and continued for1.8years.Onaverage, thyroid dysfunction was diagnosed 366 days after discontinuation of amiodarone. The mechanism of dysfunction was thought to be thyroiditis in each patient. Two patients underwent coronary angiography around the time of their diagnosis, so the iodine load may have contributed to an iodine induced thyrotoxicosis in addition to amiodarone. Patients received steroids as part

Although there are two types of amiodarone-induced thyrotoxicosis (AIT), only type II AIT has been seen at our institution in Japan so far. There have been few case reports of AIT recurrence, probably because of the fact that amiodarone is immediately discontinued once AIT has developed. Our own policy is not to discontinue amiodarone in all AIT patients, unless severe adverse effects such as pulmonary fibrosis develop. Among more than 50 patients with type II AIT we have encountered, three with arrhythmogenic right ventricular cardiomyopathy showed AIT recurrence. In these patients, the first episode of AIT developed 3, 4, and 2 years after the start of amiodarone administration, and recurrence was observed 5, 6, and 8 years after the first episode, respectively. The AIT resolved spontaneously in all cases while the patients continued to take amiodarone. In comparison with the first AIT episode, the second was milder and resolved within a shorter period. These three cases suggest that recurrence of type II AIT may not be rare in iodine-sufficient areas, and that it is relatively mild and may resolve spontaneously. Furthermore, at least in Japan, it may be possible for patients with recurrent type II AIT to continue taking amiodarone.

Summary Objective To assess diagnostic and therapeutic approaches to amiodarone-induced thyrotoxicosis (AIT) among members of the Latin American Thyroid Society (LATS). Methods LATS members responded to an online questionnaire that presented an index case (a 62-year-old man on amiodarone, with thyrotoxic symptoms and a nodular goitre) and a variant (same patient, no goitre). Results About 25% of invited members responded to the questionnaire. Most respondents lived in iodine-sufficient areas and observed that amiodarone-induced hypothyroidism (AIH) is more common than AIT. Nearly all assessed TSH, and the most used combination of tests was TSH and free T4 (37%). Thyroid autoimmunity was assessed by about 90%. Interleukin-6 (IL-6) was useful to 80%. Additional tests ordered for the index case were: radioactive iodine uptake (RAIU; 57%), echo-colour Doppler sonography (ECDS; about 50%) and fine-needle aspiration biopsy (FNAB; 44%). For the variant, ECDS and RAIU were judged unhelpful by 16%. Most defined the index case as type I AIT and the variant as type II AIT, but 16% in LATS suggested a mixed form in the index case. As initial treatment, nearly all used thionamides in the index case [with potassium perchlorate (KClO4) in one-third], while glucocorticoids were indicated to the variant by 66%. Only about 5% considered amiodarone withdrawal unnecessary. If initial strategy is ineffective in type I AIT, KClO4 (half) or glucocorticoids (a third) are added; in type II, glucocorticoids are indicated by most. Once euthyroidism is restored, ablative therapy is prescribed by a third of respondents for type I AIT. Conclusions There are several points of disagreement among thyroidologists regarding AIT management, mainly in the radiological evaluation and the approach to the already stabilized patient if amiodarone needs to be restarted.

Thyrotoxicosis is a well-documented and studied complication of treatment with amiodarone, but little has been written about the risks and treatment of recurrent thyrotoxicosis upon re-exposure to amiodarone. One such case is outlined here and discussed by a panel of experts.

Objective To determine how expert European thyroidologists assess and treat amiodarone-induced thyrotoxicosis (AIT). Design Members of the European Thyroid Association (ETA) with clinical interests were asked to answer a questionnaire on the diagnosis and management of AIT. A total of 124 responses were received: 116 from Europe, seven from USA and one from Brazil. After excluding responses coming from the same centre, 101 responses from 24 European countries were analysed, representing approximately 65% of clinically active European ETA members. Results The majority of respondents (68%) see 1-10 new cases of AIT/year, and AIT seems to be more frequent than amiodarone-induced hypothyroidism in Europe, where in many instances iodine intake is borderline or moderately deficient. A good collaboration with cardiologists exists in most centres, and patients receiving chronic amiodarone treatment are checked for thyroid function most commonly every 4-6 months. When AIT is suspected, a diffuse or nodular goitre is present or in the absence of apparent abnormalities of the thyroid, free thyroxine (FT4), free triiodothyronine (FT3) and TSH are assayed by almost 90% of respondents. Thyroid autoimmunity is evaluated in the initial assessment by > 80%, while evaluation of urinary iodine excretion is unhelpful for > 60%. Most commonly used additional diagnostic procedures include thyroid ultrasonography, particularly colour flow Doppler sonography, and, to a lesser extent, a thyroid uptake scan. If the thyroid gland is apparently normal, measurement of thyroidal radioactive iodine uptake is considered useful by a large proportion of respondents to establish the destructive nature of the process. Differentiation of type I and type II AIT is difficult and, possibly, not correct for 27% of respondents, who believe that mixed (or indefinite) forms are probably more frequent than previously recognized. Approximately 10-20% do not consider amiodarone withdrawal necessary in the therapeutic strategy of AIT, especially if the thyroid gland is apparently normal. Most respondents (82%) treat type I AIT with thionamides, either alone (51%) or in combination with potassium perchlorate (31%), while the preferred treatment for type II AIT is represented by glucocorticoids (46%). Some respondents, in view of diagnostic difficulties, initially treat all cases of AIT with a combination of thionamides and glucocorticoids. After restoration of euthyroidism, ablative therapy is recommended by 34% in type I and only 8% in type II AIT. If amiodarone therapy needs to be reinstituted, prophylactic thyroid ablation is recommended by 65% in type I AIT, while a wait-and-see strategy is adopted by 70% in type II AIT. Conclusion Areas of certainty and uncertainty concerning AIT are present among expert European thyroidologists, both from a diagnostic and a therapeutic standpoint. Diagnostic criteria need to be refined in order to improve therapeutic outcome.

Two patients with amiodarone-induced thyrotoxicosis were treated successfully with potassium perchlorate and carbimazole while treatment with amiodarone was continued. These antithyroid drugs were stopped after the patients had became clinically and biochemically euthyroid. During follow up, when treatment with amiodarone continued, thyrotoxicosis did not recur. Amiodarone-induced thyrotoxicosis seems to be a transient condition that can be treated successfully with a short course of antithyroid drugs without stopping amiodarone treatment.

The incidence of type 2 amiodarone-induced thyrotoxicosis (AIT) is increasing. A new study provides evidence that glucocorticoid therapy is safe, effective and associated with prompt restoration of euthyroidism in previously untreated type 2 AIT. The outcome of initial combined glucocorticoid and thionamide therapy can also help differentiate between type 1 and type 2 AIT.

Pathogenese, Diagnostik und Therapie der Amiodaron-induzierten Hyperthyreose (AIT) und Hypothyreose (AIH) werden kurz besprochen. Klinisch manifestieren sich AIT und AIH durch die klassischen Symptome und Zeichen der Schilddrüsendysfunktion, sind bisweilen aber auch oligosymptomatisch. Grundpfeiler der Funktionsdiagnostik sind TSH, fT4 und fT3. Bei AIT kommen wegen des hohen Jodgehalts von Amiodaron nur Medikamente und Chirurgie in Betracht. Eine Radiojodtherapie steht meist nicht zur Diskussion. Falls von kardialer Seite möglich, sollte Amiodaron abgesetzt werden. Für die medikamentöse Therapie stehen Thionamide, Perchlorat (nicht in der Schweiz), Steroide (vor allem Typ II und gemischte Formen von AIT) und Lithium (Reservemedikament) zur Verfügung. Die zwei Typen von AIT sind auch therapeutisch unterschiedlich anzugehen. Die chirurgische Therapie gilt heute als valable Option für die Therapie schwerer Formen von AIT mit schlechtem Ansprechen auf medikamentöse Therapie. Hauptvorteil der chirurgischen Therapie der AIT ist die umgehende Behebung der Hyperthyreose verbunden mit der Möglichkeit, eine kardial klar indizierte und wirksame Amiodarontherapie weiterzuführen. Bei AIH muß Amiodaron nicht sistiert werden, wenn es kardiologisch wirklich indiziert und wirksam ist. Die Therapie der AIH erfolgt wie bei den meisten andern Hypothyreoseformen in erster Linie mit Levothyroxin.

Purpose: We examined the relationship between renal impairment and high-sensitivity troponin T levels (hsTnT) in patients presenting to an emergency department with no known acute cause of hs-TnT elevation. Methods: We identified all patients presenting to the emergency department over a two-year period who had hs-TnT and serum creatinine measured. eGFR values were determined using the MDRD175 equation. We reviewed all individuals with eGFR 60ml/min/1.73m2 and applied the same exclusion criteria to give fourequal sized groups for comparison. Results: After excluding acute causes of hsTnT elevation, we identified 101 patients with an eGFR 60 group, 12 (4–19) in the eGFR 45–59 group, 16 (8–32) in the eGFR 30–44 group and 40 (21–77) in the eGFR 13ng/L (OR=4.2). Conclusions: Renal impairment is an independent cause of raised hs-TnT levels in the emergency department that needs to be considered prior to classifying a patient as having an acute coronary syndrome.

Aims Amiodarone is an iodine-rich drug widely used for the management of various cardiac arrhythmias and severe congestive heart failure. Thyroid dysfunction is an important side-effect of amiodarone therapy. Amiodarone-induced thyrotoxicosis is a complex diagnostic and therapeutic challenge. It can occur in apparently normal thyroid glands and in glands with pre-existing abnormalities. The aim of this study was to investigate the histo-pathological and immunohistochemical features of a total thyroid-ectomy specimen in a 70-year-old man with amiodarone-induced thyrotoxicosis. Methods Paraffin embedded thyroid tissues were stained with haematoxylin and eosin and special immunohistochemical and histochemical stains. Results Histological examination revealed destruction of the thyroid follicles with areas of degeneration and involution of the follicles. Together with chronic inflammatory changes and fibrosis, foamy cells containing fine-brown pigments filled approximately 50% of the follicles. Discussion The histological features of our case were in keeping with amiodarone-induced thyrotoxicosis.

Summary Context Two main forms of amiodarone-induced thyrotoxicosis (AIT) exist. Type 1 AIT is a form of iodine-induced hyperthyroidism. Its management is complex and includes thionamides, potassium perchlorate and, occasionally, thyroidectomy. Type 2 AIT is a destructive thyroiditis, responds to glucocorticoids, and usually does not require further thyroid treatment once euthyroidism has been restored. Objective To assess retrospectively the prevalence and relative proportion of type 1 and type 2 AIT over a 27-year period at a tertiary referral centre in Italy. Patients Consecutive AIT patients (n = 215) seen at the department of endocrinology of the University of Pisa between 1980 and 2006. Results Type 1 AIT constituted the most frequent AIT form (60%) during the first years covered by this study. The annual mean number of type 1 AIT patients was 3·6 at the beginning of the study period, and 2·5 during the later years. In contrast, the mean annual number of new cases of type 2 AIT progressively increased from 2·4 to 12·5. Likewise, the proportion of type 2 AIT increased in a significant linear manner (P

We describe a case of amiodarone-induced thyrotoxicosis following heart valve replacement in a patient with a multinodular goitre. He responded to medical therapy with carbimazole and potassium perchlorate. Subsequent therapy with radio-iodine was followed 30 weeks later by the development of anaplastic thyroid carcinoma. It is possible that amiodarone caused a low uptake of radio-iodine by the thyroid. It is not known whether this possible low dose exposure to ionising radiation played a part in the development of the anaplastic carcinoma.