Iodine Excess and Hyperthyroidism (original) (raw)
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The Characteristics of Amiodarone-induced Thyrotoxicosis in a Moderate Iodine Deficit Area
Acta Medica Marisiensis, 2013
Introduction: Amiodarone (AMI), a class III anti-arrhythmic drug, is associated with a number of side effects, including thyroid dysfunction (both hypo- and hyperthyroidism), which is due to amiodarone's high iodine content and its direct toxic effect on the thyroid. Objective: To evaluate the incidence of Amiodarone induced thyrotoxicosis (AIT) (type, rate of occurrence) and to identify the risk factors involved in its occurrence. Material and method: We examined patients treated with amiodarone, between January 2002 and December 2011, who presented to our Department of Endocrinology Târgu Mures for thyroid dysfunctions. Results: The retrospective study included 87 patients with thyroid dysfunctions; 58 (66.7%) patients had AIT and 29 (33.3%) had Amiodarone induced hypothyroidism (AIH). In the AIT group: 35 were women (60.3%), 23 were men (39.7%); the average age was 61.60 ± 12.39 years. Risk factors identified for the AIT group were male gender (RR = OR = 3.8; Chi-squer = 5.7,...
Clinical Endocrinology, 2008
To determine how expert European thyroidologists assess and treat amiodarone-induced thyrotoxicosis (AIT). 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. 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. 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.
Radioactive iodine in the treatment of type-2 amiodarone-induced thyrotoxicosis
Journal of the National Medical Association, 2008
Amiodarone-induced thyrotoxicosis (AIT) is usually classified into two types: type 1, in which a high iodine content triggers the autonomous production of thyroid hormone; and type 2, in which destructive thyroiditis causes the release of preformed thyroid hormone. AIT is a difficult management problem that sometimes requires ablative thyroid therapy. The use of radioactive iodine (RAI) therapy in patients with type-1 AIT who had a 24-hour radioactive iodine uptake (RAIU) value of >10% has been previously reported. Despite its documented efficacy at usual doses (10-30 mCi) in patients with type-1 AIT, the efficacy of RAI in those with type-2 AIT has never been questioned, because type-2 patients usually have low RAIU. We thought that high adjusted-dose RAI might be an attractive alternative to thyroid gland ablation in patients with type-2 AIT. Four patients with type-2 AIT who required thyroid ablation were included in the study. These individuals were either poor candidates for...
Amiodarone-Induced Thyrotoxicosis in a Patient with Autonomously Functioning Nodular Goiter
Annals of Pharmacotherapy, 2009
A miodarone is an effective antiarrhythmic agent for treatment and prophylaxis of life-threatening ventricular arrhythmias. It contains 37% organic iodine in its molecular mass, or about 75 mg of iodine per 200-mg tablet, 10% of which is released as unbound iodide. 1 A dosage of 200 mg of amiodarone daily provides roughly 50 times the recommended iodine requirement determined by the World Health Organization (150 µg/day for adults). 2-4 Amiodarone is also highly lipophilic and accumulates in adipose tissue after ingestion, leading to its long elimination half-life (~100 days). 3,5 This "iodine-rich" characteristic is believed to be the major etiology of amiodarone-induced thyroid dysfunction, which includes failure to escape from the Wolff-Chaikoff effect, iodine-induced potentiation of thyroid autoimmunity, and unregulated hormone synthesis (Jod-Basedow effect). In addition, amiodarone inhibits type 1 5'-deiodinase activity, thereby decreasing the peripheral conversion of thyroxine (T 4 ) to triiodothyronine (T 3 ) and the clearance of both T 4 and reverse T 3 . Amiodarone can act as a competitive antagonist of T 3 and inhibit the entry of thyroid hormones into peripheral tissues. Cytotoxic effects that cause lysis of thyroid follicles have also been described. 1,3, Adverse reactions to amiodarone are complex and include amiodarone-induced thyrotoxicosis (AIT) and hy-pothyroidism (AIH). In iodine-sufficient geographic areas, AIT is less common than AIH. 1,7 Although the overall incidence of thyroid dysfunction by amiodarone is about 2-24%, 3,8 AIT should be considered in patients taking amiodarone who develop symptoms and signs of thyrotoxicosis including weight loss, tremors, restlessness, and tachycardia. Laboratory tests usually demonstrate depressed thyroid-stimulating (TSH) levels with elevated T 4 and T 3 levels. AIT is further classified as type 1 or type 2 based on different etiologies. Type 1 AIT is due to unregulated hor-Author information provided at the end of the text.
Thyroid ultrasonography in patients with a previous episode of amiodarone induced thyrotoxicosis
Journal of Endocrinological Investigation, 1994
Amiodarone induced thyrotoxicosis (AIT) occurs most frequently in euthyroid patients with nodular goiter or Graves' disease due to release of iodine from this iodine rich drug. However, some cases of AIT have been attributed to an inflammatory process of the thyroid gland due to amiodarone itself. We have studied the echographic pattern of the thyroid in 11 euthyroid patients who had an episode of AIT 32.4±3.6 months earlier due to amiodarone induced thyroiditis. There was a significant increase in dyshomogeneous echo patterns and hyperechogenecity which suggests fibrotic lesions. These findings were similar to those observed in 10 euthyroid
AMIODARONE IODINE-INDUCED HYPOTHYROIDISM: RISK FACTORS AND FOLLOW-UP IN 28 CASES
Clinical Endocrinology, 1987
Amiodarone, an iodine-rich drug widely used for the treatment of cardiac tachyarrhythmias, may induce either hyperthyroidism or hypothyroidism. Of 467 patients chronically treated with this drug referred to our institution, amiodarone iodine-induced hypothyroidism (AIIH) developed in 28 patients (6%). AIIH patients were subdivided into two groups according to the presence (group A) or absence (group B) of underlying thyroid abnormalities. Thyroid autoantibodies were present in 10 of 19 patients from group A and 0 of 9 patients from group B. The thyroid 24-h radioiodine uptake (RAIU) was evaluated in 15 patients: low values (<4%) were found in three patients and detectable values (7–50%) were observed in 12. Perchlorate discharge tests were positive in all four patients tested. Follow-up data were available in 20 patients (16 in group A and four in group B). Hypothyroidism was transient in 12 (60%) and persistent for several months after amiodarone withdrawal in eight (40%). While all patients in group B had transient hypothyroidism, 50% of patients with underlying thyroid abnormalities (group A) had persistent hypothyroidism. Thyroid autoantibodies were found in seven of eight patients with persistent hypothyroidism and in only three of 12 patients with transient hypothyroidism. Conversely, seven of 10 patients with positive thyroid autoantibodies had persistent hypothyroidism and 9 of 10 patients with undetectable thyroid autoantibodies had transient hypothyroidism. These data indicate that: (i) AIIH may develop in patients with or without underlying thyroid abnormalities; (ii) RAIU is inappropriately elevated in many patients with AIIH; (iii) intrathyroidal iodine is not organified; (iv) serum thyroid autoantibodies represent a risk factor for the development of AIIH; (v) AIIH spontaneously remits after amiodarone withdrawal in patients without thyroid abnormalities, but may persist in patients with concomitant thyroid disorders, especially those with circulating thyroid autoantibodies.
Radioiodine therapy in patients with amiodarone-induced thyrotoxicosis (AIT)
Neuro Endocrinology Letters, 2009
INTRODUCTION: Amiodarone (AM) is frequently used in the therapy of patients with cardiac disorders. However, due to high iodine content, it has side effects on thyroid function. The use of radioiodine therapy (RIT) in amiodarone-induced thyrotoxicosis (AIT) with low radioactive iodine uptake (RAIU) is still controversial. In these patients therapeutic choices for refractory disease include surgery, antithyroid drugs, or glu ocorticosteriods. AIM: The aim of the study was to evaluate the efficacy of RIT in patients presenting AIT and low RAIU in two-year follow-up. PATIENTS AND METHODS: 40 patients (25 men and 15 women) aged from 63 to 83 years (x ± SD: 66.2 ± 5.0 years; median: 65 years) treated with RIT were included into the study. In these patients AM therapy was essential for the underlying heart disorder, while surgery, antithyroid drugs or glucocorticosteroids, were contraindicated. Forty seven patients with toxic multinodular goiter (TMNG) (39 women and 8 men), matched for age (67 ± 12 yr; range 54-89 yr), were enrolled into the study as a comparative group. The diagnostic procedures included baseline thyroid function tests (thyrothropin-TSH, free triiodothyronine-fT 3 and free thyroxine-fT 4 levels), thyroid autoantibodies measurement (antithyroglobulin autoantibodies-TgAb, antithyroid peroxidase autoantibodies-TPOAb, anti-TSH receptor autoantibodies-TRAb), thyroid ultrasonography, thyroid scintiscan and RAIU assessment. RESULTS: Serum values of TSH, TgAb, TPOAb and TRAb were undetectable in both groups. In patients with AIT fT 4 level was 18.7 to 38.7 pmol/l (mean: 27.1 ± 5.8) and fT 3 concentration was 3.9 to 5.6 pmo/l (mean: 5.7 ± 1.4), while in TMNG patients level of fT 4 was 31.5 to 22.2 pmol/l (mean: 25,3 ± 5,8) and fT 3 concentration was 3.8 to 4,2 pmo/l (mean: 4,2 ± 0,2). Mean RAIU values after 5h and 24h in AIT patients were 2.3 ± 0.5 and 3.1 ± 0.9%, while in TMNG patients were 18,0 ± 3,8 and 35,7 ± 9,1%, respectively. A significant difference (p<0.001) between 5h and 24h RAIU in AIT compared to TMNG was noted. In all patients 210
Clinical Endocrinology, 2007
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. 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. Consecutive AIT patients (n = 215) seen at the department of endocrinology of the University of Pisa between 1980 and 2006. 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 &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001), currently accounting for 89% of AIT cases. Type 2 AIT patients showed a male preponderance, higher serum FT4/FT3 ratio (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.002), lower 3-h and 24-h thyroidal radioactive iodine uptake values (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001), and received a higher cumulative dose of amiodarone (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.0001) than type 1 AIT patients. Over a 27-year period, the epidemiology of AIT changed, as the prevalence of type 2 AIT progressively increased and that of type 1 remained constant. Thus, under most circumstances, endocrinologists nowadays deal with type 2 AIT, which is a destructive thyroiditis, generally treated successfully with glucocorticoids. Although no additional treatment is usually required after the destructive process subsides, periodic assessment of thyroid function is warranted, because of the occurrence of hypothyroidism (up to 17%) during long-term follow-up of these patients.