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Abstract Graves` disease
In 1811, France was at war, and Bernard Courtois was producing saltpeter for gunpowder for Napoleon’s army. He was burning seaweed to isolate sodium bicarbonate and when he added sulfuric acid to the ash, he produced an intense violet vapor that crystallized on cold surfaces. He sent the crystals to Gay-Lussac, who subsequently identified it as a new element and named it iodine, from the Greek for violet. Iodine (atomic weight 126.9 g/atom) is an essential component of the hormones produced by the thyroid gland and is therefore essential for mammalian life. The ancient Greeks, including Galen, used the marine sponge to treat swollen glands, but Italian physicians of the School of Salerno were the first to report the specific use of the sponge and dried seaweed to treat goiter. Chatin and goiter prophylaxis in France The French chemist Chatin was the first to publish, in 1851, the hypothesis that iodine deficiency was the cause of goiter. Chatin, the director of the School of Pharmacy in Paris, had measured iodine in a large number of foodstuffs and water supplies throughout Western Europe and concluded: ‘‘Too low a concentration of iodine in the drinking waters of certain areas appears to be the principal cause of goiter. Changing the water source and animal foods and above all of eggs are rational treatments against this condition.’’ French authorities in 3 Departments where goiter was severe (Bas-Rhin, Seine-Inferieure, and Haute-Savoie) began distributing iodine tablets and salt together with other prophylactic measures. The program was clearly effective; in a survey of 5000 goitrous children, 80% were cured or improved by the iodine treatment. Endemic goiter is characterized by enlargement of the thyroid gland in a significantly large fraction of a population group, and is generally considered to be due to insufficient iodine in the daily diet. Endemic goiter exists in a population when >5% of 6-12 year-old children have enlarged thyroid glands Congenital hypothyroidism (CH) occurs in approximately 1:2,000 to 1:4,000 newborns. The clinical manifestations are often subtle or not present at birth. This likely is due to trans-placental passage of some maternal thyroid hormone, while many infants have some thyroid production of their own. Common symptoms include decreased activity and increased sleep, feeding difficulty, constipation, and prolonged jaundice. On examination, common signs include myxedematous facies, large fontanels, macroglossia, a distended abdomen with umbilical hernia, and hypotonia. CH is classified into permanent and transient forms, which in turn can be divided into primary, secondary, or peripheral etiologies. Thyroid dysgenesis accounts for 85% of permanent, primary CH, while inborn errors of thyroid hormone biosynthesis (dyshormonogeneses) account for 10-15% of cases. Secondary or central CH may occur with isolated TSH deficiency, but more commonly it is associated with congenital hypopitiutarism. Transient CH most commonly occurs in preterm infants born in areas of endemic iodine deficiency. In countries with newborn screening programs in place, infants with CH are diagnosed after detection by screening tests. The diagnosis should be confirmed by finding an elevated serum TSH and low T4 or free T4 level. Other diagnostic tests, such as thyroid radionuclide uptake and scan, thyroid sonography, or serum thyroglobulin determination may help pinpoint the underlying etiology, although treatment may be started without these tests. Levothyroxine is the treatment of choice; the recommended starting dose is 10 to 15 mcg/kg/day. The immediate goals of treatment are to rapidly raise the serum T4 above 130 nmol/L (10 ug/dL) and normalize serum TSH levels. Frequent laboratory monitoring in infancy is essential to ensure optimal neurocognitive outcome. Serum TSH and free T4 should be measured every 12 months in the first 6 months of life and every 3-4 months thereafter. In general, the prognosis of infants detected by screening and started on treatment early is excellent, with IQs similar to sibling or classmate controls. Studies show that a lower neurocognitive outcome may occur in those infants started at a later age (> 30 days of age), on lower l-thyroxine doses than currently recommended, and in those infants with more severe hypothyroidism. Macroglossia Graves' disease Graves' disease, the most common form of hyperthyroidism in the United States, is an autoimmune disorder caused by an overactive thyroid gland, which secretes more thyroid hormones than your body needs. If you have Graves' disease, your immune system mistakenly attacks the thyroid gland — and sometimes the tissue behind your eyes or the skin on your lower legs. Primary hyperthyroidism – diagnosis and treatment. Edyta Gurgul, Jerzy Sowinski Department of Endocrinology, Metabolism and Internal Diseases,Poznan, Poland Primary hyperthyroidism in young patients (20–40 years old) is mainly due to Graves-Basedow disease. Toxic goitre and autonomous thyroid nodules are the major causes of hyperthyroidism in the elderly and in patients living in iodine deficient areas. Thyroiditis, drug-induced thyroid disorders (amiodarone, interferon gamma), and pregnancy may be connected with hyperthyroidism. Graves-Basedow disease is an autoimmunological disorder caused by increased level of thyrotropin-receptor antibody (TRAb), which leads to continuous thyrotropin (TSH) receptor stimulation and excessive thyroid hormones production. Diagnosis of primary hyperthyroidism Ordinarily, typical symptoms suggest hyperthyroidism. However, the diagnosis has to be confirmed by hormonal tests: — TSH level is reduced or even undetectable; — free triiodothyronine and tetraiodothyronine (fT3 and fT4) concentrations are elevated in overt hyperthyroidism and normal in subclinical thyroid disorders. Graves’ orbitopathy (GO, endocrine orbitopathy, thyroid eye disease) is an inflammatory fibrosing disease of the predominantly retro-orbital contents. It is commonly associated with autoimmune hyperthyroidism, disorders associated with hyperthyroidism (Hashimoto’s thyroiditis, myxedema without previous thyrotoxicosis), and rarely occurs in patients without a history of thyroid disease. Autoimmune hyperthyroidism (Graves’ disease) is considered an autoimmune disease due to the production of antibodies against thyroid stimulating hormone receptors located in the retroorbital contents. These antibodies subsequently induce inflammatory and fibrotic reactions. THYROID EYE DISEASE Superior limbic keratoconjunctivitis (SLK) INFILTRATION 1. soft tissue involvement :chemosis, conjunctival injection over the recti insertions, puffy lids Corticosteroids have been used successfully in the treatment of acute congestive orbitopathy. J Clin Res Pediatr Endocrinol. 2012 Nov 15. Hyperthyroidism In Childhood: Causes, When and How To Treat. Léger J, Carel JC. Abstract Graves' disease (GD) is the most common cause of hyperthyroidism in children. This review gives an overview and update of management of GD. Antithyroid drugs (ATD) are recommended as the initial treatment, but the major problem is the high relapse rate (30%) as remission is achieved after a first course of ATD. More prolonged medical treatment may increase the remission rate up to 50%. Alternative treatments, such as radioactive iodine or thyroidectomy, are considered in cases of relapse, lack of compliance, or ATD toxicity. Therefore, clinicians have sought prognostic indicators of remission. Relapse risk decreases with longer duration of the first course of ATD treatment, highlighting the positive impact of a long period of primary ATD treatment on outcome. The identification of other predictive factors such as severe biochemical hyperthyroidism at diagnosis, young age, and absence of other autoimmune conditions has made it possible to stratify patients according to the risk of relapse after ATD treatment, leading to improvement in patient management by facilitating the identification of patients requiring long-term ATD or early alternative therapy. Neonatal autoimmune hyperthyroidism is generally transient, occurring in only about 2% of the offspring of mothers with GD. Cardiac insufficiency, intrauterine growth retardation, craniostenosis, microcephaly and psychomotor disabilities are the major risks in these infants and highlight the importance of TRAb determination throughout pregnancy in women with GD, as well as highlighting the need for early diagnosis and treatment of hyperthyroidism. World J Nucl Med. 2012 Jan-Jun; 11(1): 7–11. Radioiodine Thyroid Ablation in Graves’ Hyperthyroidism: Merits and Pitfalls J. F. Nwatsock,1,2 D. Taieb,1 L. Tessonnier,1 J. Mancini,3 F. Dong-A-Zok,2 and O. Mundler1 Abstract Ablative approaches using radioiodine are increasingly proposed for the treatment of Graves′ disease (GD) but their ophthalmologic and biological autoimmune responses remain controversial and data concerning clinical and biochemical outcomes are limited. The aim of this study was to evaluate thyroid function, TSH-receptor antibodies (TRAb) and Graves′ ophthalmopathy (GO) occurrence after radioiodine thyroid ablation in GD. We reviewed 162 patients treated for GD by iodine-131 (131I) with doses ranging from 370 to 740 MBq, adjusted to thyroid uptake and sex, over a 6-year period in a tertiary referral center. Collected data were compared for outcomes, including effectiveness of radioiodine therapy (RIT) as primary endpoint, evolution of TRAb, and occurrence of GO as secondary endpoints. The success rate was 88.3% within the first 6 months after the treatment. The RIT failure was increased in the presence of goiter (adjusted odds ratio = 4.1, 95% confidence interval 1.4–12.0, P = 0.010). The TRAb values regressed with time (r = −0.147; P = 0.042) and patients with a favorable outcome had a lower TRAb value (6.5 ± 16.4 U/L) than those with treatment failure (23.7 ± 24.2 U/L, P < 0.001). At the final status, 48.1% of patients achieved normalization of serum TRAb. GO occurred for the first time in 5 patients (3.7%) who were successfully cured for hyperthyroidism but developed early and prolonged period of hypothyroidism in the context of antithyroid drugs (ATD) intolerance (P = 0.003) and high TRAb level (P = 0.012). On the basis the results of this study we conclude that ablative RIT is effective in eradicating Graves’ hyperthyroidism but may be accompanied by GO occurrence, particularly in patients with early hypothyroidism and high pretreatment TRAb and/or ATD intolerance. In these patients, we recommend an early introduction of LT4 to reduce the duration and the degree of the radioiodine-induced hypothyroidism. Mechanism underlying the effect of thyroid hormone on the cardiovascular system Besides its metabolic and thermoregulatory tissue effects, thyroid hormone regulates cardiac performance by acting on the heart and vascular system. In fact, thyroid hormone influences cardiac performance by genomic and non-genomic effects and increases cardiac output by affecting stroke volume and heart rate. Genomic effects: Several important cardiac structural and functional proteins are transcriptionally regulated by T3, namely, sarcoplasmic reticulum calcium ATPase (SERCA2), a-myosin heavy chain (aMHC), b1 adrenergic receptors, sodium/potassium ATPase, voltage-gated potassium channels, malic enzyme and atrial and brain natriuretic hormone. The non-genomic effects exerted by TH on cardiac myocyte and peripheral vascular resistance are the effects that do not require the binding to nuclear receptors (26). These effects start very quickly and involve the transport of ions (calcium, sodium and potassium) across the plasma membrane, glucose and amino acid transport, mitochondrial function and a variety of intracellular signalling pathways. Vie di sintesi ormoni tiroidei Biosintesi degli ormoni tiroidei Schematica rappresentazione della biosintesi degli ormoni tiroidei nei follicoli tiroidei e potenziali funzioni della GPx3 nel rimuovere l’eccesso di H2O2. Il sodio ioduro sinporter (NIS) accumula ioduro a livello della membrana basolaterale del tirocita. Lo ione ioduro è trasportato fino all’apice della membrana per entrare poi nel lume colloidale attraverso una proteina trasportatrice di anioni la pendrina. La Tiroide ossidasi (Duox) genera acqua ossigenata sulla superficie della membrana apicale che è utilizzata dalla thyroperoxidase (TPO) per iodinare la thyroglobulin (TG) secreta nel lume colloidale con la formazione di residui MIT e DIT nella catena della TG. La TPO inoltre catalizza l’accoppiamento tra una molecola di MIT e DIT portando alla fomazione di iodiotironina precursore di T4 e T3. La TG contenente gli ormoni T4 e T3 è internalizzata attraverso micropinocitosi a livello della membrana apicale. La T4 e T3 sono liberate attraverso proteolisi della TG dalla catepsina e secrete nel circolo sanguigno. Lo ioduro è liberato dal MIT e dal DIT attraverso la dealogenasi (Dehal1) e riciclato per la iodinazione della TG. La selenioproteina GPx3 degrada l’eccesso di acqua ossigenata non utilizzata per la iodinazione e l’accoppiamento di DIT e MIT. Gli enzimi intracellulari deiodinasi seleniodipendenti formano la T3 e liberano ioduro dalla T4. Inoltre altre selenio-proteine quali il TrxRd, la GPx1 e la selenio-proteina P15 (Sep15) sono coinvolte nelle reazioni redox e nella difesa antiossidante. L’ormone ipofisario TSH è il regolatore della biosintesi, l’immagazzinamento e della secrezione degli ormoni tiroidei. Farmaci tiroidei e Antitiroidei TPO= Tiroperossidasi; SePP = Selenioproteina; GPx3 = Glutatione perossidasi; NIS = Sodio-ioduro sinporter; Tg = Tiroglobulina Formazione della T4 Metabolismo della T4 Sintomi dell’ipotiroidismo Fatica Aumentata sensibilità al freddo Costipazione Pelle secca e scolorita Elevati livelli di colesterolo Aumento di peso Dolori muscolari Dolori articolari Debolezza muscolare Lunghi periodi di mestruazione Depressione Medici della scuola di salerno furono i primi a riportare l’uso specifico di spugne marine e alghe per il trattamento del gozzo. J. Nutr. 138: 2060–2063, 2008. L’ipotiroidismo primario è risultante da una tiroidite cronica autoimmunitaria mentre l’ipotiroidismo centrale può essere dovuto a tumore dell’ipofisi. Il trattamento con T4 ristabilisce l’equilibrio tiroideo (eutiroidismo). S W I S S M E D W K LY 2 0 0 9 ; 1 3 9 ( 2 3 – 2 4 ) : 3 3 9 – 3 4 4 Trattamento ipotiroidismo Il trattamento standard nei casi di ipotiroidismo è l’uso giornaliero di levotirossina. Dopo una o due settimane di trattamento il soggetto sente meno la fatica e i livelli di colesterolo e il peso corporeo diminuiscono. I livelli di TSH devono essere misurati dopo 2 o 3 mesi onde evitare un’eccessiva stimolazione. I test di fnzionalità tiroidea mostravano a due giorni dalla nascita i seguenti valori: T3 = 3.0 nmol/l (normal range: 1.042.5), T4= 23.2 nmol/l (normal: 65-160), fT4 (T4 libera) 2.6 pmol/l (normal range: 10-25), TSH= 165.1 mIU/l (normal range: 0.15-3.2), Tiroglobulina 2,093 ng/ml. Il bambino è stato sottoposta ad una terapia con 50 μg/giorno di L-tiroxina. Ipertiroidismo Con il termine di ipertiroidismo si intende una elevata concentrazione di T4 e T3 libera circolante nel sangue. Le maggiori cause di ipertiroidismo sono: 1) Il morbo di Graves, 2) Adenomi tiroidei 3) Gozzo multinodulare. Il trattamento può essere farmacologico o chirurgico. Il trattamento farmacologico può essere fatto con: 1) Iodio radioattivo (131I) 2) Farmaci antitiroidei (Propiltiouracile, metimazolo, carbimazolo) 3) Beta Bloccanti (propanololo) Lo iodio radioattivo è somministrato per os e assorbito dalla ghiandola tiroidea dove ne diminuisce il volume nell’arco di tre-sei mesi. Il propiltiouracile e il metimazolo vengono somministrati per os e nell’arco delle seidodici settimane migliorano il quadro clinico dell’ipertiroideo. Il trattamento può continuare per un intero anno o più a lungo. Questi farmaci possono essere epatotossici. Si deve preferire il metimazolo in quanto è meno epatotossico del propiltiouracile. Lo iodio radioattivo è il farmaco di elezione nel morbo di Graves e nelle sue forme di recrudescenza. E’ utilizzato anche nel trattamento dell’ipertiroidismo da noduli tossici ( Hong Kong Med J. 2009 Aug;15(4):267-73). Il metimazolo e il propiltiouracile sono degli inibitori selettivi della iodinazione della tirosina presente nella tiroglobulina da parte della tiroperossidasi. Queste tionamidi inibiscono l’accoppiamento dei residui iodotirosinici nel formare iodotironine. Inoltre, il propiltiouracile, al contrario del metimazolo, inibisce la deiodinazione della tiroxina (T4) a triiodotironina (T3) porzione più attiva della T4. Il Carbimazolo è il profarmaco che da origine a metimazolo. Il metimazolo possiede un’emivita maggiore del propiltiouracile e può essere somministrato una volta al giorno. Gli effetti collaterali sono minori rispetto al propiltiouracile. . Propiltiouracile Methimazole Actions, Dosing, and Efficacy Il Trattamento con iodio radioattivo è il trattamento di scelta nell’ipertiroidismo ma in alcuni casi il metimazolo è la terapia di scelta. Il metimazolo blocca la sintesi dell’ormone tiroideo (T3 e T4) attraverso l’inibizione della tiroide perossidasi, enzima coinvolto nell’ossidazione dello ioduro a iodio, nell’incorporazione dello iodio nella tiroglobulina e l’accoppiamento dei residui di tirosina per formare la T4 e la T3. Il Metimazolo non blocca il rilascio degli ormoni tiroidei già formati. Questo spiega il ritardo di 2-4 settimane prima che la concentrazione plasmatica di T4 si normalizzi. Il metimazolo non diminuisce la dimensione del gozzo, anzi questo diventa ancora più grande nel tempo malgrado la terapia. Clin Tech Small Anim Pract 21:22-28 © 2006 Expert Opin Pharmacother. 2005 Jun;6(6):851-61. An update on the pharmacological management of hyperthyroidism due to Graves' disease. Bartalena L, Tanda ML, Bogazzi F, Piantanida E, Lai A, Martino E. Division of Endocrinology, Department of Clinical Medicine, Ospedale di Circolo, University of Insubria, Viale Borri, 57, 21100 Varese, Italy. Abstract Una delle migliori terapie per il trattamento del morbo di Graves’ è usualmente tramite l’uso delle tionamidi quali carbimazolo, metimazolo e propiltiouracile in aggiunta alla terapia con radioiodio e la tiroidectomia. Le tionamidi rappresentano il trattamento di scelta nelle donne gravide, durante l’allattamento, nei bambini e adolescenti in preparazione alla terapia con iodio radioattivo o alla tiroidectomia. Gli effetti collaterali sono relativamente frequenti ma in genere lievi e transitori. Due regimi posologici sono disponibili: il metodo della titolazione ( si usa la dose più bassa per mantenere l’eutiroidismo di durata tra I 12 e I 18 mesi) e il metodo del blocco e rimpiazzo. Nessuno dei due metodi ha chiari vantaggi in termini di risultati terapeutici ma al secondo sono associati meno effetti collaterali. Ricorrenza di episodi di ipertiroidismo è del 50% dei casi nei confronti dei quali la terapia di asportazione dovrebbe essere offerta. Abstract Graves’ disease (GD) is the most common cause of thyrotoxicosis in children and adolescents. Caused by immunologic stimulation of the thyroid-stimulating hormone receptor, lasting remission occurs in only a minority of pediatric patients with GD, including children treated with antithyroid drugs (ATDs) for many years. Thus the majority of pediatric patients with GD will need thyroidectomy or treatment with radioactive iodine (RAI; 131 I). When ATDs are used in children, only methimazole should be used. Propylthiouracil is associated with an unacceptable risk of severe liver injury in children and should never be used as first-line therapy. If remission (defined as normal thyroid function off ATDs) is not achieved after 1 or 2 years of ATD therapy, 131 I or surgery may be considered, with the choice influenced by the age of the individual. When 131 I is used, administered doses should be 1 150 Ci/g of thyroid tissue. When surgery is performed, near total or total thyroidectomy is recommended. Conclusion: Choosing a treatment approach for childhood GD is often a difficult and highly personal decision. Discussion of the advantages and risks of each therapeutic option is essential to help the patient and family select a treatment option. Endocr Pract. 2002 May-Jun;8(3):222-4. Methimazole-induced hepatotoxicity. Woeber KA. Department of Medicine, University of California, San Franscisco, California 94143-1640, USA. Abstract To present the case of a patient with Graves' hyperthyroidism in whom treatment with methimazole led to severe cholestasis. In a 36-year-old woman with severe hyperthyroidism, treatment with methimazole (20 mg twice daily) was initiated. Nineteen days later, pruritus, scleral icterus, dark urine, and abdominal discomfort prompted discontinuation of the therapy. Laboratory investigations and abdominal ultrasonography showed findings consistent with a cholestatic reaction to methimazole. Recovery was slow but complete. Of the 30 previously published cases of hepatotoxicity related to treatment with methimazole or carbimazole in which the nature of the hepatic injury was described, 19 were also cholestatic. Physicians should be aware that thionamide drugs can be associated with hepatotoxicity. Analysis of the known cases suggests that older age of the patient and higher dose of the drug are risk factors for cholestatic injury. Concerns about the safety of carbimazole in pregnancy were raised in 1985 [Milham (1985): Teratology 32:321]. Since this timemanyreports of children believed to have been affected by carbimazole in utero have appeared in the medical literature. Initial reports were of an increased incidence of scalp defects in the infants of treated mothers, but many other anomalies have now been described. Choanal atresia, gastrointestinal anomaliesparticularly esophageal atresia, athelia/hypothelia, developmental delay, hearing loss, and dysmorphic facial features have all been reported. The phenotype associated with exposure to carbimazole appears to be rare but specific with distinctive facial features. We report on two new cases of carbimazole embryopathy with strikingly similar facial features. Propylthiouracil and methimazole are frequently used in the management of hyperthyroidism. Two patients in whom adverse immunologic effects other than isolated agranulocytosis developed during treatment with propylthiouracil are described. Rash, fever, arthralgias and granulocytopenia were the most common manifestations. Vasculitis, particularly with cutaneous manifestations, occurs and may be fatal. The clinical evidence suggests that an immunologic mechanism is involved. Serum protein electrophoresis showed slight hypergammaglobulinemia (gamma-globulin level 19 [normally 9 to 18] g/L), with elevation of the IgG fraction. CMAJ, VOL. 136, JANUARY 15,1987 Lo Iodio radioattivo può essere somministrato come capsule o in forma liquida (per bocca o per via endovenosa). Per la misurazione del dosaggio e della cinetica dello iodio radioattivo, un suo attento monitoraggio della sua attività in tutto il corpo e sull’attività della tiroide è necessario. Dopo la somministrazione di radioiodio questo lo si ritrova in tutto il corpo, ma dopo ventiquattro ore la maggior parte del radioiodio è intrappolato nella tiroide. La determinazione dell’emivita e dell’uptake di iodio 131 è importante per calcolare la sua dose preterapeutica e l’effettiva emivita che può variare da 1 a 8 giorni mentre l’uptake tiroideo di 131I va da <10% a >80%. Amiodarone, a benzofuranic iodine-rich antiarrhythmic drug, causes thyroid dysfunction in 15–20% of cases. Although amiodarone-induced hypothyroidism poses no particular problem, amiodarone-induced thyrotoxicosis (AIT) is a diagnostic and therapeutic challenge. There are two main forms of AIT: type 1, a form of iodine-induced hyperthyroidism, and type 2, a drug-induced destructive thyroiditis. However, mixed/indefinite forms exist that maybe caused by both pathogenic mechanisms. Type 1 AIT usually occurs in abnormal thyroid glands, whereas type 2 AIT develops in apparently normal thyroid glands (or small goiters). Diagnosis of thyrotoxicosis is easy, based on the finding of increased free thyroid hormone concentrations and suppressed TSH levels. Thyroid radioactive iodine (RAI) uptake values are usually very low/suppressed in type 2 AIT, most commonly low or low-normal, but sometimes normal or increased in type 1 AIT despite the iodine load. Successful Treatment of Amiodarone-Induced Thyrotoxicosis Faizel Osman, MB, MRCP; Jayne A. Franklyn, MD, PhD, FRCP;Michael C. Sheppard, PhD, FRCP; Michael D. Gammage, MD, FRCP +Author Affiliations>From the Division of Medical Sciences, University of Birmingham, Birmingham, UK. Correspondence to Dr M.D. Gammage, Department of Cardiovascular Medicine, Queen Elizabeth Hospital, Birmingham B15 2TH, England UK. Amiodarone treatment results in a large iodine load and affects thyroid status by decreasing peripheral deiodination of thyroxine (T4) to tri-iodothyronine (T3), leading to an increase in serum T4 and decrease in T3.1,2 Serum thyrotropin (TSH) levels increase in the early phase of treatment (1 to 3 months) and typically return to normal thereafter.3 These changes are found in euthyroid subjects. Amiodarone also can induce thyroid dysfunction, with the relative proportion of patients developing thyrotoxicosis or hypothyroidism dependent on dietary iodine content. In iodine-replete areas, such as the United Kingdom and United States, about 3% become thyrotoxic,4 with a higher prevalence in iodinedeficient areas.5Development of thyrotoxicosis in patients taking amiodarone is associated with significant morbidity.6 Withdrawal of amiodarone often is undesirable because it may provoke life-threatening arrhythmias and may worsen cardiovascular manifestations caused by thyrotoxicosis. Even if withdrawal is possible, the half-life of the drug (≈50 days) means that it influences thyroid function for months. This makes amiodarone-induced thyrotoxicosis (AIT) a difficult condition to manage, especially because data on optimal treatment are limited as the result of a lack of controlled trials.