potassium-perchlorate and Thyrotoxicosis

Amiodarone-induced thyrotoxicosis (AIT) is a common clinical disorder that may be life threatening and whose clinical manifestations and response to treatment may vary among patients.. We present three patients treated with amiodarone for atrial fibrillation who developed AIT at least 36 months after beginning the treatment. Thyrotoxicosis worsened the underlying cardiac disorders and was resistant to treatment based on the combination of dexamethasone 8-12 mg/day i.v., thioamides 45 mg/day p.o., beta blockers and potassium perchlorate at doses of 800 to 1000 mg per day p.o. Two of the patients attained sustained euthyroidism after 12 and 32 days of combined treatment, while the third required total thyroidectomy.. The combination of thioamides with potassium perchlorate is an appropriate form of therapy for AIT in patients resistant to thioamides. The use of this combination should be evaluated in patients with mixed AIT or AIT of unclear etiology.

Topics: Acenocoumarol; Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Algorithms; Amiodarone; Atrial Fibrillation; Cardiovascular Agents; Comorbidity; Dexamethasone; Drug Therapy, Combination; Female; Humans; Male; Middle Aged; Pacemaker, Artificial; Perchlorates; Potassium Compounds; Thioamides; Thyroid Hormones; Thyroidectomy; Thyrotoxicosis; Thyrotropin

Amiodarone (AM), a potent class III anti-arrhythmic drug, is an iodine-rich compound with a structural resemblance to thyroid hormones triiodothyronine (T3) and thyroxine (T4). At the commonly employed doses, AM causes iodine overload up to 50-100 times the optimal daily intake, which may be responsible of a spectrum of effects on thyroid function often counterbalancing its heart benefits. Although most patients on chronic AM treatment remain euthyroid, a consistent proportion may develop thyrotoxicosis (AM-induced thyrotoxicosis, AIT) or hypothyroidism. AIT is more prevalent in iodine-deficient areas and is currently subdivided in two different clinico-pathological forms (AIT I and AIT II). AIT I develops in subjects with underlying thyroid disease, and is caused by an exacerbation by iodine load of thyroid autonomous function; AIT II occurs in patients with no underlying thyroid disease and is probably consequent to a drug-induced destructive thyroiditis. Mixed or indeterminate forms of AIT encompassing several features of both AIT I and AIT II may be also observed. The differential diagnosis between AIT I and AIT II (which is important for the choice of the appropriate therapy) is currently made on radioiodine uptake (RAIU), which may be high, normal or low but detectable in AIT I, while is consistently very low or undetectable in AIT II and on colour-flow Doppler sonography (CFDS) showing normal or increased vascularity in AIT I and absent vascularity in AIT II. Quite recently, studies carried out in our Units at the University of Cagliari (Italy) showed that sestaMIBI thyroid scintigraphy may represent the best single test to differentiate AIT I (showing increased MIBI retention) from AIT II (displaying no significant uptake). Treatment of AIT is dependent from its etiology. AIT usually responds to combined thionamides and potassium perchlorate (KClO4) therapy, AIT II generally responds to glucocorticoids, while indeterminate forms may require both therapeutic approaches. In patients with AIT I definitive treatment of hyperthyroidism by administration of (131)I, initially not feasible for the low RAIU and/or the risk of thyrotoxicosis exacerbation, is advised after normalization of iodine overload. To control severe AIT additional treatment with lithium carbonate, the use of short course of iopanoic acid and plasmapheresis have been also proposed. In cases resistant to medical treatment and/or in patients with severe cardiac diseases who cannot inter

Topics: Amiodarone; Anti-Arrhythmia Agents; Humans; Interleukin-6; Iodine; Iodine Radioisotopes; Iopanoic Acid; Lithium Carbonate; Perchlorates; Plasmapheresis; Potassium Compounds; Technetium Tc 99m Sestamibi; Thyroid Diseases; Thyroidectomy; Thyrotoxicosis; Ultrasonography, Doppler, Color

Amiodarone is an iodine-rich drug. Its chronic administration may lead to disturbances in thyroid hormone metabolism and/or overt gland dysfunction. It causes an increased in serum fT4, rT3, and TSH concentrations and a decreased serum level of fT3 without thyroid dysfunction. Amiodarone may induce thyrotoxicosis (AIT--Amiodarone-induced thyrotoxicosis) or hypothyroidism (AIH--Amiodarone-induced hypothyroidism) in some persons. AIT occurs more frequently in areas with low iodine intake. The excess iodine contributes to excessive thyroid hormone synthesis-type I AIT or may lead to thyroiditis and a destructive process of thyroid follicular cells, resulting in excess thyroid hormone release-type II AIT. The mixed form of AIT also occurs. Type I AIT should be treated with antithyroid drugs alone or in association with potassium perchlorate, type II AIT benefits from treatment with glucocorticoids, whereas the mixed form of AIT is most effectively treated with a combination of thionamides, potassium perchlorate, and glucocorticoids. AIT often requires thyroidectomy after restoration of euthyroidism or radioiodine therapy, provided that 24-h thyroid radioactive iodine uptake values permit. AIH prevails in areas with high dietary iodine intake. It requires a discontinuation of amiodarone therapy and thyroid hormone (levothyroxine) replacement. It can remit spontaneously. Amiodarone and L-thyroxine therapy is also possible. Baseline thyroid function tests, thyroid antibodies, and imaging examinations such as thyroid ultrasound on initial evaluation and follow-ups every 6 months must be carefully monitored before starting amiodarone therapy.

Topics: Amiodarone; Animals; Anti-Arrhythmia Agents; Antithyroid Agents; Female; Glucocorticoids; Humans; Hypothyroidism; Perchlorates; Potassium Compounds; Pregnancy; Thyroid Gland; Thyroid Hormones; Thyroidectomy; Thyroiditis; Thyrotoxicosis

Amiodarone-induced thyrotoxicosis (AIT) is a complex therapeutic challenge. Two major forms have been described: type I and type II. Methimazole (MMI) and potassium perchlorate (KCLO(4)) is the treatment of choice for the former, whereas corticosteroids are used for the latter. However, mixed forms appear frequently and it is not easy to prescribe corticosteroids because of side effects. The present study investigated the validity of a stepwise therapeutic approach to AIT. Twenty patients with AIT were given 30-50 mg/d of MMI and 1000 mg/d of KCLO(4) initially for a month. Euthyroidism or a significant decrease in serum thyroid hormone levels could be achieved in 12 of the patients (7 with type I, 5 type II). Prednisolone, 40-48 mg/d was added for the 8 nonresponding patients (7 type I, 1 type II) and euthyroidism was achieved in all. The prednisolone dose was decreased when free thyroxine (T(4)) levels normalized, and MMI was titrated, maintaining euthyroidism until urinary iodine excretion normalized. Mixed forms of AIT may prevail in iodine-deficient areas. Initial classification of the patients may cause unnecessary corticosteroid use in a substantial number of patients with AIT. A stepwise approach is feasible; however, when the patient is gravely ill, MMI, KCLO(4), and prednisolone could be prescribed simultaneously.

Topics: Amiodarone; Anti-Arrhythmia Agents; Anti-Inflammatory Agents; Antibodies; Antithyroid Agents; Female; Humans; Iodides; Iodine; Male; Methimazole; Middle Aged; Perchlorates; Potassium Compounds; Prednisolone; Prospective Studies; Thyroid Gland; Thyrotoxicosis; Thyroxine; Ultrasonography

Amiodarone can induce severe hyperthyroidism that justifies its withdrawal and the introduction of antithyroid drugs. Continuing amiodarone use, failure to control hyperthyroidism and poor clinical progress may require thyroidectomy. This study aimed to evaluate patients' post-operative development and mid-term outcome after thyroidectomy for amiodarone-associated thyrotoxicosis.. Prospective case series.. Tertiary care centre.. We prospectively collected cases of amiodarone-associated thyrotoxicosis requiring thyroidectomy due to failure of antithyroid treatment, despite amiodarone discontinuation. Post-thyroidectomy complications were compared immediately, 30 days and one year post-operatively, and also for scheduled versus emergency surgery cases.. Of 11 total cases, nine scheduled thyroidectomy cases had no morbidity after elective surgery. Two cases required emergency surgery for multiple organ failure and cardiac problems. Immediate post-operative complications (mostly haemodynamic) occurred in both cases (emergency vs routine surgery, p = 0.018).. In such cases, pre-operative medical treatment is vital to limit peri- and post-operative complications, but surgery should not be delayed if the haemodynamic status deteriorates. Surgery, with careful anaesthesia, is the cornerstone of the treatment.

Topics: Adult; Aged; Aged, 80 and over; Amiodarone; Anti-Arrhythmia Agents; Antithyroid Agents; Arrhythmias, Cardiac; Drug Therapy, Combination; Female; Glucocorticoids; Humans; Male; Methylprednisolone; Middle Aged; Perchlorates; Postoperative Complications; Potassium Compounds; Preoperative Care; Prospective Studies; Severity of Illness Index; Thyroid Hormones; Thyroidectomy; Thyrotoxicosis; Time Factors; Treatment Outcome

TWO TYPES: Hyperthyroidism may develop in around 10% of patients in excess iodine. It may reveal an undetected pretoxic thyroid disease (type I) or have been induced by excess iodine in previously normal thyroid gland or in an euthyroid goiter (type II). IODINE EXCESSE REVEALING THYROTOXICOSIS: In the former situation, symptoms appear shortly after the iodine load, thyroid scintigraphy shows significant uptake and therapy includes discontinuation of iodine excess, antithyroid drugs, potassium perchlorate and, if necessary, thyroidectomy or a therapeutic dose of iodide 131. IODINE-INDUCED THYROTOXICOSIS: In the latter situation (type II) hyperthyroidism may occur several years after the initiation of iodine excess, scintigraphy shows very low or no uptake, spontaneous remission is observed within six months, despite the persistence of iodine excess, and treatment is based on corticosteroids.

Topics: Antithyroid Agents; Follow-Up Studies; Humans; Hyperthyroidism; Iodine; Perchlorates; Potassium Compounds; Risk Factors; Thyroid Diseases; Thyroid Function Tests; Thyroidectomy; Thyrotoxicosis

Topics: Amiodarone; Anti-Arrhythmia Agents; Antithyroid Agents; Glucocorticoids; Humans; Interleukin-6; Iodine; Perchlorates; Potassium Compounds; Thyroid Gland; Thyroid Hormones; Thyrotoxicosis; Ultrasonography, Doppler, Color

Amiodarone-induced thyrotoxicosis (AIT) occurs both in abnormal thyroid glands (nodular goiter, latent Graves' disease) (type I AIT) or in apparently normal thyroid glands (type II AIT). Differentiation of the two forms is crucial, because type I AIT responds well to methimazole and potassium perchlorate combined treatment, whereas type II AIT is effectively managed by glucocorticoids. Differential diagnosis is often difficult, although thyroid radioactive iodine uptake is usually low-to-normal in type I and low-suppressed in type II, and serum interleukin-6 levels are normal/slightly elevated in type I, markedly elevated in type II. Color flow Doppler sonography (CFDS) is a technique that shows intrathyroidal blood flow and provides real-time information on thyroid morphology and hyperfunction. To investigate the usefulness of CFDS in differentiating the two types of AIT, 27 consecutive AIT patients, 11 type I and 16 type II, were evaluated by CFDS before starting antithyroid treatment. Gender, age, severity of thyrotoxicosis, and cumulative amiodarone dose were similar in the two groups. All type II AIT patients had a CFDS pattern 0 (ie, absent vascularity), in agreement with the pathogenesis of the disease, due to thyroid damage. Likewise, nine patients with subacute thyroiditis, another destructive process of the thyroid gland, also had a CFDS pattern 0. Eleven patients with type I AIT had a CFDS pattern ranging from pattern I (presence of parenchymal blood flow with patchy uneven distribution) (7 patients, 64%) to pattern II (ie, mild increase of color flow Doppler signal with patchy distribution) (1 patient, 9%) and pattern III (markedly increased color flow Doppler signal with diffuse homogeneous distribution)(3 patients, 27%), similar to that found in patients with untreated Graves' disease patients, thus indicating a hyper-functioning gland. Control subjects and euthyroid patients under long-term amiodarone treatment had absent thyroid hypervascularity and a CFDS pattern 0. These findings demonstrate that CFDS distinguishes type I and II AIT. Because of its rapidity and noninvasive features, CFDS represents a valuable tool for a quick differentiation between the two types of AIT. This can avoid any delay in initiating the appropriate treatment for a rapid control of thyrotoxicosis in patients whose tachyarrhythmias or other cardiac disorders make thyroid hormone excess extremely deleterious.

Topics: Adult; Aged; Amiodarone; Antithyroid Agents; Diagnosis, Differential; Female; Glucocorticoids; Goiter, Nodular; Graves Disease; Humans; Male; Methimazole; Middle Aged; Perchlorates; Potassium Compounds; Thyrotoxicosis; Ultrasonography, Doppler, Color

Amiodarone-induced thyrotoxicosis (AIT) occurs in both abnormal (type I) and apparently normal (type II) thyroid glands due to iodine-induced excessive thyroid hormone synthesis in patients with nodular goiter or latent Graves' disease (type I) or to a thyroid-destructive process caused by amiodarone or iodine (type II). Twenty-four consecutive AIT patients, 12 type I and 12 type II, were evaluated prospectively. Sex, age, severity of thyrotoxicosis, and cumulative amiodarone dose were similar. Type II patients had higher serum interleukin-6 (IL-6; median, 440 vs. 173 fmol/L; P < 0.001), but lower serum thyroglobulin levels. Several weeks of thionamide therapy in eight type II or prolonged glucocorticoid administration in two type I patients had previously failed to control hyperthyroidism. Type II patients were given prednisone (initial dose, 40 mg/day) for 3 months and achieved normal free T3 and IL-6 after an average of 8 and 6 days, respectively. Exacerbation of thyrotoxicosis with increased serum IL-6 values, observed in 4 patients while tapering steroid, was promptly corrected by increasing it. Type I patients, given methimazole (30 mg/day) and potassium perchlorate (1 g/day), achieved normal free T3 and IL-6 concentrations after an average of 4 weeks. Exacerbation of thyrotoxicosis with markedly increased IL-6 was controlled by prednisone in 3 of 4 cases. Distinction of different forms of AIT is essential for its successful management. Type II AIT should be treated with glucocorticoids; type I AIT should be treated with methimazole and potassium perchlorate. Exacerbation of thyrotoxicosis, which may occur in both forms and is probably related to destructive processes, should be controlled by the addition/increase in glucocorticoids.

Topics: Adult; Aged; Amiodarone; Drug Therapy, Combination; Female; Humans; Interleukin-6; Male; Methimazole; Middle Aged; Perchlorates; Potassium Compounds; Prednisone; Prospective Studies; Thyrotoxicosis; Triiodothyronine

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.

Topics: Adolescent; Amiodarone; Carbimazole; Humans; Male; Middle Aged; Perchlorates; Potassium Compounds; Tachycardia; Thyrotoxicosis

Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with underlying thyroid disease and is generally believed to be due to the iodine contamination of amiodarone and iodine released by the metabolism of the drug. We and others have suggested that the thyrotoxicosis may also be secondary to amiodarone-induced thyroiditis. To further determine the etiology of AIT, we administered large doses of iodides [10 drops saturated solution of potassium iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT believed to be due at least in part to amiodarone-induced thyroiditis. Six of these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI administration, indicating a subtle defect in the thyroidal organification of iodide. During SSKI administration, 6 patients developed marked iodine-induced basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and TRH-stimulated TSH values, and 2 had normal TSH responses compared to SSKI-treated euthyroid subjects with no history of amiodarone ingestion or thyroid disease. Serum T4 and T3 concentrations remained normal and unchanged during SSKI administration in both the AIT patients and control subjects. These results strongly suggest that excess iodine may not be the cause of the hyperthyroidism associated with amiodarone therapy, especially in those patients with probable amiodarone-induced thyroiditis. Furthermore, like patients with a previous history of subacute thyroiditis and postpartum thyroiditis, the present results suggest that some patients with a previous history of AIT may be at risk to develop hypothyroidism when given excess iodine.

Topics: Amiodarone; Female; Humans; Hypothyroidism; Iodine; Iodine Radioisotopes; Middle Aged; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis; Time Factors

Topics: Aged; Amiodarone; Humans; Male; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis

Amiodarone iodine induced thyrotoxicosis occurs frequently in patients residing in areas of mild iodine deficiency and in patients with preexisting goiter. Drug therapy of the hyperthyroidism is often unsuccessful. Twenty-three patients with amiodarone induced thyrotoxicosis were either not treated, treated with 40 mg methimazole daily or with methimazole and 1 gm potassium perchlorate daily for up to 40 days and then with methimazole alone. Thyrotoxicosis was more likely to spontaneously remit in patients without goiter. Therapy with methimazole alone was unsuccessful in inducing euthyroidism in 5 patients with goiter. However, combined therapy with methimazole and potassium perchlorate rapidly alleviated hyperthyroidism in almost all patients with goiter. This drug combination is successful because perchlorate inhibits the active transport of iodine into the thyroid and methimazole blocks the intrathyroidal synthesis of thyroid hormones.

Topics: Adult; Aged; Amiodarone; Drug Synergism; Drug Therapy, Combination; Female; Goiter; Humans; Male; Methimazole; Middle Aged; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis

Topics: Anemia, Aplastic; Antithyroid Agents; Drug Hypersensitivity; Geriatrics; Humans; Hyperthyroidism; Penicillins; Perchlorates; Potassium; Potassium Compounds; Sulfonamides; Thyrotoxicosis; Toxicology

Topics: Antithyroid Agents; Humans; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Disease Management; Humans; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Anemia; Anemia, Aplastic; Humans; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Antithyroid Agents; Exophthalmos; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis; Thyroxine

Topics: Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Anemia, Aplastic; Humans; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Antineoplastic Agents, Hormonal; Antithyroid Agents; Carbimazole; Humans; Hyperthyroidism; Methylthiouracil; Perchlorates; Potassium Compounds; Thiouracil; Thyrotoxicosis

Topics: Hyperthyroidism; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis

Topics: Hyperthyroidism; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis

Topics: Hyperthyroidism; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis

Topics: Antineoplastic Agents, Hormonal; Antithyroid Agents; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Chlorine; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Chlorine; Hyperthyroidism; Perchlorates; Potassium Compounds; Thyrotoxicosis

Topics: Adolescent; Child; Humans; Hyperthyroidism; Infant; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis

Topics: Hyperthyroidism; Perchlorates; Potassium; Potassium Compounds; Reserpine; Thyrotoxicosis

Topics: Hyperthyroidism; Perchlorates; Potassium; Potassium Compounds; Thiouracil; Thyrotoxicosis

Topics: Chlorine; Hyperthyroidism; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis

Topics: Hyperthyroidism; Perchlorates; Potassium; Potassium Compounds; Thyrotoxicosis