Effect of amiodarone on circulating antithyroid antibodies.

Safran, Marjorie; Martino, Enio; Aghini-Lombardi, F.; Bartalena, Luigi; Balzano, S.; Pinchera, Aldo; Braverman, Lewis E.

doi:10.1136/bmj.297.6646.456

Cited by 28 publications

(9 citation statements)

References 3 publications

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“…Although some studies have described induction of thyroid auto‐antibodies following short‐term amiodarone administration, others have failed to confirm this finding. 3,16 Modulation of lymphocyte activity and induction of a cell‐mediated autoimmune response is also a possible mechanism for the pathogenesis of type II AAT. 17…”

Section: Discussionmentioning

confidence: 99%

Refractory Amiodarone‐associated Thyrotoxicosis: An Indication for Thyroidectomy

Claxton

Sinha

Donovan

et al. 2000

Aust. N.Z. J. Surg.

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Section: Discussionmentioning

confidence: 99%

Refractory Amiodarone‐associated Thyrotoxicosis: An Indication for Thyroidectomy

Claxton

Sinha

Donovan

et al. 2000

Aust. N.Z. J. Surg.

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“…This phenomenon was attributed to early and transient toxic effects of amiodarone on the thyroid, leading to release of thyroid autoantigens and subsequent triggering of thyroid autoimmune reactions (39). Safran et al (40) failed to find an increased incidence of antithyroid autoantibodies in 47 patients submitted to both short-term and long-term amiodarone treatment in geographical areas of different ambient iodine intake. Safran et al (40) failed to find an increased incidence of antithyroid autoantibodies in 47 patients submitted to both short-term and long-term amiodarone treatment in geographical areas of different ambient iodine intake.…”

Section: Effect On Thyroid Autoimmunitymentioning

confidence: 99%

The Effects of Amiodarone on the Thyroid*

et al. 2001

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Amiodarone is a benzofuranic-derivative iodine-rich drug widely used for the treatment of tachyarrhythmias and, to a lesser extent, of ischemic heart disease. It often causes changes in thyroid function tests (typically an increase in serum T(4) and rT(3), and a decrease in serum T(3), concentrations), mainly related to the inhibition of 5'-deiodinase activity, resulting in a decrease in the generation of T(3) from T(4) and a decrease in the clearance of rT(3). 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. Preexisting Hashimoto's thyroiditis is a definite risk factor for the occurrence of AIH. The pathogenesis of iodine-induced AIH is related to a failure to escape from the acute Wolff-Chaikoff effect due to defects in thyroid hormonogenesis, and, in patients with positive thyroid autoantibody tests, to concomitant Hashimoto's thyroiditis. 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), but mixed forms frequently exist. Treatment of AIH consists of L-T(4) replacement while continuing amiodarone therapy; alternatively, if feasible, amiodarone can be discontinued, especially in the absence of thyroid abnormalities, and the natural course toward euthyroidism can be accelerated by a short course of potassium perchlorate treatment. In type I AIT the main medical treatment consists of the simultaneous administration of thionamides and potassium perchlorate, while in type II AIT, glucocorticoids are the most useful therapeutic option. Mixed forms are best treated with a combination of thionamides, potassium perchlorate, and glucocorticoids. Radioiodine therapy is usually not feasible due to the low thyroidal radioiodine uptake, while thyroidectomy can be performed in cases resistant to medical therapy, with a slightly increased surgical risk.

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“…Predisposing factors include micronodular and macronodular goiter, which are common in older patients who most often require amiodarone. Thyroid autoimmunity has also been incriminated as a predisposing factor and antithyroid antibodies have been found following amiodarone administration in some patients (63) but not in others (64). Amiodarone may also induce destructive thyroiditis resulting in thyrotoxicosis as suggested by clinical, histologic, and in vitro studies (64)(65)(66).…”

Section: Amiodarone-induced Thyroid Diseasementioning

confidence: 99%

Iodine Excess and Hyperthyroidism

Roti¹,

Uberti²

2001

Thyroid

241

132

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150 microg iodine are daily required for thyroid hormone synthesis. The thyroid gland has intrinsic mechanisms that maintain normal thyroid function even in the presence of iodine excess. Large quantities of iodide are present in drugs, antiseptics, contrast media and food preservatives. Iodine induced hyperthyroidism is frequently observed in patients affected by euthyroid iodine deficient goiter when suddenly exposed to excess iodine. Possibly the presence of autonomous thyroid function permits the synthesis and release of excess quantities of thyroid hormones. The presence of thyroid autoimmunity in patients residing in iodine-insufficient areas who develop iodine-induced hyperthyroidism has not been unanimously observed. In iodine-sufficient areas, iodine-induced hyperthyroidism has been reported in euthyroid patients with previous thyroid diseases. Euthyroid patients previously treated with antithyroid drugs for Graves' disease are prone to develop iodine-induced hyperthyroidism. As well, excess iodine in hyperthyroid Graves' disease patients may reduce the effectiveness of the antithyroid drugs. Occasionally iodine-induced hyperthyroidism has been observed in euthyroid patients with a previous episode of post-partum thyroiditis, amiodarone destructive or type II thyrotoxicosis and recombinant interferon-alpha induced destructive thyrotoxicosis. Amiodarone administration may induce thyrotoxicosis. Two mechanisms are responsible for this condition. One is related to excess iodine released from the drug, approximately 9 mg of iodine following a daily dose of 300 mg amiodarone. This condition is an iodine-induced thyrotoxicosis or type I amiodarone-induced thyrotoxicosis. The other mechanism is due to the amiodarone molecule that induces a destruction of the thyroid follicles with a release of preformed hormones. This condition is called amiodarone-induced destructive thyrotoxicosis or type II thyrotoxicosis. Patients developing type I thyrotoxicosis in general have preexisting nodular goiter whereas those developing type II thyrotoxicosis have a normal thyroid gland. The latter group of patients, after recovering from the destructive process, may develop permanent hypothyroidism as the consequence of fibrosis of the gland.

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Effect of amiodarone on circulating antithyroid antibodies.

Cited by 28 publications

References 3 publications

Refractory Amiodarone‐associated Thyrotoxicosis: An Indication for Thyroidectomy

Refractory Amiodarone‐associated Thyrotoxicosis: An Indication for Thyroidectomy

The Effects of Amiodarone on the Thyroid*

Iodine Excess and Hyperthyroidism

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