Amiodarone-treated patients with suppressed TSH test are at risk of thyrotoxicosis

Stäubli, M; Studer, H

doi:10.1007/bf01732171

Cited by 17 publications

(4 citation statements)

References 29 publications

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“…Whether such decreased serum levels of TSH or a suppressed response of TSH to TRH test [25] may predict the development of clinically overt AIT remains to be elucidated in a prospective study in a greater number of patients.…”

Section: Discussionmentioning

confidence: 99%

Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan.

et al. 1999

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Abstract.Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing.We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6 years. AIT and AAH developed after 39±21 and 20± 16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole.Their thyrotoxicosis persisted for 3 to 9 months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months.Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment.In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high (< 12 yg/dl), accompanied by suppressed TSH (< 0.1 yU/ml) and high thyroglobulin levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical thyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies revealed no nodular lesion in the thyroid, and color flow Doppler sonography demonstrated no hypervascularity in the thyroid gland in any AIT patient. Although it is postulated in Europe that there are two types of AIT, namely type I, which develops in patients with latent Graves' disease or toxic multinodular goiter, and type II, which develops in an apparently normal thyroid as destructive thyroiditis, all AIT patients we have seen so far had developed destructive type AIT. Sufficient intake of iodide and a very low incidence of toxic multinodular goiter may account for the rare incidence of type I AIT in our country. Mild to moderate AIT resolved spontaneously without discontinuing amiodarone, but it was discontinued in two of 13 AIT patients because of extrathyroidal adverse reactions.

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Section: Discussionmentioning

confidence: 99%

Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan.

et al. 1999

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“…Trip et al (44) observed that the average length of amiodarone treatment before the occurrence of AIT was about 3 yr, with a probability of 0.025 after 18 months and 0.335 after 48 months. There are no parameters allowing predictability of AIT (44), although it has been suggested that the baseline lack of a TSH response to TRH may represent a risk factor for the subsequent occurrence of AIT (70). Mariotti et al (66) reported the occurrence of AIT after 21-47 months of amiodarone therapy.…”

Section: April 2001mentioning

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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“…TSH binding-inhibiting autoanti bodies (TBIAb) were measured by radioreceptor as say using a commercial kit (TBIAb Kit, Byk Mallinckrodt, Milan, Italy). Thyroid stimulating autoanti bodies (TSAb) were assayed by adenylate cyclase stimulation in human thyroid plasma membranes [57]. Urinary iodine excretion was measured by the modified method of Zac and the results were ex pressed as microgram iodine per gram creatinine.…”

Section: Methodsmentioning

confidence: 99%

“…However, either suppressed basal TSH values or absent TSH response to TRH were often found also in euthyroid subjects chronically treated with amiodarone [35]. This finding was interpreted as a prognostic index for the possible evolution toward thy rotoxicosis [57]. Radioiodine Uptake Twenty-four-hour RAIU was available in 43 AIIT patients.…”

Section: Serum Thyroid Hormone Concentrationsmentioning

confidence: 99%

Amiodarone: A Common Source of Iodine-Induced Thyrotoxicosis

Martino¹,

Aghini-Lombardi²,

Mariotti³

et al. 1987

Horm Res

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Amiodarone, a iodine-rich drug widely used in the treatment of tachyarrythmias, represents one of the most common sources of iodine-induced thyrotoxicosis. The data concerning 58 patients with amiodarone-iodine-induced thyrotoxicosis (AIIT) were analyzed in the present study. Prevalence of AIIT was higher in males than in females (M/F = 1.23/1). Thyrotoxicosis occurred either during treatment with or at various intervals after withdrawal of amiodarone. AIIT developed not only in patients with underlying thyroid disorders, but also in subjects with apparently normal thyroid gland. Classical symptoms of thyrotoxicosis were often lacking, the main clinical feature being a worsening of cardiac disorders. Biochemical diagnosis of AIIT was established by the finding of elevated serum total and free triiodothyronine levels, since elevated serum total and free thyroxine could be found also in euthyroid amiodarone-treated subjects. Twenty-four-hour thyroid radioiodine uptake was very low or undetectable in AIIT patients with apparently normal thyroid glands, while it was inappropriately elevated in patients with underlying thyroid disorders, despite iodine contamination. The role of autoimmune phenomena in the pathogenesis of AIIT appeared to be limited, because circulating thyroid autoantibodies were undetectable in AIIT patients without underlying thyroid disorders or with nodular goiter. Conversely, humoral features of thyroid autoimmunity were mostly found in AIIT patients with diffuse goiter. Treatment of AIIT appeared to be a difficult challenge. Among the 11 patients given no treatment, thyrotoxicosis spontaneously subsided in the 5 patients with apparently normal thyroid gland, whereas the 6 patients with nodular or diffuse goiter were still hyperthyroid 6–9 months after discontinuation of the drug. The administration of high doses (40 mg/day) of methimazole alone proved to be ineffective in most (14/16) patients given this treatment. Twenty-seven patients were treated by methimazole combined with potassium perchlorate (1 g/day). With one exception, euthyroidism was restored within 15–90 days in all cases with underlying thyroid abnormalities, and within 6–55 days in subjects with apparently normal thyroid gland. Thus, the combined treatment appears to be the most effective one, but, due to the potential toxicity of potassium perchlorate, it should be reserved to patients with severe thyrotoxicosis and should be carefully monitored.

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Amiodarone-treated patients with suppressed TSH test are at risk of thyrotoxicosis

Cited by 17 publications

References 29 publications

Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan.

Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan.

The Effects of Amiodarone on the Thyroid*

Amiodarone: A Common Source of Iodine-Induced Thyrotoxicosis

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