Prednisone in amiodarone-induced thyrotoxicosis.

Wimpfheimer, C; Stäubli, M; Schädelin, J; Studer, H

doi:10.1136/bmj.284.6332.1835-a

Cited by 56 publications

(14 citation statements)

References 3 publications

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“…It is not unusual for AIT to require multiple drugs (consecutively or in combination) treatment before metabolic control is attained (2, 3). Nevertheless, some evidence suggests that type II AIT can more easily be treated by glucocorticoid regimen alone (4,5). With the exception of the isolated small thyroid nodule, our patient fulfilled the diagnostic criteria of type II AIT: reduced or absent 123 I-uptake, no hypoechogenic pattern by ultrasound, negative thyroid antibodies.…”

mentioning

confidence: 80%

Type II amiodarone-induced thyrotoxicosis and concomitant papillary cancer of the thyroid

Cattaneo¹

2000

European Journal of Endocrinology

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confidence: 80%

Type II amiodarone-induced thyrotoxicosis and concomitant papillary cancer of the thyroid

Cattaneo¹

2000

European Journal of Endocrinology

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“…Although some authors have reported successful control of IIT, including AIIT, by thyroidectomy, it should be taken into account that surgery carries high risk in cardiac patients with un controlled thyrotoxicosis. Recently, Wimpfheimer et al [71 ], Léger et al [ 15] and Simon et al [72] reported in small series that the administration of systemic corticosteroids in association with thionamides produced fa vorable effects. These results, however, need to be confirmed in larger series of AIIT patients.…”

Section: Therapy O F Aiitmentioning

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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“…In contrast to AIT, AIH is more frequent in females with a female to male ratio of 1.5:1 [86]. AIH patients are also older than AIT with circulating thyroid autoantibodies seen in almost 53% of AIH patients with underlying thyroid abnormalities especially Hashimoto's thyroiditis [87].…”

Section: Tips and Tricksmentioning

confidence: 99%

Thyroid Ultrasound: State of the Art Part 1 – Thyroid Ultrasound reporting and Diffuse Thyroid Diseases

et al. 2017

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Accurate differentiation of focal thyroid nodules (FTL) and thyroid abnormalities is pivotal for proper diagnostic and therapeutic work-up. In these two part articles, the role of ultrasound techniques in the characterization of FTL and evaluation of diffuse thyroid diseases is described to expand on the recently published World Federation in Ultrasound and Medicine (WFUMB) thyroid elastography guidelines and review how this guideline fits into a complete thyroid ultrasound exam.

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Prednisone in amiodarone-induced thyrotoxicosis.

Abstract: under intensive care observation may be a safe alternative to mechanical ventilation in patients with severe pneumatosis cystoides and chronic respiratory insufficiency.

Cited by 56 publications

References 3 publications

Type II amiodarone-induced thyrotoxicosis and concomitant papillary cancer of the thyroid

Type II amiodarone-induced thyrotoxicosis and concomitant papillary cancer of the thyroid

Amiodarone: A Common Source of Iodine-Induced Thyrotoxicosis

Thyroid Ultrasound: State of the Art Part 1 – Thyroid Ultrasound reporting and Diffuse Thyroid Diseases

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