Abstract
Patients with the syndrome of resistance to thyroid hormone (RTH) have clinical (tachycardia and anxiety) and biochemical (elevated thyroid hormones level) features of hyperthyroidism. Based on previous reports in pediatric patients with the RTH, antithyroid treatment in these patients is not indicated. Clinical and biochemical sequel of antithyroid therapy in an adult patient with RTH was not previously reported. A 63-year-old African American female with history of RTH was treated with a therapy consisting of methimazole 15 mg daily and atenolol. Methimazole treatment resulted in reduction in thyroid hormone level while the patient’s TSH increased with a peak of 24.88 mIU/L. Having achieved biochemical euthyroidism, the patient developed thyroid gland enlargement associated with progressive symptoms of dysphagia and dyspnea. Examination demonstrated globally enlarged firm thyroid gland with areas of nodularity in both lobes. A computed tomography of the neck showed enlarged thyroid gland with extension around bilateral sternocleidomastoid muscles and compression onto the trachea. Methimazole therapy was discontinued and patient was treated just on atenolol. Over 12 months following discontinuation of methimazole, the patient experienced marked clinical and radiographic improvement of the goiter size associated with TSH reduction to 1.26 mIU/L and modest free thyroxine increase as expected in RTH. It seems appealing to treat patients with the RTH with antithyroid medications. However, in these patients decrease in thyroid hormone levels will stimulate TSH production, which can, in turn, predispose to goiter formation. Our report supports prior observations in children with RTH that treatment with methimazole is not indicated in adult patients with RTH.
Highlights
Resistance to thyroid hormone (RTH) is a rare syndrome characterized by decreased tissue sensitivity to thyroid hormone
It is imperative to understand the pathophysiology of RTH with specific focus on changes in thyroid stimulating hormone (TSH) level when antithyroid therapy is being considered
While peripheral tissues retain their sensitivity to thyroid hormones, higher concentrations of circulating thyroid hormones need to be present to provide a response at the level of the hypothalamus, pituitary, and liver in order to provide negative feedback in TSH release
Summary
Resistance to thyroid hormone (RTH) is a rare syndrome characterized by decreased tissue sensitivity to thyroid hormone. RTH can manifest with symptoms of thyrotoxicosis, including tachycardia or irritability Treatment of these syndromes has relied on the use of β-adrenergic blockers to control hyperadrenergic symptoms or levo-triiodothyronine to provide enough circulating thyroid hormone to reduce goiter size via suppression of TSH.[1]. A 63-year-old African American female with history of RTH presented to our endocrinology clinic in April 2012 for a second opinion on the management of thyroid goiter She complained of increased size of her goiter with symptoms of dysphagia, dyspnea while lying flat, tightness in her throat, and hoarse voice. She initially presented to an outside endocrinology clinic in September of 2005 with symptoms of hyperthyroidism and elevated level of free thyroxine and was started on methimazole 15 mg daily and atenolol 50 mg twice daily. Follow-up laboratory showed a decrease and normalization of TSH associated with expected increase in FT4 of 2.31 mIU/L during the most recent clinical assessment (Figure 1)
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