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Methimazole-Induced Goitrogenesis in an Adult Patient With the Syndrome of Resistance to Thyroid Hormone.

Glymph K, Gosmanov AR - J Investig Med High Impact Case Rep (2014)

Bottom Line: Having achieved biochemical euthyroidism, the patient developed thyroid gland enlargement associated with progressive symptoms of dysphagia and dyspnea.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.

View Article: PubMed Central - PubMed

Affiliation: University of Tennessee Health Science Center, Memphis, TN, USA.

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.

No MeSH data available.


Related in: MedlinePlus

Time course of TSH and free T4 levels during methimazole therapy and after its discontinuation.
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fig1-2324709614555768: Time course of TSH and free T4 levels during methimazole therapy and after its discontinuation.

Mentions: Given the recent onset of increase in thyroid gland size causing compressive symptoms, we reevaluated her previous laboratory data. On initial evaluation in 2005 and before initiation of methimazole therapy by an outside provider, laboratory studies revealed an elevated TSH of 6.96 (0.35-5.50 mIU/L), free T4 (FT4) of 1.55 (0.61-1.76 ng/dL; Figure 1), and total triiodothyronine (TT3) of 260 (85-205 ng/dL). Thyroid peroxidase antibodies were negative and thyroglobulin level was 129 (2-38 ng/mL) with negative thyroglobulin antibodies. When she was seen in our office in 2012 while continuing to receive methima-zole, her TSH was elevated at 16.57 mIU/L and FT4 was normal at 1.10 mIU/L. We ordered computed tomography (CT) of the neck that revealed a significantly enlarged thyroid with multiple bilateral nodules present with a moderate amount of tracheal compression (Figure 2A).


Methimazole-Induced Goitrogenesis in an Adult Patient With the Syndrome of Resistance to Thyroid Hormone.

Glymph K, Gosmanov AR - J Investig Med High Impact Case Rep (2014)

Time course of TSH and free T4 levels during methimazole therapy and after its discontinuation.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License 1 - License 2 - License 3
Show All Figures
getmorefigures.php?uid=PMC4528878&req=5

fig1-2324709614555768: Time course of TSH and free T4 levels during methimazole therapy and after its discontinuation.
Mentions: Given the recent onset of increase in thyroid gland size causing compressive symptoms, we reevaluated her previous laboratory data. On initial evaluation in 2005 and before initiation of methimazole therapy by an outside provider, laboratory studies revealed an elevated TSH of 6.96 (0.35-5.50 mIU/L), free T4 (FT4) of 1.55 (0.61-1.76 ng/dL; Figure 1), and total triiodothyronine (TT3) of 260 (85-205 ng/dL). Thyroid peroxidase antibodies were negative and thyroglobulin level was 129 (2-38 ng/mL) with negative thyroglobulin antibodies. When she was seen in our office in 2012 while continuing to receive methima-zole, her TSH was elevated at 16.57 mIU/L and FT4 was normal at 1.10 mIU/L. We ordered computed tomography (CT) of the neck that revealed a significantly enlarged thyroid with multiple bilateral nodules present with a moderate amount of tracheal compression (Figure 2A).

Bottom Line: Having achieved biochemical euthyroidism, the patient developed thyroid gland enlargement associated with progressive symptoms of dysphagia and dyspnea.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.

View Article: PubMed Central - PubMed

Affiliation: University of Tennessee Health Science Center, Memphis, TN, USA.

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.

No MeSH data available.


Related in: MedlinePlus