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N. Stathatos, R. Gaz, D. S. Ross, G. H. Daniels, High Radioactive Iodine Uptake Despite a Fully Suppressed TSH in a Patient with Thyroid Cancer, The Journal of Clinical Endocrinology & Metabolism, Volume 96, Issue 3, 1 March 2011, Page 589, https://doi.org/10.1210/jc.2010-2053
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A 20-yr-old woman presented with a history of heat intolerance, tremors, and palpitations. A 2-cm left, level III, cervical lymph node was palpated. Thyroid function tests confirmed hyperthyroidism due to Graves' disease: thyroid-stimulating Ig (TSI), 4.7 IU/liter (normal, <1.3 IU/liter); and thyroid-binding inhibiting Ig, 27 IU/liter (normal, <1.37 IU/liter). A fine-needle aspiration of the lymph node revealed papillary thyroid cancer. A total thyroidectomy and a left-sided neck dissection were performed (final pathology: papillary cancer with diffuse hyperplasia consistent with Graves' disease).
Two months after withdrawal of thyroid hormone, the patient's TSH was 0.09 μU/ml, free T4 was 0.6 ng/dl (7.72 pmol/liter; normal = 0.9–1.8 ng/dl), a total T3 was 77 ng/dl (1.18 nmol/liter; normal = 60–181 ng/dl), and serum thyroglobulin was 165 ng/ml. Twenty-four hours after 3 mCi 131I, the overall uptake was 40%, with uptake in the thyroid bed (Fig. 1, arrow 1), mediastinal nodes (arrow 2), and diffusely in her lungs (arrow 3). The ability to take up iodine despite a fully suppressed serum TSH, both in the thyroid bed and in the metastases, is due to the presence of TSIs that stimulate the TSH receptor and increase iodine uptake by the thyrocytes (1). Despite hypothyroidism, her TSH likely remained suppressed due to the prior long-standing hyperthyroidism. Although TSIs may be beneficial by increasing radioiodine uptake, they may stimulate further cancer growth by stimulating the TSH receptor (2). There is no way to inhibit TSI production.
