Endocrine Abstracts

Background: We present a rare case of a 64-year-old patient diagnosed with longstanding untreated Graves’ disease and co-occurrence of metastatic thyroid cancer. Very few cases are reported in literature where the thyrotoxicosis in due to the distant metastasis and optimal treatment remains challenging.

Case Presentation: The patient came to the endocrine unit for thyrotoxicosis treatment. He was diagnosed with Graves’ disease and following treatment initiation and hormone normalization, he underwent total thyroidectomy. The histological evaluation revealed a follicular variant of papillary thyroid cancer with capsular invasion (T3aNxMx). Post-surgery, aberrations in thyroid function parameters persisted, marked by suppressed thyroid-stimulating hormone (TSH), elevated free thyroxine (FT4), positive anti-thyroglobulin antibodies, and remarkably elevated thyroglobulin levels (50, 000 ng/ml). Levothyroxine was initially tapered down and later suspended due to persistent hyperthyroidism. However, two months after suspention TSH remained suppressed (0.01 mUI/ml) and FT4 elevated (22 pg/ml). Iodine-131 therapy (100 mCi) was scheduled it was discussed whether the therapy should be postponed since the TSH target was not met. However, Given the high levels of anti-TSH receptor antibodies (40 UI/ml), the decision to proceed with I131 treatment was made, revealing multiple lung and bone metastases on post-I131 imaging. Two months post-I131, symptomatic hyperthyroidism prompted the initiation of a low dose of methimazole, effectively normalizing thyroid function. At 6 months post-I131, thyroglobulin levels decreased to 19, 753 ng/ml with a TSH of 0.5 mUI/ml showing good biochemical response to therapy. However dispite improving Tg remains very high and close follow-up is fondamental and posing a challenge in determining the optimal approach for pre-I131 treatment, especially in countries were where recombinant TSH is not availability

Discussion: This case underscores the intricate balance required in addressing both cancer and hyperthyroidism. Despite the convention of advocating a lower TSH in metastatic thyroid cancer, the persistence of elevated TSH receptor antibodies suggests continued stimulation of residual thyroid cancer cells.

Conclusion: Given the scarcity of such cases, further exploration through additional cases and an extensive literature review is crucial for refining optimal management strategies.