A rare case of thyrotropinoma inappropriately treated as Graves

Sahar Alwakil; Ahmed Haroun; Dina Farouk; Christina Samir; Randa Salam

doi:10.1530/endoabs.110.EP1535

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Endocrine Abstracts (2025) 110 EP1535 | DOI: 10.1530/endoabs.110.EP1535

ECEESPE2025 ePoster Presentations Thyroid (198 abstracts)

A rare case of thyrotropinoma inappropriately treated as Graves’ disease

Sahar Alwakil ¹ , Ahmed Haroun ² , Dina Farouk ³ , Christina Samir ⁴ & Randa Salam ¹

Author affiliations

¹Professor of Internal Medicine, Endocrinology and Diabetes Cairo University, Cairo, Egypt; ²Assistant Professor of Internal Medicine, Endocrinology and Diabetes Cairo University, Cairo, Egypt; ³Lecturer of Internal Medicine, Endocrinology and Diabetes Cairo University, Internal Medicine Department, Cairo, Egypt; ⁴Assistant Lecturer of Internal Medicine, Endocrinology and Diabetes Cairo University, Cairo, Egypt

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Introduction: Thyrotropinoma, TSHoma, TSH secreting pituitary tumor, is considered a very rare cause of hyperthyroidism. They account for less than 1 % of all pituitary adenomas. Almost all TSHomas express a variable number of somatostatin receptors.

Case report: A 44 year old male patient presented to Endocrinology unit for consultation about total thyroidectomy. The patient presented three years ago with goiter, palpitations, heat intolerance, irritability and tremors. Despite his initial thyroid profile showed elevated TSH, Free T3 and free T4, he was falsely considered Graves’ disease kept on carbimazole 30 mg/day for 3 years. Patient’s symptoms were not controlled, and he developed atrial flutter. Total thyroidectomy was considered so he was referred to surgery department who consulted us about the decision of total thyroidectomy.

Examination: BP: 120/70 mmHg, irregular pulse at rate of 90/mint Diffuse goiter, not tender, no palpable thrill, with no thyroid orbitopathy. Cardiac examination: accentuated heart sounds and mitral regurge. Complete blood picture, liver, kidney function, blood glucose, and lipid profile were normal. TSH 43 U/ml (0.5 - 4.8), Free T3: 12.7 pg/ml (2.3 - 4.2), Free T4: 3.5 ng/dl (0.8 – 1.7). ACTH 9 am: 42pg/ml (up to 65), serum Cortisol 9 am: 5.9 mg/dl (4- 22), serum prolactin: 5.5 ng/ml (2 -17.7 ), FSH: 4.36 mIU/ml (1.4 – 18), LH: 6.2 mIU/ml (1.5 -9.3). TSH receptor antibodies 0.9 IU/l (0-1.75) excluding coexisting primary thyrotoxicosis. Thyroid ultrasound showed enlarged heterogeneous thyroid gland, (4.2x3.5 cm) with increased vascularity. Dynamic MRI Sella with gadolinium showed a 7 mm right sided pituitary microadenoma. To confirm that the pituitary microadenoma is functioning, and as somatostatin scintigraphy was not available, a dynamic test using long-acting somatostatin analogue injection (somatostatin LAR) was done, thyroid profile was measured 28 days after with marked reduction of the thyroid hormones; TSH 27 U/ml (0.5 - 4.8 ), Free T3: 3.02 pg/ml (2.3 - 4.2 ), Free T4: 0.58 ng/dl (0.8 – 1.7), with improvement of the symptoms and reduction of the thyroid gland size. This step is considered a bridging therapy until transsphenoidal surgery is performed.

Conclusion: Thyrotropinoma is a very rare cause of secondary thyrotoxicosis and is frequently misdiagnosed as Graves’ disease. Definite diagnosis depends on positive pituitary imaging and dynamic tests to differentiate TSHoma from other causes of central hyperthyroidism. Early diagnosis is important to prevent inappropriate management.