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Endocrine Abstracts (2021) 73 EP160 | DOI: 10.1530/endoabs.73.EP160

ECE2021 Eposter Presentations Pituitary and Neuroendocrinology (32 abstracts)

A pituitary TSH and GH co-secreting adenoma presenting with thyrotoxicosis, but no symptoms of acromegaly: a case report

Rea Nagy 1 , Anna Vágvölgyi 1 , Nikolette Szucs 2 , Balint Scheich 3 , Gergely Nyari 4 , Tibor Hortobagyi 4 , Pal Barzo 5 & Zsuzsanna Valkusz 1


1University of Szeged Faculty of Medicine, Department of Internal Medicine, Szeged, Hungary; 2Semmelweis University Faculty of Medicine, Department of Internal Medicine and Oncology, Budapest, Hungary; 3Semmelweis University Faculty of Medicine, I. Department of Pathology, Budapest, Hungary; 4University of Szeged Faculty of Medicine, Department of Pathology, Szeged, Hungary; 5University of Szeged Faculty of Medicine, Department of Neurosurgery, Szeged, Hungary


TSH producing pituitary adenomas are a rare cause of thyrotoxicosis. These tumors account for only 1–2% of the pituitary adenomas. Co-secretion occurs in 30% of thyrotropinomas and requires careful investigation and subsequent follow up.

A 43-year-old male presented with hand tremor and tachycardia. He was found to have elevated TSH, free T4 (FT4) and free T3 (FT3), but did not get treatment for years. In 2019 he developed atrial fibrillation. TSH was 7.65 mIU/l (0.55–4.78 mIU/l), FT4 was 28.5 pmol/l (11.5–22.7 pmol/l), FT3 was 13.69 pmol/l (3.5–6.5 pmol/l). In early 2020 he underwent an MRI of the brain, which showed a 25×18×18 mm pituitary macroadenoma. Basal growth hormone (GH) level was 0.99 ng/ml, and during an oral glucose tolerance test it remained 0.48 ng/ml at 60 min and decreased below 0.4 ng/ml at the other time points. In May 2020 he had transsphenoidal surgery. Histology showed plurihormonal hypophysis adenoma with extensive GH and focal prolactin (PRL) and TSH expression with immunohistochemistry, consistent with type 3 plurihormonal adenoma. Following the surgery he continued to have elevated TSH and FT3 levels and required beta-blocker therapy for symptom control. Thiamazole therapy was also attempted, but the patient did not tolerate it. Somatostatin analog therapy was also considered, but was not started. He continued to have heat intolerance, palpitations, anxiety and generalized weakness. On the 4-month postoperative sella MRI there was no significant change in the size of the pituitary tumor (25×16×15 mm). His TSH, FT4 and FT3 level increased to 9.4 mIU/l (0.27–4.2 mIU/l), 33.0 pmol/l (12.0–22.0 pmol/l) and 14.7 pmol/l (3.1–6.8 pmol/l) respectively. Basal GH level was 0.48 ng/ml, and during an oral glucose tolerance test it decreased below 0.4 ng/ml at all time points. In December 2020 he had a reoperation of the persistent tumor. Histology revealed GH immunohistochemistry positive hypophysis adenoma, but TSH positivity could not be verified. 6 days after surgery his TSH decreased to 0.03 mIU/l, FT3 to 3.0 pmol/l and FT4 to 18.6 pmol/l. One month after the surgery his TSH level was 0.81 mIU/l, FT3 was 2.6 pmol/l and FT4 was 6.3 pmol/l, therefore he was started on thyroid hormone supplementation. No other pituitary hormonal derangements were observed. First-line treatment of thyroptopinomas is pituitary adenomectomy followed by irradiation in the case of surgical failure. Our case highlights the importance of attempting definitive cure by removal of the tumor to avoid long-term effects of pituitary irradiation.

Volume 73

European Congress of Endocrinology 2021

Online
22 May 2021 - 26 May 2021

European Society of Endocrinology 

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