Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2018) 56 GP117 | DOI: 10.1530/endoabs.56.GP117

ECE2018 Guided Posters Endocrine Case Reports (10 abstracts)

A rare case report of Graves disease with coexisting TSH producing pituitary adenoma

Rujuta Katkar , Thinzar Lin & Antoine Makdissi


University at Buffalo, Buffalo, New York, USA.


Background: Only 10 cases of Grave’s disease coexistencing with a TSH-secreting pituitary adenoma (TSHoma) have been reported to date. We present a patient with a TSHoma identified based on the biochemical pattern developing while on treatment with anti-thyroid medications initiated after establishing the diagnosis Grave’s disease.

Case report: A 44-year-old Caucasian lady presented with unintentional weight loss. Physical examination revealed diffuse goiter without bruit. TSH was 0.158 (0.4–4.5, free T4 (FT4) 3.5 mg/dl (0.8–1.8) with TSI antibodies elevated 345%. I123 thyroid uptake and scan showed a diffuse uptake of 84% at 24 h. While on treatment with Methimazole(MMI), thyroid function tests (TFTs) normalized initially, however, a pattern of elevated FT4 with inappropriately normal TSH was noted. Assay interference and thyroid hormone resistance were ruled out by negative HAMA antibodies and negative RTH mutation analysis. Alpha subunit was1.2 ng/ml (normal <1.02) with elevated α-TSH/TSH molar ratio at 5 (normal range <1). MRI revealed a 1.7×1.4×1.6 cm pituitary macroadenoma. Transsphenoidal resection of the pituitary adenoma was done. TFTs normalized postoperatively without medications. However, four months after surgery, FT4 was found to be elevated at 6.5 with suppressed TSH <0.005. Patient was treated again with MMI with successful achievement of biochemical and clinical euthyroid state. Discussion: Hyperthyroidism caused by excess TSH is uncommon. TSH- secreting pituitary adenoma accounts for less than 2% of pituitary adenomas. The association of TSHoma with Graves’ disease is exceedingly rare\. It is recommended that surgery as primary therapy for TSHoma but there is no established management guideline for coexisting condition of Grave’s disease and TSHoma at this time. In our case, it is possible that the coexistance of the two conditions is incidental. However, the interruption of normal negative feedback mechanism caused by antithyroid medications leading to the progression of preexisting TSHoma has been postulated. Similarly, it has been postulated that a rapid decrease TSH level after pituitary tumor removal may induce autoimmune activation against the thyroid gland

Conclusion: We emphasize the importance of re-evaluation of the primary diagnosis and consideration of coexisting diagnoses including rare entities if there is any deviation of clinical and laboratory findings from the primary diagnosis.

Volume 56

20th European Congress of Endocrinology

Barcelona, Spain
19 May 2018 - 22 May 2018

European Society of Endocrinology 

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