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Abstract Disclosure: V.A. Mendpara: None. P.P. Rao: None. M.D. Lundholm: None. Background: Thyroid-stimulating hormone-secreting pituitary adenoma (TSH-oma) is a rare cause of hyperthyroidism, forming 0.5-3% of all functioning pituitary tumors and 1% of hyperthyroid cases. Here, TSH secretion is autonomous and unresponsive to the normal negative feedback of thyroid hormones, leading to inappropriate TSH, T4 and T3 elevation. In the absence of clinical symptoms it can be difficult to distinguish between thyroid hormone resistance (THR) and lab errors. Clinical Case: A 44-year-old Swahili-speaking female with a history of type 2 diabetes was admitted for hypoglycemia requiring insulin adjustment. In her workup, thyroid function tests were obtained, revealing normal or low TSH (0.28 mIU/L) and high free T4 levels (2.7 ng/dL). At outpatient follow-up, repeat labs showed elevated TSH, T3 and FT4 (5.22 mIU/L, 377 ng/dL and 4.7 ng/dL, respectively). She reported weight loss, occasional palpitations, and chronic insomnia but denied other symptoms. Graves' antibodies (TSI, TSHR Ab) were negative. On exam, she had a 30-40 gm, smooth, non-tender thyroid without adenopathy, and a BMI of 23 kg/m2. The initial differential diagnosis included TFT lab error, THR or TSH-oma. A FT4 by equilibrium dialysis was high at 7.8 ng/dL (1.1-2.4 ng/dL). N-telopeptide (NTX) and sex hormone-binding globulin (SHBG) were elevated, consistent with a true hyperthyroid state. Genetic testing for THR posed time and cost barriers. Elevated alpha-subunit levels (87 ng/mL, normal ≤1.8 ng/mL) with normal levels of other pituitary hormones prompted a pituitary MRI, unveiling a 4.7 cm suprasellar bilobed pituitary mass abutting the optic chiasm and invading the cavernous and sphenoidal sinuses. She denied peripheral vision loss or headaches. Hyperthyroidism was managed with methimazole until surgical intervention for the TSH-oma. A transsphenoidal resection was performed with histopathological confirmation of a TSH-staining pituitary adenoma. She was started on levothyroxine for central hypothyroidism thereafter. Discussion: It is challenging to find the cause of abnormal TFTs when patients are asymptomatic and the differential includes THR, lab errors or TSH-oma. Inaccurate diagnosis can lead to delays in care or unnecessary thyroid ablation or pituitary surgery. Conversely, early identification and appropriate treatment of TSH-omas can prevent neurological and endocrinological complications, such as optic chiasm compression, visual disturbances, headache and hypopituitarism. Despite a lack of convincing symptoms of hyperthyroidism, we used confirmatory labs (NTX, SHBG) to rule in biochemical hyperthyroidism along with alpha-subunit testing and pituitary MRI to solidify the TSH-oma diagnosis, leading to surgical intervention. This case highlights the vital steps in the diagnosis of a TSH-oma, emphasizing the need for logical evaluation and differentiation of this rare condition. Presentation: 6/1/2024
Mendpara et al. (Tue,) studied this question.