Endocrine Abstracts

A 51-year-old asymptomatic man presented in 1998 with elevated thyroid stimulating hormone (TSH) 6.34 mIU/l (0.34–5.6 mIU/l), FT₄ 54.1 pmol/l (7.5–21.1 pmol/l), FT₃ 20.1 pmol/l (3.0–5.0 pmol/l) and TSH-α subunits 3.6 mcg/l (<2.0 mcg/l). After the first visit, he was lost to follow-up.

He presented 10 years later in 2008 with 1-week history of symptoms of heart failure and hyperthyroidism. Clinically he was thyrotoxic with no goitre, in fast atrial fibrillation and biventricular failure. Visual fields were normal. Chest radiograph showed pulmonary oedema and echocardiogram, moderate left ventricular systolic dysfunction (ejection fraction 49%). His TSH was 8.2 mIU/l, FT₄ 48.3 pmol/l, FT₃ 14.42 pmol/l and TSH-α subunits 4 mcg/l. MRI revealed a 16x14mm left sided pituitary tumour. The provisional diagnosis was high output cardiac failure secondary to thyrotoxicosis from a thyrotropin-secreting pituitary tumour (TSH-oma).

His peak cortisol and GH were 615 nmol/l and 47.1 mU/l following glucagon stimulation. His IGF1 was 13 nmol/l (11.3–30.9) and prolactin 81 mIU/l (60–278). Interestingly, he had raised gonadotrophins: FSH 6.0 IU/L (1.27–19.26) and LH 9.47 IU/l (1.2–8.6). Testosterone was 40.6 nmol/l (6.1–27.2) and SHBG 145 nmol/l (13–71), which was in keeping with the effect of excess thyroxine on SHBG. Unfortunately, he failed to attend his glucose tolerance test for GH levels although notably he had normal IGF1.

He continued to have poor attendance but underwent transspenoidal surgery in March 2009. Surprisingly, histology revealed a pituitary adenoma with immunohistochemistry positive for GH only. Post-operatively, thyroid status improved: TSH 4.7 mIU/l, FT₄ 24.2 pmol/l and FT₃ 3.4 pmol/l. Repeat glucagon stimulation showed adequate cortisol (545 nmol/l) and GH (11.9 mcg/l) responses. Repeat MRI showed a small residual pituitary adenoma.

This case illustrates indolent clinical progression of a TSH-oma over a 10 years interval. We can also assume from the size of the adenoma on MRI scan that it was slow-growing. Although this was clinically and biochemically a TSH-oma, immunohistochemistry stained for GH alone.