A 46-yr-old postmenopausal woman with acromegaly and hyperthyroidism had serum levels of TSH which were repeatedly measurable (2.0-3.4 μU/ml) and, therefore, inappropriately elevated. In addition, serum concentrations of the a-subunit were persistently elevated (10.7-18.8 ng/ml). Although there was a reciprocal relationship between serum T4 and TSH levels during treatment with antithyroid drugs, the concentration of a-subunit did not appear to vary with either T4 or TSH. Transsphenoidal surgery documented the presence of a pituitary adenoma but failed to cure either the acromegaly or the hyperthyroidism. While she was hyperthyroid, a-subunit fell to <1 μU/ml after prednisolone, but was unaffected by the administration of T3. α-Subunit was minimally suppressed by prednisolone and was not affected by T3. Secretion of TSH, α-subunit, and GH were unresponsive to TRH stimulation. When the patient became hypothyroid on antithyroid drugs, TRH increased TSH from 22.5 to >40 μU/ml, increased a-subunit from 14.6 to 21.8 ng/ml, and increased GH from 9 to 25 ng/ml. The patient was subsequently treated with both pituitary irradiation and 131I. Eighteen months later, she was euthyroid with serum TSH levels of 1.0 μU/ml, α-subunit levels of 4.3 ng/ml, and GH levels of 9 ng/ml. These data indicate that the patient had a pituitary tumor that secreted GH, TSH, and α-subunit and that there was a discordance between the feedback inhibitory effects of glucocorticoids and T3 on TSH secretion, and suggest that the tumor had an altered receptor for thyroid hormone.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical