A 46-year-old woman had signs of
thyrotoxicosis and galactorrhoea. Serum immunoreactive TSH and its alpha-subunit increased in the presence of high serum
triiodothyronine (T3),
thyroxine (T4), and free T4 concentrations, whereas beta-subunit TSH was undetectable. Exogenous TRH failed to increase serum TSH. Serum TSH was markedly suppressed by
glucocorticoid, but was increased by
antithyroid drug.
L-Dopa or
bromocriptine partially suppressed, but
nomifensine had no influence on serum TSH. Serum
prolactin (Prl) was above normal and markedly increased by TRH, but depressed by
bromocriptine and not suppressed by
nomifensine. Plasma TRH was normal in the
hyperthyroid state, but was increased by
glucocorticoid and
antithyroid drug. Excess
thyroid hormone depressed plasma TRH concentrations. Basal serum GH levels were constantly low. Transsphenoidal removal of the tumour normalized serum
hormones (T3, T4 free T4,
TSH, alpha-subunit and Prl), and eradicated the clinical signs of
hyperthyroidism and galactorrhoea. Histological study of the tumour tissue demonstrated both thyrotrophes and somatotrophes. A reciprocal relationship between serum TSH and T4 concentrations shifted to a higher level before but was normalized after removal of the tumour. Ten months later, the clinical signs of
thyrotoxicosis and the increase in serum
thyroid hormone recurred without a concomitant increase in serum TSH and its alpha-subunit. Thyroidal auto-
antibodies were slightly positive, but
thyrotrophin-binding inhibitor
immunoglobulin (TBII) was negative. Administration of
antithyroid drug produced a euthyroid state, but 3 years later, discontinuation of the treatment resulted in recurrent
hyperthyroidism without suppressed plasma TRH and with no evidence of regrowth of the pituitary tumour. It is suggested that the patient initially had
hyperthyroidism owing to excessive TSH secretion from the tumour caused by abnormal TRH secretion, and subsequently had
hyperthyroidism owing to
Graves' disease.