Successful treatment of hyperthyroidism due to nonneoplastic pituitary TSH hypersecretion with 3,5,3′-triiodothyroacetic acid (TRIAC)

The effects of 3,5,3′-triiodothyroacetic acid (TRIAC) or bromocriptine oral administration on serum TSH and thyroid hormone concentrations were studied in a 47 yr old woman affected with hyperthyroidism due to nonneoplastic pituitary hypersecretion of TSH. The diagnosis was made on the basis of elevated thyroid hormone levels (total T4 and T3:170–198 and 2.9–3.5 nmol/l;free T4 and T3:20.7–25.5 and 12.5–14.5 pmol/l, respectively) and inappropriately high serum TSH (9.7–15.6 μU/ml) in the absence of radiological evidence of pituitary tumor. Typical alterations of several parameters of peripheral thyroid hormone action [BMR: + 25%, pulse wave arrival time: 130 msec, pre-ejection period/left ventricular ejection time (PEP/LVET): 0.26] were indicative of hyperthyroidism. Abnormal thyroid stimulators, as well as substances known to interfere in RIA determination were absent. TSH secretion was suppressed by T3 (-90%), dopamine (-52%), bromocriptine (-44%), somatostatin (-45%) and dexamethasone (-36%) administration, and stimulated by TRH (+ 438%), domperidone (+ 123%) and methimazole (+426%). As these findings were suggestive of intact regulatory mechanisms for TSH secretion operating at a higher set point, therapeutical trials with either TRIAC or bromocriptine were carried out owing to the ability of these compounds to suppress TSH secretion. No significant variations in serum TSH, total and free thyroid hormone concentrations were observed after 2 months of bromocriptine treatment (10 mg/day). On the contrary, during TRIAC administration (3 mg/day for 3 weeks) serum TSH, total and free thyroid hormone concentrations fell to within the euthyroid range (TSH: 4.8 μU/ml; total T4 and T3:142 and 2.5 nmol/l; free T4 and T3:14.2 and 7.8 pmol/l, respectively) and all the parameters of peripheral thyroid hormone action reverted to normal (BMR: + 5%, pulse wave arrival time: 198 msec, PEP/LVET: 0.34), without any appreciable untoward effect. Lower TRIAC dose (1 mg/day was ineffective and its withdrawal was followed by a rapid elevation of serum TSH and thyroid hormone levels and reappearance of hyperthyroidism. Long term treatment with 2.1 mg/day caused the remission of clinical hyperthyroidism, though serum TSH levels still remained little above the normal range (5.2–7.1 μU/ml). It is concluded that the nonneoplastic pituitary TSH hypersecretion can be successfully treated with TRIAC.