Background: rhTSH, in doses from 0.01 mg to 0.9 mg have been used to augment the effect of radioiodine (¹³¹I) therapy in patients with a benign nontoxic nodular goiter. Transient thyroid enlargement and thyrotoxicosis may be seen following ¹³¹I therapy.

Aim: To investigate whether rhTSH per se causes goiter enlargement, until now an issue evaluated only in healthy nongoitrous subjects.

Methods: In random order, ten patients with nontoxic nodular goiter (mean 39.8 ± 20.5(SD) ml) received either 0.3 mg rhTSH or isotonic saline in a double-blinded cross-over design. Thyroid volume (by ultrasound) and function were closely monitored during the following 28 days.

Results: Saline injection did not affect thyroid function or size. Following rhTSH, median serum TSH increased from baseline 0.97 mU/l (range: 0.39 -1.56) to 37.0 mU/l (range: 18.5 - 55.0) at 24 h, (P < 0.01), with a subsequent decline to subnormal levels at day seven. Mean free T4 and free T3 increased significantly from baseline to a maximum at 48 h. Twenty-four hours after rhTSH the mean goiter volume was significantly increased by 9.8 ± 2.3(SEM)% (P = 0.01), and after 48 h by 24.0 ± 5.1% (P = 0.002). The goiter enlargement had reverted at day seven. Nine patients had symptoms of hyperthyroidism and/or cervical compression following rhTSH, as opposed to one during placebo treatment (P < 0.02).

Conclusion: A transient average goiter enlargement of up to 24% is seen after 0.3 mg rhTSH. This may lead to a significant cervical compression when used for augmentation of ¹³¹I therapy in patients with goiter. The use of lower doses of rhTSH needs to be explored.