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Administration of a Single Low Dose of Recombinant Human Thyrotropin Significantly Enhances Thyroid Radioiodide Uptake in Nontoxic Nodular Goiter¹

Departments of Nuclear Medicine (D.A.H., J.W.B.), Internal Medicine (B.B.), and Clinical Chemistry (A.P.S.), Catharina Hospital, 5602 ZA Eindhoven; Department of Internal Medicine, St. Joseph Hospital (R.J.E.), 5500 MB Veldhoven; and Department of Endocrinology, University Hospital (W.A.N., A.R.H.), 6500 HB Nijmegen, The Netherlands

Address all correspondence and requests for reprints to: Dr. D. Huysmans, Department of Nuclear Medicine, Catharina Hospital, P.O. Box 1350, 5602 ZA Eindhoven, The Netherlands. E-mail: hermus.huysmans{at}freeler.nl

Radioiodine (¹³¹I) is increasingly used as treatment for volume reduction of nontoxic, nodular goiter. A high dose of ¹³¹I is often needed because of low thyroid radioiodide uptake (RAIU). We investigated whether pretreatment with a single, low dose of recombinant human TSH (rhTSH; Thyrogen, Genzyme Transgenics Corp.) enhances RAIU in 15 patients with nontoxic, nodular goiter (14 women and 1 man; aged 61 ± 11 yr). Four patients were studied twice, and 1 patient was studied 3 times. RAIU was measured both under basal conditions and after pretreatment (im) with rhTSH, given either 2 h (0.01 mg; n = 7) or 24 h [0.01 mg (n = 7) or 0.03 mg (n = 7)] before ¹³¹I administration (20–40 µCi). Serum levels of TSH, free T₄ (FT₄), and total T₃ were measured at 2, 5, 8, 24, 48, 72, 96, and 192 h after rhTSH administration.

After administration of 0.01 mg rhTSH, serum TSH rose from 0.7 ± 0.5 to a peak level of 4.4 ± 1.1 mU/L (P < 0.0001), FT₄ rose from 16.0 ± 2.6 to 18.5 ± 3.7 pmol/L (P < 0.0001), and T₃ rose from 2.10 ± 0.41 to 2.63 ± 0.66 nmol/L (P < 0.0001). After administration of 0.03 mg rhTSH, TSH rose from 0.6 ± 0.4 to 15.8 ± 2.3 mU/L (P < 0.0001), FT₄ rose from 15.2 ± 1.5 to 21.7 ± 2.9 pmol/L (P < 0.0001), and T₃ rose from 1.90 ± 0.43 to 3.19 ± 0.61 nmol/L (P < 0.0001). Peak TSH levels were reached at 5–8 h and peak FT₄ and T₃ levels at 8–96 h after rhTSH administration.

Administration of 0.01 mg rhTSH 2 h before ¹³¹I increased 24-h RAIU from 30 ± 11% to 42 ± 10% (P < 0.02), 0.01 mg rhTSH administered 24 h before ¹³¹I increased 24-h RAIU from 29 ± 10% to 51 ± 10% (P < 0.0001), and 0.03 mg rhTSH administered 24 h before ¹³¹I increased 24-h RAIU from 33 ± 11% to 63 ± 9% (P < 0.0001). After administration of 0.01 mg rhTSH 2 h before ¹³¹I, 24-h RAIU did not increase in 1 patient, whereas the increase in 24-h RAIU was less than 10% in 2 other patients. In contrast, administration of rhTSH 24 h before ¹³¹I increased 24-h RAIU by more than 10% in all 14 patients (by >20% in 10 and by >30% in 6).

In conclusion, pretreatment with a single, low dose of rhTSH in patients with nontoxic, nodular goiter increased RAIU considerably. Our observations hold promise that administration of rhTSH before ¹³¹I therapy for nontoxic, nodular goiter will allow treatment with lower doses of ¹³¹I in these patients.

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