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The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 2 506-510
Copyright © 2006 by The Endocrine Society

123I Thyroid Uptake and Thyroid Size at 24, 48, and 72 Hours after the Administration of Recombinant Human Thyroid-Stimulating Hormone to Normal Volunteers

Samara Pena, Seth Arum, Mary Cross, Barbarajean Magnani, Elizabeth N. Pearce, M. Elizabeth Oates and Lewis E. Braverman

Section of Endocrinology, Diabetes, and Nutrition (S.P., S.A., E.N.P., L.E.B.), Section of Nuclear Radiology (M.C., M.E.O.), Department of Radiology, and Department of Laboratory Medicine (B.M.), Boston University Medical Center, Boston, Massachusetts 02118

Address all correspondence and requests for reprints to: Elizabeth N. Pearce, M.D., M.Sc., Section of Endocrinology, Diabetes, and Nutrition, Evans 201, 88 East Newton Street, Boston, Massachusetts 02118. E-mail: elizabeth.pearce{at}bmc.org.


   Abstract
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 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Context: Recombinant human TSH (rhTSH) is used to evaluate thyroid carcinoma patients and off-label for 131I thyroid ablation and nontoxic goiter therapy.

Objective: Our objective was to determine the optimal time for 131I administration after rhTSH.

Participants: Twenty-five euthyroid nongoitrous volunteers participated in the study.

Design: Baseline 24-h thyroid 123I uptake (RAIU) was measured, and then 0.1 mg rhTSH was administered. 123I was administered 24, 48, or 72 h after rhTSH, and a repeat 24-h RAIU was obtained.

Setting: The study was conducted at an academic research center.

Main Outcome Measures: Thyroid function tests, thyroid ultrasounds, and electrocardiograms were measured before rhTSH, then daily for 4 d, and finally 7 d after rhTSH.

Results: Serum TSH concentrations 24 h after rhTSH increased from 1.7 ± 0.5 µU/ml (mean ± SD) to 13.3 ± 4. The 24-h RAIUs rose from 25 ± 5 to 47 ± 8% (88% increase) when the 123I was given at 24 h after rhTSH and from 29.8 ± 7 to 40.5 ± 13% (36% increase) when the 123I was given at 48 h and were unchanged when the 123I was given at 72 h. The post-rhTSH RAIU increase was greater at 24 than at 72 h (P < 0.005) and marginally greater than at 48 h (P = 0.057). Thyroid volumes significantly increased 48 h after rhTSH (10 ± 3.8 vs. 11.1 ± 3.7 ml; P < 0.009). Electrocardiograms were normal.

Conclusions: Marked increases in RAIU occurred when 123I was given 24 h after rhTSH administration to euthyroid volunteers. Smaller increases were observed at 48 h and none at 72 h.


   Introduction
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 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
RECOMBINANT HUMAN TSH (rhTSH) is used to augment the thyroid radioiodine uptake (RAIU) in the surveillance of thyroid cancer without rendering the patient hypothyroid. Its combined use with serum thyroglobulin (Tg) measurements has been established as a safe and effective way to monitor for metastatic or recurrent differentiated thyroid cancer or residual thyroid bed tissue, although stimulation of Tg release without thyroid scanning is often recommended (1). Because of its ability to increase the RAIU, other potential uses have been proposed including the pretreatment of multinodular goiter before 131I therapy, the ablation of residual thyroid bed tissue after thyroidectomy, and the treatment of metastatic thyroid cancer in those patients unable to increase endogenous TSH after thyroid hormone withdrawal or in those who cannot tolerate hypothyroidism (2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13).

Since its introduction in the 1990s, the physiological effects of rhTSH have been studied in both animal models and humans. It has been well established that the 24-h thyroid RAIU approximately doubles when the radioactive iodine is given 24 h after administration of rhTSH to normal subjects (14, 15, 16). However, the duration and timing of this effect beyond 24 h has not been studied in normal volunteers. In vitro studies in FRTL-5 cells exposed to rhTSH demonstrated that a minimum of 12 h is needed to stimulate iodine uptake, reaching a maximum at 72 h. Sodium iodide symporter mRNA expression after addition of rhTSH was detected at 3–6 h, reaching a maximum after 24 h (17, 18). Thus, it has been suggested that the thyroid 4-h RAIU is 4-fold higher when radioactive iodine is given at 72 h compared with 24 h after rhTSH administration in patients with multinodular goiters (19, 20). To determine the optimal time to administer radioiodine after a single injection of rhTSH, we have measured the 123I thyroid uptake when the 123I was given 24, 48, and 72 h after the administration of a small dose of rhTSH to healthy volunteers.


   Subjects and Methods
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 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Experimental subjects

Twenty-five healthy subjects with no history of thyroid disease were enrolled. There were 10 men and 15 women with a mean age of 31 ± 5.7 (SD) yr. The study was approved by the Boston University Medical Center’s Institutional Review Board, and informed consent was obtained from all subjects before participating in the study. Baseline studies included serum TSH, total T4, total T3, T3 uptake (T3U), free T4 index (FTI), Tg, Tg antibodies, TPO antibodies, complete blood count (CBC), creatinine, serum ß-human chorionic gonadotropin (in women), spot urinary iodine and creatinine, and a thyroid ultrasound (US).

All enrolled volunteers were biochemically euthyroid, had no evidence of goiter or thyroid nodules on US, were not pregnant, and had normal CBC and serum creatinine values.

Study design

A baseline 24-h 123I RAIU was performed on all subjects. Four days later, subjects were administered 0.1 mg rhTSH im. They were then arbitrarily assigned into three groups. Group I was given 100 µCi 123I 24 h after the rhTSH injection, and a 24-h RAIU was then obtained. Group II was given 100 µCi 123I 48 h after the rhTSH, and a 24-h RAIU was obtained. Group III was given 100 µCi 123I 72 h after the rhTSH, and a 24-h RAIU was obtained. All subjects had vital signs and electrocardiograms (ECGs) before and daily for 4 d after rhTSH and on the seventh day. USs were obtained before and on d 2, 4, and 7 after rhTSH. Thyroid function tests and serum Tg were measured before and daily for 4 d and on d 7 after rhTSH. Spot urine iodine and creatinine concentrations were measured at the time of each 123I administration.

Methods

Thyroid hormone tests (total T3, total T4, FTI, and TSH) were measured at the Boston Medical Center laboratory by chemiluminescence using the Bayer Advia Centaur automated system (Bayer Healthcare, Tarrytown, NY). Reference ranges are as follows: T4, 4.5–10.9 µg/dl; T3 uptake, 22.5–37.0%; FTI, 1.0–4.0; TSH, 0.35–5.5 µIU/ml; total T3, 60–181 ng/dl. The FTI is the product of the T4 concentration and the T3 uptake divided by 100. Tg, antithyroid peroxidase antibodies (TPO-Ab) and anti-Tg antibodies (TgAb) were measured using chemiluminescence on the Nichols Advantage (Nichols Institute Diagnostics, San Juan Capistrano, CA). Reference range for serum Tg is 4–40 ng/ml, TPO-Ab 0.0–2.0 IU/ml, and TgAb less than 1 IU/ml. Urinary iodine was measured using the Sandell-Kolthoff reaction for iodine in the laboratory of one of the authors (L.E.B.). CBC and chemistry analyses were conducted at the Boston Medical Center Laboratory.

The 24-h thyroid RAIUs were measured before and after rhTSH administration with an Atomlab 950 thyroid uptake system after an oral dose of 100 µCi 123I sodium iodine.

Thyroid USs were performed on a Toshiba JustVision 400 by two different operators. The operators were not blinded. Thyroid volume was calculated using maximal measurements of length (l), width (w), and depth (d). The formula used was (l x w x d) x {pi}/6 (21).

rhTSH (Thyrogen) was supplied by the Genzyme Corp. (Cambridge, MA) and reconstituted with 1.2 ml sterile water and diluted to a final concentration of 0.1 mg/1.1 ml, which was administered as an im injection in the gluteus muscle.

Daily ECGs were evaluated for changes in rhythm or signs of ischemia. Mean heart rate was calculated for each visit, and a mean increase of more than 10% from baseline was considered significant. Subjects were questioned about hyperthyroid symptoms and monitored for tachycardia and thyroid tenderness.

Statistical analysis

All statistical analyses were performed using SAS version 8.2 (SAS Institute, Cary, NC). Repeated-measures ANOVA was used to determine changes in thyroid volume and RAIU over time by treatment group. ANOVA was used to assess for differences in the maximal posttreatment change in serum TSH, T3, Tg, and FTI by treatment group. Values are presented as the mean ± SD.


   Results
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 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
There were no significant differences in age, thyroid function tests, thyroid volume, or baseline 123I RAIUs between the three groups (Table 1Go). Small changes in urinary iodine excretion in individual subjects before and after rhTSH administration did not correlate with thyroid 123I RAIUs. Median spot urinary iodine excretion for all subjects was 166 µg/liter at baseline and was 130 µg/liter at the time of the post-rhTSH 123I RAIUs. None of the subjects experienced adverse events. Mean heart rate did not change significantly over the course of the study (P = 0.484), and there were no signs of ischemia or rhythm disturbances on ECG. No thyroid tenderness was observed. Subjects did not report any symptoms of thyroid hormone excess.


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  		TABLE 1. Mean baseline values per group

 
Mean peak serum TSH values did not differ across the three groups; group I was 14.9 ± 3.4, group II 12.3 ± 4.8, and group III 11.8 ± 3.1 µIU/ml (Fig. 1Go). Maximal TSH was reached 24 h after administration of rhTSH, and there was no difference in the maximal TSH response between the three groups. There were also no significant differences in the maximal total T3, FTI, and Tg responses between the three groups. Figure 2Go depicts the mean serum Tg, T3, and FTI concentrations in the three groups combined. Mean peak T3 was 204 ± 46.4 ng/dl, mean peak Tg was 63 ± 54 ng/ml, mean peak T4 was 10.4 ± 2.4 µg/dl, and mean peak FTI was 3.2 ± 0.6.


Figure 1
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  		FIG. 1. Effect of 0.1 mg rhTSH on serum TSH concentrations in the three groups given 123I 24, 48, and 72 h after 0.1 mg rhTSH im. Peak TSH was 14.9 ± 3.4 µIU/ml in group I, 12.3 ± 4.8 µIU/ml in group II, and 11.8 ± 3.1 µIU/ml in group III. Maximal TSH was reached 24 h after administration of rhTSH, and there was no difference in the maximal TSH response between the three groups (P = 0.4).

 

Figure 2
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  		FIG. 2. Effect of 0.1 mg rhTSH on the 24-h thyroid 123I uptakes in the three groups. In group I, RAIUs rose from a mean of 25 ± 7 to 47.0 ± 8% (P = 0.0008). Group II RAIUs rose from 29.8 ± 7 to 40.5 ± 13% (P = 0.03). There was no significant increase in RAIU from baseline in group III (29.9 ± 0.07 vs. 31.1 ± 0.06). There was a borderline significant difference in the RAIU increase between 24 and 48 h (P = 0.057).

 
The thyroid 123I uptakes are shown in Fig. 2Go. In group I, there was a significant increase (88%) from the basal 24-h RAIU after rhTSH administration. RAIUs rose from a mean of 25 ± 7 to 47.0 ± 8% (P = 0.0008). Group II had a 36% increase in the RAIU after rhTSH administration. RAIUs rose from 29.8 ± 7 to 40.5 ± 13% (P = 0.03). There was no significant increase in RAIU from baseline in group III (29.9 ± 0.07 vs. 31.1 ± 0.06). The RAIU increase was significantly greater at 24 h than at 72 h. There was a borderline significant difference in the RAIU increase between 24 and 48 h (P = 0.057).

Thyroid volume by US increased slightly but significantly 2 d after the administration of 0.1 mg rhTSH (11.1 ± 3.7 vs. 10.0 ± 3.8 ml; P = 0.0068) in all groups combined and returned to baseline on d 4 and 7 (Fig. 3Go).


Figure 3
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  		FIG. 3. The effect of 0.1 mg rhTSH on thyroid volume in the combined three groups. Thyroid volume by US increased significantly 2 d after the administration of 0.1 mg rhTSH (11.1 ± 3.7 vs. 10.0 ± 3.8 ml; P = 0.0068).

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Our study demonstrates that there is a significant 88% increase in the 24-h thyroid RAIU when the 123I is given 24 h after the administration of 0.1 mg rhTSH. There was also a significant 36% increase in the RAIU 48 h after rhTSH administration, an increase that was less than that observed at 24 h, suggesting that radioiodine is most efficaciously given 24 h after rhTSH. When the 123I was given 72 h after rhTSH, no rise in the thyroid RAIU was observed. These findings are not consistent with those reported recently in nodular goitrous patients, some of whom had hyperthyroidism (19, 20). Upon careful inspection of the data in the most recent report, it is evident that the baseline thyroid 4- and 24-h RAIUs were defined as those occurring when the 123I and 0.1 mg or 0.3 mg rhTSH were given simultaneously. This would almost certainly affect the baseline thyroid uptakes. Furthermore, their defined 72-h uptake after rhTSH was based upon the administration of 123I 48 h after rhTSH, which corresponds to our group II subjects who received the 123I 48 h after rhTSH and had the 123I thyroid measured 24 h later. The stated 4-fold increase in the thyroid RAIU after rhTSH was observed in the 4-h uptake, whereas the 24-h thyroid RAIU doubled, as observed in the present and earlier studies, when 123I was given 24 h after rhTSH to normal subjects (15, 16). In an earlier study (20), the same authors reported that the 4-h thyroid 123I uptake obtained before rhTSH did increase a mean of 4-fold 72 h after the injection of rhTSH in six patients with nodular goiter with or without subclinical hyperthyroidism; the thyroid RAIU increased two times in three patients, four times in two patients, and 10 times in one patient. The 24-h thyroid RAIUs were not obtained in these six patients. In both studies, the 4-h thyroid RAIUs before or simultaneously with rhTSH were relatively low for patients with nodular goiter. Urinary iodine excretion was not assessed, and an increase of iodine intake affecting the 123I uptake could have been a confounding factor.

Our findings in normal individuals may be different from those observed in goitrous patients, and the present protocol should be applied to patients with nodular goiters to determine the optimal time to give radioiodine after the administration of rhTSH. Whether in vitro findings in the rat FTRL-5 cell line suggesting that sodium iodide symporter is not increased for 12–24 h and peaks 72 h after the addition of rhTSH to the media can be extrapolated to humans remains unclear (17, 18).

In one previous study in normal subjects, the thyroid volume by US increased by 35% 48 h after the administration of 0.9 mg rhTSH (22). In a recent study of patients with nontoxic multinodular goiter treated with 0.3 mg rhTSH, goiters increased in size by 24% at 48 h after rhTSH administration (23). The greater increases in thyroid size than that observed in the present study (10%) may have been because of the larger dose of rhTSH administered, 0.9 vs. 0.1 mg. In two earlier studies in normal volunteers, US measurements were not carried out (15, 16). In some studies employing rhTSH in goitrous subjects before therapy with 131I, there was a decrease in thyroid size secondary to the 131I therapy (3, 13, 24, 25, 26). In these studies, because thyroid size was not measured shortly after rhTSH administration, it is unknown whether there was a short-term increase in volume.

Consistent with other studies in normal subjects in the United States (15, 16), there was a marked increase in mean peak serum total T4 and T3 concentrations within 24 h after rhTSH, whereas the serum Tg concentration peaked at 48 h. These increases in serum T4 and T3 concentration were not associated with either symptoms or ECG changes in the present normal, healthy subjects. Patients with goiters, who are often elderly and may have underlying cardiovascular disease, could be at risk for cardiac complications after rhTSH administration. However, recent studies have not observed any serious side effects in patients with nodular goiters given rhTSH (3, 13, 19, 20, 24), although some patients in those studies were treated with ß-blocking drugs.


   Footnotes
 
This study was supported in part by a grant from Genzyme Corp. (Cambridge, MA) and by National Institutes of Health Grants 5K23DK064611 (to E.N.P.) and M01RR 00533.

First Published Online November 29, 2005

Abbreviations: CBC, Complete blood count; FTI, free T4 index; RAIU, radioiodine uptake; rhTSH, recombinant human TSH; Tg, thyroglobulin; TgAb, anti-Tg antibodies; TPO-Ab, antithyroid peroxidase antibodies; US, ultrasound.

Received September 6, 2005.

Accepted November 21, 2005.


   References
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Wartofsky L 2002 Management of low risk well differentiated thyroid cancer based only on thyroglobulin measurement after recombinant human thyrotropin. Thyroid 12:583–590[CrossRef][Medline]
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V. E. Nielsen, S. J. Bonnema, H. Boel-Jorgensen, P. Grupe, and L. Hegedus
Stimulation With 0.3-mg Recombinant Human Thyrotropin Prior to Iodine 131 Therapy to Improve the Size Reduction of Benign Nontoxic Nodular Goiter: A Prospective Randomized Double-blind Trial.
Arch Intern Med, July 24, 2006; 166(14): 1476 - 1482.
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