Differentiated Thyroid Carcinoma: Is There Any Evidence for the Use of Recombinant Human TSH in Thyroid Hormone–Secreting Metastasis?

TO THE EDITOR: We are thankful for the interesting and highly relevant article by Douglas Van Nostrand and colleagues, published in the March 2012 issue (1). The objective of this study was to compare administration of recombinant human thyroid-stimulating hormone (rhTSH) versus thyroid hormone withdrawal for the identification of metastasis in differentiated thyroid cancer (DTC) on ¹³¹I planar whole-body imaging and ¹²⁴I PET. The authors observed that ¹³¹I planar whole-body scans and ¹²⁴I PET scans identified significantly more foci of metastasis in patients after preparation with thyroid hormone withdrawal than with rhTSH injections. The conclusion drawn by the authors that “physicians should be cautious in using rhTSH for patient preparation before diagnostic scanning for the detection of DTC or treating distant metastasis secondary to DTC with ¹³¹I” appears well founded on the data presented. Furthermore, such a study is important, because recently there has been a shift toward the use of rhTSH in increasing numbers of indications in patients with DTC.

However, we have several concerns regarding the authors’ conclusion that “the use of rhTSH is appropriate for patients…[to] increase their endogenous TSH because their metastases are producing significant thyroid hormone.” First, none of the patients in the evaluated study cohort was identified as a patient with thyroid hormone–secreting metastasis. Second, there is no corresponding discussion to support this conclusion. Furthermore, DTC with thyroid hormone–secreting metastases is exceedingly rare. Only a few cases have been reported since the first patient with adenocarcinoma of the thyroid with thyroid hormone–secreting metastasis and postoperative thyrotoxicosis was described by Leiter et al. in 1946 (2). Because of the small number of cases reported so far, patients with hormone-producing metastasis represent a challenge for the further treatment of DTC. Recently, we reported the case of a patient with thyroid hormone–secreting metastasis leading to persistent TSH suppression after thyroidectomy and radioiodine remnant ablation. As suggested by Van Nostrand et al., we assumed that rhTSH was the appropriate preparation to elevate the TSH level before ¹³¹I whole-body imaging. However, we observed that when applied before the second radioiodine treatment, rhTSH increased the ¹³¹I uptake into the thyroid hormone–secreting metastasis and prolonged the effective half-life of ¹³¹I in relation to measurements from the first radioiodine therapy without rhTSH (3). Compared with the original therapy without rhTSH, the ¹³¹I uptake after rhTSH increased from 8.4% to 39% and the effective half-life increased from 2.2 to 4.1 d. Subsequent radiation exposure caused bone marrow toxicity with myelosuppression. To prevent grade IV neutropenia, the patient was successfully treated with pegfilgrastim, a long-acting granulocyte-stimulating growth factor.

On the basis of the data presented by van Nostrand et al. and our own experience, we cannot agree with their recommendation regarding the use of rhTSH in the subgroup of patients with thyroid hormone–secreting metastasis. We would propose adding the following clarifications to the article: rhTSH might not be necessary for diagnostic ¹³¹I whole-body imaging in patients with TSH suppression due to thyroid hormone–secreting metastasis, because thyroid hormone–secreting metastases generally show a high ¹³¹I uptake. Furthermore, in patients undergoing ¹³¹I treatment, the use of rhTSH needs to be handled carefully as it can increase ¹³¹I uptake and prolong the effective half-life of ¹³¹I, leading to an increased exposure to radiation and bone marrow toxicity. Because this subgroup of patients is extremely rare, further studies regarding their optimal diagnostic work-up and treatment should be performed before any general recommendation is given.

• © 2012 by the Society of Nuclear Medicine and Molecular Imaging, Inc.