Diabetes and Endocrine Service, Liverpool Health Service, Liverpool, NSW 2170, Australia
Address correspondence to: Barbara Depczynski, Diabetes and Endocrine Service, Liverpool Health Service. E-mail: barbara.depczynski{at}swsahs.nsw.gov.au.
To the editor:
In their recent article in JCEM, Driedger and Kotowycz (1) reported that 131I uptake by thyroid carcinoma metastases and thyroglobulin production was not stimulated by recombinant human TSH (rhTSH). Potential mechanisms that were proposed included variation in receptor binding sites of rhTSH compared with endogenous TSH and serial exposure to rhTSH exerting progressive selection pressure on the TSH receptor (TSHR). Although changes in the TSHR are likely to be responsible for the variation in response seen, it is important to consider a role for the difference in circulating thyroid hormone levels between thyroid hormone withdrawal and rhTSH administration.
Levels of circulating T4 and T3 were not reported by Driedger and Kotowycz (1). This may also be a potential factor in the variation of response of thyroid carcinoma to stimulation with hypothyroidism compared with rhTSH. In vitro, T3 has been shown to down-regulate the expression of TSHR gene (2). Although thyroid hormone receptor expression is reduced in thyroid cancers (3), evidence exists for T3 exerting its effect on TSHR by thyroid hormone receptor-independent means (2). In the presence of higher circulating T3 levels when thyroid hormone is not withdrawn, the potential exists for T3 to reduce TSHR expression. This would result in a reduced response to exogenous TSH, as manifested by reduced iodine uptake and thyroglobulin production.
Received May 17, 2004.
References
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