Abstract

Experimental studies and clinical data have demonstrated that thyroid-cell proliferation is dependent on thyroid-stimulating hormone (TSH), thereby providing the rationale for TSH suppression as a treatment for differentiated thyroid cancer. Several reports have shown that hormone-suppressive treatment with the L-enantiomer of tetraiodothyronine (L-T₄) benefits high-risk thyroid cancer patients by decreasing progression and recurrence rates, and cancer-related mortality. Evidence suggests, however, that complex regulatory mechanisms (including both TSH-dependent and TSH-independent pathways) are involved in thyroid-cell regulation. Indeed, no significant improvement has been obtained by suppressing TSH in patients with low-risk thyroid cancer. Moreover, TSH suppression implies a state of subclinical thyrotoxicosis. In low-risk patients, the goal of L-T₄ treatment is therefore to obtain a TSH level in the normal range (0.5–2.5 mU/l). Only selected patients with high-risk papillary and follicular thyroid cancer require long-term TSH-suppressive doses of L-T₄. In these patients, careful monitoring is necessary to avoid undesirable effects on bone and heart.

Author affiliations

1. B Biondi is Associate Professor at the Department of Clinical and Molecular Endocrinology and Oncology, University of Naples Federico II, Naples, Italy.
2. S Filetti is the Chairman of the Internal Medicine Department, University La Sapienza, Rome, Italy.
3. M Schlumberger is the Chairman of the Nuclear Medicine and Endocrine Tumor Department, Institut Gustave Roussy, Villejuif, France.

Correspondence to: Bernadette Biondi¹ Department of Clinical and Molecular Endocrinology and Oncology, Via S Pansini, 5, 80131 Naples, Italy
Email: bebiondi@unina.it

Received 18 May 2005 | Accepted 30 August 2005