Thyroid-hormone therapy and thyroid cancer: a reassessment.
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-T(4)) 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-T(4) 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-T(4). In these patients, careful monitoring is necessary to avoid undesirable effects on bone and heart.
Biondi
Bernadette
B
Department of Clinical and Molecular Endocrinology and Oncology, University of Naples Federico II, Naples, Italy. bebiondi@unina.it
Filetti
Sebastiano
S
Schlumberger
Martin
M
D006801:Humans; D013963:Thyroid Hormones / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D013964:Thyroid Neoplasms / Q000188:drug therapy* / Q000473:pathology; D013972:Thyrotropin / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D013974:Thyroxine / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D014284:Triiodothyronine / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use
D013963:Thyroid Hormones; D014284:Triiodothyronine; D013972:Thyrotropin; D013974:Thyroxine