Thyroid-hormone therapy and thyroid cancer: a reassessment

Nat Clin Pract Endocrinol Metab. 2005 Nov;1(1):32-40. doi: 10.1038/ncpendmet0020.


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.

Publication types

  • Review

MeSH terms

  • Humans
  • Thyroid Hormones / adverse effects
  • Thyroid Hormones / pharmacology
  • Thyroid Hormones / therapeutic use*
  • Thyroid Neoplasms / drug therapy*
  • Thyroid Neoplasms / pathology
  • Thyrotropin / antagonists & inhibitors
  • Thyrotropin / pharmacology
  • Thyrotropin / therapeutic use
  • Thyroxine / adverse effects
  • Thyroxine / pharmacology
  • Thyroxine / therapeutic use
  • Triiodothyronine / adverse effects
  • Triiodothyronine / pharmacology
  • Triiodothyronine / therapeutic use


  • Thyroid Hormones
  • Triiodothyronine
  • Thyrotropin
  • Thyroxine