Thyroxine therapy for thyroid cancer

The most common forms of thyroid cancer are differentiated thyroid cancers (papillary and follicular cancers) that arise from thyroid follicular cells. Many differentiated thyroid cancers respond to thyroid stimulating hormone (TSH) suppression, so a major therapeutic objective in the follow-up of these cancers is to limit potential TSH-mediated growth of residual tumour. To suppress TSH, a higher dose of levothyroxine than the usual replacement dose is used, and the serum TSH target concentration is at least less than 0.1 milliunits/L.

If TSH suppression is indicated, ensure that all clinicians involved in the patient’s care understand the goal of treatment, to avoid the levothyroxine dose being incorrectly lowered from a suppressive dose to a replacement dose.

Not all patients with differentiated thyroid cancers should be treated with TSH-suppressive thyroxine therapy. The managing specialist will consider the likely benefits of treatment related to the thyroid cancer versus the risk of harms of treatment. Patients at highest risk of complications or harm from TSH suppression include those with atrial fibrillation and reduced bone density (both of which can be worsened by levothyroxine treatment). Patients unlikely to benefit from TSH suppression include those with low-risk thyroid cancer (eg patients with low initial risk of recurrent disease, patients restratified as low risk after a prolonged disease-free period).

If TSH suppression is not indicated, levothyroxine therapy may still be used to reduce the serum TSH concentration, but with a less aggressive target concentration of 0.5 to 2 milliunits/L. An intermediate serum TSH target concentration of 0.1 to 0.5 milliunits/L is reasonable for patients with both high risk of complications from TSH-suppressive therapy and high-risk thyroid cancer, or for patients transitioning away from full TSH suppression.

The appropriate individualised serum TSH target concentration for both short- and long-term follow-up of thyroid cancer should be determined with endocrinologist consultation. The dose should be reviewed if symptoms suggestive of thyrotoxicosis develop, or if thyroid cancer risk status changes. If long-term TSH-suppressive therapy is essential, assess bone density and start appropriate treatment to prevent osteoporosis if required. Patients with persistent or progressive thyroid cancer require subspecialist management.

Some thyroid cancer subtypes are not responsive to TSH suppression (eg medullary and anaplastic cancers).