Thyroid-Stimulating Hormone Suppression Therapy after Thyroid Cancer Surgery

Historically:
- Almost all patients were given thyroid hormone:
  - To fully suppress serum thyroid-stimulating hormone (TSH)
- The rationale for this approach:
  - Was based on the theory that TSH is a stimulant for thyroid cell proliferation and suppression of thyrotropin will inhibit tumor growth:
    - Indeed, early studies supported the role of TSH suppression in reducing the likelihood of disease progression and improving survival:
      - Particularly in those with high-risk disease
    - More recent analyses, however, have failed to demonstrate a benefit of such suppressive therapy in those with low-risk tumors:
      - In fact, such treatment may prove harmful
    - A long-term observational study showed a three-fold increased risk of cardiovascular death for each ten-fold reduction in mean TSH level
    - Patients with subclinical thyrotoxicosis:
      - Are also at increased risk of atrial fibrillation, ventricular hypertrophy, diastolic dysfunction, and impaired cardiac reserve
      - Additionally, bone turnover may be adversely affected by suppressive doses of levothyroxine:
        
        Higher rates of osteoporosis may be seen in thyroid cancer patients:
        
        There is an increased risk of fracture when suppressive doses of levothyroxine are used
- As a consequence of the myriad negative effects of excess levothyroxine:
  - The target TSH range should be determined on an individual basis
  - It is also worthy of note that lowering TSH to undetectable levels probably does not confer additional benefit beyond that seen with less aggressive suppression below 0.1 mU/L
  - The optimal TSH range should consider the initial risk for recurrence, the response to therapy, and the risk for thyrotoxicosis-related morbidities in the individual patient
  - Furthermore, this target TSH for the individual patient may evolve over time, depending on the response to therapy