In people with normal thyroid function, taking L-dopa does not result in a detectable change in thyroid-stimulating hormone levels because any changes are too small to be measured by standard tests.

In people taking thyroid hormone medication who have normal thyroid function, the pituitary gland releases less TSH in response to TRH, but releases the same amount of prolactin as before, indicating that the two hormones are regulated differently during hormone replacement.

When high thyroid hormone levels are caused by taking too much thyroid medication (exogenous thyrotoxicosis), the underlying biochemical changes differ from those caused by an overactive thyroid gland (endogenous hyperthyroidism). Because of these differences, relying only on TSH levels to assess risk can lead to incorrect conclusions in one condition versus the other.

In people with thyrotoxicosis caused by taking too much thyroid hormone medication, the brain's control system for thyroid hormone levels behaves differently than in people whose thyroid gland overproduces hormones on its own. Specifically, TSH stays low even when thyroid hormone levels are higher than normal.

In patients who have had their thyroid removed and are taking levothyroxine, those whose TSH levels remain above 2.0 mU/L show higher indicators of reduced pituitary sensitivity to thyroid hormones in the blood.

A blood test called the thyroid-stimulating hormone index (TSHI) can moderately predict which patients continue to have high TSH levels after thyroid removal and levothyroxine treatment, even when the treatment dose is considered adequate.