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.

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 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.

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.

People taking synthetic thyroid hormone after thyroid removal have higher levels of FT4 but similar levels of FT3 compared to people with overactive thyroid glands due to Graves' disease or toxic adenoma, suggesting different ways the body processes these two thyroid hormones.

When older adults get more thyroid hormone—either through a shot or a pill—their prolactin levels drop by about 8–12% in just a couple of days, and this drop is bigger in men, suggesting thyroid hormone naturally lowers prolactin no matter how you give it or whether you're male or female.