Secondary Hypothyroid: Labs
Advanced, Organ-Based and Clinical Sciences
Secondary hypothyroidism results from a failure at some point of the hypothalamic-pituitary axis and not as a result of dysfunction in the thyroid itself. In the normal pathway, the hypothalamus secretes TRF (thyrotropin-releasing factor) and TRH (thyrotropin releasing hormone), which prompt the anterior pituitary to produce TSH (throid-stimulating hormone).
Both primary and secondary hypothyroidism have the end effect of low thyroid activity and therefore low T4 and T3 levels (T4 being the less active precursor of T3).
In primary hypothyroidism (more common than secondary), the thyroid itself is dysfunctional and does not respond appropriately to TSH. TSH levels are therefore high as the HPA attempts to stimulate the thyroid.
In secondary hypothyroidism the problem stems from a lack of TSH to stimulate an otherwise functional thyroid gland, and therefore the TSH is low.
A “euthyroid sick” phenomenon can also occur in critical illness, during which the TSH levels are normal but T3 is low. Failure of autoregulation with the hypothalamic pituitary axis is one potential component of the underlying mechanism of this phenomenon.