TRH: Pathophysiologic and clinical implications

Thyrotropin releasing hormone is thought to be a tonic stimulator
of the pituitary TSH secretion regulating the setpoint of the
thyrotrophs to the suppressive effect of thyroid hormones. The
peptide stimulates the release of normal and elevated prolactin.
ACTH and GH may increase in response to exogenous TRH in pituitary
ACTH and GH hypersecretion syndromes and in some extrapituitary
diseases. The pathophysiological implications of extrahypothalamic
TRH in humans are essentially unknown. The TSH response to TRH is
nowadays widely used as a diganostic amplifier in thyroid diseases
being suppressed in borderline and overt hyperthyroid states and
increased in primary thyroid failure. In hypothyroid states of
hypothalamic origin, TSH increases in response to exogenous TRH
often with a delayed and/or exaggerated time course. But in
patients with pituitary tumors and suprasellar extension TSH may
also respond to TRH despite secondary hypothyroidism. This TSH
increase may indicate a suprasellar cause for the secondary
hypothyroidism, probably due to portal vessel occlusion. The TSH
released in these cases is shown to be biologically inactive.