Prolactin as a Marker of Dopaminergic Activity at Different Levels of Thyroid Function in Man

Summary

To investigate the hypothesis of an altered dopaminergic activity in hypothyroidism, seven patients without thyroid tissue were studied by means of three consecutive tests: 1) an iv bolus of TRH (200 μg); 2) a continuous iv infusion (5 mg during 30 min) of metoclopramide (MCP); and 3) a second, post-MCP, iv bolus of TRH (200 μg). The study was performed three times: (A) without treatment; (B) on the 15th day while on L-T₄ (150 μg i.d.);and (C) on the 30th day with the same treatment. Each time was a different situation of thyroid function; on the basis of basal serum TSH (P < 0.001, A vs B vs C).

The response of PRL to the first (non-primed) TRH, expressed as the sum of increments in ng/ml (mean ± SE), was significantly higher in A (659 ± 155) than in C (185 ± 61). Individual PRL responses correlated with circulating T₃ (P < 0.02), but not with T₄. A significant increase of PRL occurred after MCP in the three situations, but there were no differences among them. Likewise, the responses to the second (MCP-primed) TRH showed no differences. Although there was an expected high correlation (P < 0.001) between basal TSH and circulating thyroid hormones, the maximal response of TSH to both non-primed and MCP-primed TRH was in B. After MCP, no measurable increase of TSH could be demonstrated at any of the three levels of thyroid function.

These results do not support the hypothesis of an altered dopaminergic activity in hypothyroidism. They suggest that: 1) PRL hyperresponse to TRH in hypothyroidism is mediated by circulating T₃, rather than by T₄, and 2) dopaminergic modulation of TSH secretion is of minor relevance in comparison with the predominant role of other factors, such as serum thyroid hormones and the availability of TSH in the pituitary.

Key-Words:

Thyroid Function - Dopaminergic Modulation - Prolactin - Thyrotropin