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Prolactin and Thyrotropin in Thyroid Diseases: Lack of Evidence for a Physiological Role of Thyrotropin-Releasing Hormone in the Regulation of Prolactin Secretion

M. L’Hermite, C. Robyn, J. Golstein, G. Rothenbuchner, Jesper B. Birk, U. Loos, M. Bonnyns, L. Vanhaelst

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Abstract

The purpose of the present study was to investigate whether thyrotropin-releasing hormone (TRH) could play a role in the regulation of prolactin (PRL) secretion, and whether thyroid hormones would exert a feedback effect on the PRL response to TRH. Therefore, serum thyrotropin (TSH) and PRL levels were measured in basal conditions in patients with thyroid diseases, and after TRH stimulation in hyperthyroid patients and in normal subjects treated with triiodothyronine (T3). Mean basal PRL levels of the adults with asymptomatic thyroiditis (n = 10), with spontaneous myxoedema (n = 28), and with hyperthyroidism (n = 34) were not significantly different from that of normal euthyroid adults (n = 30). On the contrary, mean PRL levels of 6 children with congenital myxoedema (athyreosis) were significantly (p < 0.001) elevated. In 4 normal men, short-term (3 days) pretreatment with 100 µg T3 failed to inhibit the PRL response to synthetic TRH, whereas T3 inhibited the TSH response to TRH. The mean TRH-induced PRL response observed in 7 hyperthyroid women was lower than expected for normal euthyroid women. The lack of short-term effect of thyroid hormones on TRH-induced PRL release argues against their direct action on the lactotropes. Moreover, the present data do not favour the hypothesis of a physiological role of TRH in the regulation of PRL secretion, and suggest that it rather acts as a pharmacological PRL releaser.

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What this paper is about

The purpose of the present study was to investigate whether thyrotropin-releasing hormone (TRH) could play a role in the regulation of prolactin (PRL) secretion, and whether thyroid hormones would exert a feedback effect on the PRL response to TRH. Therefore, serum thyrotropin (TSH) and PRL levels were measured in basal conditions in patients with thyroid diseases, and after TRH stimulation in hyperthyroid patients and in normal subjects treated with triiodothyronine (T3). Mean basal PRL levels of the adults with asymptomatic thyroiditis (n = 10), with spontaneous myxoedema (n = 28), and with hyperthyroidism (n = 34) were not significantly different from that of normal euthyroid adults (n = 30). On the contrary, mean PRL levels of 6 children with congenital myxoedema (athyreosis) were significantly (p < 0.001) elevated. In 4 normal men, short-term (3 days) pretreatment with 100 µg T3 failed to inhibit the PRL response to synthetic TRH, whereas T3 inhibited the TSH response to TRH. The mean TRH-induced PRL response observed in 7 hyperthyroid women was lower than expected for normal euthyroid women. The lack of short-term effect of thyroid hormones on TRH-induced PRL release argues against their direct action on the lactotropes. Moreover, the present data do not favour the hypothesis of a physiological role of TRH in the regulation of PRL secretion, and suggest that it rather acts as a pharmacological PRL releaser.

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Available abstract

The purpose of the present study was to investigate whether thyrotropin-releasing hormone (TRH) could play a role in the regulation of prolactin (PRL) secretion, and whether thyroid hormones would exert a feedback effect on the PRL response to TRH. Therefore, serum thyrotropin (TSH) and PRL levels were measured in basal conditions in patients with thyroid diseases, and after TRH stimulation in hyperthyroid patients and in normal subjects treated with triiodothyronine (T3). Mean basal PRL levels of the adults with asymptomatic thyroiditis (n = 10), with spontaneous myxoedema (n = 28), and with hyperthyroidism (n = 34) were not significantly different from that of normal euthyroid adults (n = 30). On the contrary, mean PRL levels of 6 children with congenital myxoedema (athyreosis) were significantly (p < 0.001) elevated. In 4 normal men, short-term (3 days) pretreatment with 100 µg T3 failed to inhibit the PRL response to synthetic TRH, whereas T3 inhibited the TSH response to TRH. The mean TRH-induced PRL response observed in 7 hyperthyroid women was lower than expected for normal euthyroid women. The lack of short-term effect of thyroid hormones on TRH-induced PRL release argues against their direct action on the lactotropes. Moreover, the present data do not favour the hypothesis of a physiological role of TRH in the regulation of PRL secretion, and suggest that it rather acts as a pharmacological PRL releaser.

Key concepts: Internal medicine, Endocrinology, Thyrotropin-releasing hormone, Prolactin, Euthyroid, Hormone, TRH stimulation test, Thyroid

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