Prolactin Response to Metoclopramide in Hyperthyroidism

Sawers, J. S. A.; Kellett, H A; Brown, N. S.; Seth, John; Toft, A. D.

doi:10.1210/jcem-55-1-175

Cited by 14 publications

(14 citation statements)

References 9 publications

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“…This study confirmed that thyroid hormones exert neg ative feedback effects on the basal and TRH-stimulated PRL secretion in humans [1][2][3][4][5][6][7], In the hyperthyroid patients, not only the basal PRL level but also the PRL responsiveness to TRH were significantly lower during the hyperthyroid state than during the euthyroid state. In turn, in the hypothyroid patients both variables were sig nificantly higher during the hypothyroid state compared to the euthyroid state.…”

Section: Discussionsupporting

confidence: 79%

Effect of Thyroid Status on the Prolactin-Releasing Action of Vasoactive Intestinal Peptide in Humans: Comparison with the Action of Thyrotropin-Releasing Hormone

Watanobe

Sasaki²

1995

Neuroendocrinology

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Recent studies have shown that primary hypothyroidism induced in the rat was able to stimulate the biosynthesis of vasoactive intestinal peptide (VIP) in the anterior pituitary (AP). Since the AP VIP is known to stimulate prolactin (PRL) secretion through a paracrine and/or autocrine mechanism, it is interesting to hypothesize that hyperprolactinemia seen in hypothyroid patients may at least in part be due to a paracrine effect of elevated VIP on AP PRL secretion. Prompted by this information, we in the present study examined the effect of VIP load on PRL secretion in patients with primary hyperthyroidism or hypothyroidism, and compared the data with those from thyrotropin-releasing hormone (TRH) load performed in the same patients. Eight female patients with Graves’ disease and 8 females with chronic thyroiditis received intravenous bolus injections of VIP (100 µg) and TRH (500 µg) 2-3 days apart from each other, during both the dysthyroid and euthyroid (attained by medical treatment) states. Compared to the data in the euthyroid state of the respective group, hyperthyroidism was associated with a lower basal PRL level and a lower PRL responsiveness (estimated by net percent increase in PRL) to TRH, whereas hypothyroidism was associated with higher values of these parameters. With respect to VIP, although the peptide was able to significantly stimulate PRL secretion during both the dysthyroid and euthyroid states of hyper- and hypothyroid patients, PRL responsiveness to VIP was essentially the same regardless of thyroid status. Although these results can not exclude a possible role for AP VIP in the thyroid hormone regulation of the basal PRL secretion, we would suggest at least that the AP PRL responsiveness to VIP may not be as sensitively regulated by thyroid hormones as that to TRH in humans.

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Section: Discussionsupporting

confidence: 79%

Effect of Thyroid Status on the Prolactin-Releasing Action of Vasoactive Intestinal Peptide in Humans: Comparison with the Action of Thyrotropin-Releasing Hormone

Watanobe

Sasaki²

1995

Neuroendocrinology

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“…The rise in both TSH and PRL is reported as significantly greater in subclinical than in overt hypothy roidism and interpreted as a stimulation of hypothalamic DA release induced by thyroid hormones [3]. This hypothe sis appears to be in line with the blunted PRL response to metoclopramide in hyperthyroidism [10]. In our study, after exogenous administration of thyroxine, the magnitude of the TSH rise in response to TRH was reduced to values found in euthyroid subjects, and the marked rise in plasma TSH after the DA receptor antagonist administration com pletely disappeared.…”

Section: Discussionmentioning

confidence: 60%

“…It has also been suggested that an altered thyroid function can modify the control of TSH and PRL, both at the hypothalamic and pituitary levels [3,10].…”

mentioning

confidence: 99%

Prolactin and TSH Response to TRH and Metoclopramide before and after /-Thyroxine Therapy in Subclinical Hypothyroidism

et al. 1986

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The effects of the dopamine (DA) receptor antagonist metoclopramide on the plasma thyroid stimulating hormone (TSH) and prolactin (PRL) levels were studied in 8 patients with subclinical hypothyroidism (defined as absence of clinical signs of hypothyroidism with normal thyroid hormone levels, normal or slightly increased basal plasma TSH levels and increased and long-lasting TSH response to TRH) before and after l-thyroxine replacement therapy. Metoclopramide induced a significant (p < 0.01) TSH release in the subclinical hypothyroid patients. Two weeks after l-thyroxine replacement therapy (50 µg/day), the TSH response to metoclopramide was completely blunted in subclinical hypothyroidism. In these patients a significant (p < 0.01) inhibition of TSH response to intravenous thyrotropin-releasing hormone (TRH) was also observed after treatment with thyroid hormone. In analogy to the TSH behavior, plasma PRL secretion in response to metoclopramide and TRH administration was significantly (p < 0.05) inhibited in the subclinical hypothyroid patients after l-thyroxine replacement therapy.

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“…Regarding the elevation of the basal PRL level in the hypothyroid state, the following possibilities can be considered ; 1) negative feedback effect of thyroid hormones on the lactotrophs, as it is reported that elevated thyroid hormones have a direct suppressive effect on the pituitary lactotrophs (Sawers et al 1982), 2) decreased hypothalamic dopaminergic regulation on these cells or 3) increased TRH secretion (Feek et al 1980). From these explanations, the paradoxical elevation of the basal PRL level observed in this study is difficult to understand.…”

Section: Resultsmentioning

confidence: 81%

“…Contreras et al (1981) have postulated depressed hypothalamic dopaminergic tone in patients with hypothyroidism based on their findings that the patients showed the inadequate PRL response to dopamine receptor blocker. However, the exact relationships between thyroid function and hypothalamic dopaminergic activity are not fully studied (Sawers et al 1982). In order to evaluate these relationships, we examined the changes of basal PRL, TSH and their responsiveness to sulpiride (a dopamine receptor blocker) in patients with primary hypothyroidism, untreated or treated with thyroid replacement therapy.…”

mentioning

confidence: 99%

Enhanced prolactin secretion in patients with primary hypothyroidism during thyroid replacement.

Sato

Hanew

Sasaki

et al. 1984

Tohoku J. Exp. Med.

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Thyroid hormones are known to exert some influence on prolactin (PRL) secretion indirectly via the hypothalamic dopaminergic system and directly at the level of pituitary gland. In order to study the effect of thyroid hormones on the activity of hypothalamic dopamine neurons, lactotrophs and thyrotrophs, we administered increasing doses of thyroid hormones to patients with primary hypothyroidism, and examined the changes of basal PRL, TSH and PRL responses to a dopamine receptor blocker (sulpiride).Among 24 patients with primary hypothyroidism, hyperprolactinemia was observed in 10 cases (18.0-236 ng/ml, mean +S.E. 58.6+20.0 ng/ml), while elevated TSH levels were observed in all of them (6.6-972,uU/ml, mean ±S.E. 231.4+53.9,aU/ml). There was a significant negative relationship between plasma T3 or T4 levels and basal plasma TSH levels (p <0.05), whereas a poor correlation was observed between the thyroid hormones and basal plasma PRL levels (r = -0.25, p >0.05). Following the administration of gradually increasing doses of thyroid hormones, plasma PRL showed paradoxical and transient increases, while plasma TSH decreased steadily.Plasma PRL response to sulpiride also became exaggerated during the treatment.The elevated basal PRL level and the enhanced response to sulpiride turned to be within the normal range when the patients became euthyroid by treatment.These results may indicate that thyroid hormones stimulate not only hypothalamic dopaminergic activity, but also the lactotroph activity in a long term hypothyroid state. Regarding the paradoxical elevation of basal PRL, one can postulate that the activation of lactotroph by a small dose of thyroid hormone may be able to overcome the hypothalamic dopaminergic inhibition. primary hypothyroidism ; thyroid hormone ; prolactin ; sulpiride ; dopaminergic regulation

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Prolactin Response to Metoclopramide in Hyperthyroidism

Cited by 14 publications

References 9 publications

Effect of Thyroid Status on the Prolactin-Releasing Action of Vasoactive Intestinal Peptide in Humans: Comparison with the Action of Thyrotropin-Releasing Hormone

Effect of Thyroid Status on the Prolactin-Releasing Action of Vasoactive Intestinal Peptide in Humans: Comparison with the Action of Thyrotropin-Releasing Hormone

Prolactin and TSH Response to TRH and Metoclopramide before and after /-Thyroxine Therapy in Subclinical Hypothyroidism

Enhanced prolactin secretion in patients with primary hypothyroidism during thyroid replacement.

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