Tests of Prolactin Secretion in Diagnosis of Prolactinomas

Cowden, E.A.; Thomson, John A.; Doyle, D; Ratcliffe, John G.; Macpherson, P.; Teasdale, Graham M.

doi:10.1016/s0140-6736(79)91841-5

Cited by 99 publications

(29 citation statements)

References 18 publications

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“…The provocative agents included thyrotropin releasing hormone (TRH), chlorpromazine, levodopa, carbidopa, domperidone, nomifensine and insulin induced hypoglycemia [24][25][26][27][28][29][30]. Unfortunately all of these tests are nonspecific and blunted prolactin responses occur in patients with prolactinomas, hypothalamic tumors and in non-tumoral hyperprolactinemia.…”

Section: Dynamic Tests Of Prolactin Secretionmentioning

confidence: 99%

Hyperprolactinemia

Chahal

Schlechte

2008

Pituitary

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In several respects prolactin is unique among anterior pituitary hormones. The primary regulation of prolactin secretion is mediated through hypothalamic inhibition, and the diagnosis of hyperprolactinemia can be established without the use of stimulation or suppression tests. Documenting the presence of hyperprolactinemia is not difficult-the challenge is in identifying the cause of the hormone hypersecretion. With immunoradiometric assays falsely low levels of prolactin are occasionally seen in patients with macroadenomas and very high serum prolactin (the hook effect). Macroprolactin should be suspected when a patient with hyperprolactinemia does not present with typical clinical symptoms, and all hyperprolactinemic sera should be screened for macroprolactin. With prolactinomas, prolactin levels generally parallel tumor size. Prolactin secreting macroadenomas are typically associated with levels that exceed 250 microg/l and may exceed 1,000 microg/l. Large non-functioning adenomas also lead to hyperprolactinemia but levels virtually never exceed 94 microg/l. Acquired and isolated prolactin deficiency is rare.

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Section: Dynamic Tests Of Prolactin Secretionmentioning

confidence: 99%

Hyperprolactinemia

Chahal

Schlechte

2008

Pituitary

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“…In 6 patients, the presence of a pituitary adenoma was determined by the finding of abnormalities on plain skull x-ray and/or CAT scanning but in the remaining 4 patients, radiological changes were less clear cut. All patients, however, had reduced or absent PRL responses (rise of <100% basal levels) to acute DA antagonism (domperidone, 10 mg iv) and TRH administration (200 ng iv) consistent with the diagnosis of prolactinoma (19), but not unequivocal proof of it. Each subject received the DA receptor-blocking drug domperidone (10 mg iv) at 1100 and 2300 h, and tests were carried out after a 12-h fast, with subjects lying at rest, and blood sampling was via forearm iv cannulae.…”

Section: Methodsmentioning

confidence: 89%

Exaggerated Circadian Variation in Basal Thyrotropin (TSH) and in the Dopaminergic Inhibition of TSH Release in Pathological Hyperprolactinemia: Evidence Against a Hypothalamic Dopaminergic Defect

Rodríguez-Arnao

Peters

Foord

et al. 1983

The Journal of Clinical Endocrinology & Metabolism

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In order to delineate more accurately the dopaminergic control of anterior pituitary function in normal subjects and in patients with pathological hyperprolactinemia, we investigated the nature of the circadian variation in the dopaminergic inhibition of TSH release in such subjects. Ten euthyroid women with hyperprolactinemia due to presumed PRL-secreting microadenomas (aged 18-60 yr) were compared with 11 normal, euthyroid women (aged 18-32 yr). Each received the dopamine receptor blocking drug domperidone (10 mg, iv) at 1100 and 2300 h (tests randomized and separated by at least 1 week). Blood was sampled 10, 20, 30, 45, and 60 min after drug administration. Normal women had a greater TSH response to domperidone and, hence, greater dopaminergic inhibition of TSH release at 2300 than at 1100 h (sum of TSH increments; mU/liter mean +/- SE, 8.5 +/- 1.3 vs. 4.8 +/- 0.5, P less than 0.01), whereas there was no difference in the dopaminergic inhibition of PRL release at each time of day. Hyperprolactinemic women also had a significantly greater TSH response to domperidone at 2300 than at 1100 h (42.0 +/- 10.2 vs. 19.1 +/- 2.8, P less than 0.001). The hyperprolactinemic women had a greater TSH response to domperidone than normal women at each time of day studied (1100 h, 19.1 +/- 2.8 vs. 4.8 +/- 0.5, P less than 0.001; 2300 h, 42.0 +/- 10.2 vs. 8.5 +/- 1.3, P less than 0.001). The incremental PRL responses to domperidone were significantly less in hyperprolactinemic than in normal women and did not differ at each time of day. In conclusion, the circadian change in the dopaminergic inhibition of TSH secretion is specific for TSH and not PRL. This indicates that the dopaminergic control of TSH and PRL secretion can be dissociated in normal subjects. Second, hyperprolactinemic women with presumed PRL-secreting microadenomas had qualitatively normal but quantitatively exaggerated circadian pattern of dopaminergic inhibition of TSH release. These data argue against a hypothalamic dopaminergic defect in hyperprolactinemia and support the view that the established dopaminergic defect in the inhibition of PRL release is related specifically to PRL control and may well be at the anterior pituitary level.

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“…The day-to-day reproducibility was 6%, 7%, and 9% for norepinephrine, epinephrine, and dopamine, respectively. Plasma prolactin was measured with a radioimmunoassay (RIA) kit (HPRLK-PR) (CIS, Gif-Sur-Yvette, France) (Cowden et al 1979). Accuracy was 4%-6% for within-run assay and 5%-9% for day-to-day reproducibility.…”

Section: Biochemical Measuresmentioning

confidence: 99%

Catecholamines in Autistic Disorder: Effects of Amisulpride and Bromocriptine in a Controlled Crossover Study

Dollfus¹,

Petit²,

Garnier³

et al. 1993

Journal of Child and Adolescent Psychopharmacology

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The biochemical effects on catecholaminergic systems of the dopamine antagonist amisulpride and the dopamine agonist bromocriptine were evaluated in a double-blind, randomized, crossover study in children with autistic disorder. Plasma levels of dopamine, norepinephrine, and epinephrine; urinary concentrations of homovanillic acid (HVA), vanillyImandelic acid (VMA) and 3-methoxy-4-hydroxyphenylethylene glycol (MHPG); and plasma prolactin were measured. At doses of amisulpride and bromocriptine that had the expected opposing effects on plasma prolactin, the drugs' effects on the catecholaminergic systems were similar. Both agents unexpectedly lowered urinary HVA (total, free, and sulfated) although only amisulpride decreased the HVA levels significantly. This paradoxical decrease in HVA levels suggests that both dopamine agonists and antagonists could act on autoreceptors or presynaptic dopaminergic receptors in the central nervous system. There was no significant action of either drug on plasma epinephrine, urinary VMA, or urinary MHPG, suggesting that neither drug altered norepinephrine or epinephrine systems; however, a weak increase of plasma norepinephrine occurred after amisulpride treatment, consistent with effects observed with other neuroleptics. Neither agent altered plasma dopamine, suggesting that peripheral dopamine metabolism was unchanged. The clinical effects of amisulpride and bromocriptine have been reported to be unexpectedly complementary. The complementary clinical effects of a dopamine agonist and dopamine antagonist might speculatively be related to their similar action on dopamine autoreceptors, leading to a correction of the dopaminergic hyperactivity that has been postulated in autistic children.

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Tests of Prolactin Secretion in Diagnosis of Prolactinomas

Cited by 99 publications

References 18 publications

Hyperprolactinemia

Hyperprolactinemia

Exaggerated Circadian Variation in Basal Thyrotropin (TSH) and in the Dopaminergic Inhibition of TSH Release in Pathological Hyperprolactinemia: Evidence Against a Hypothalamic Dopaminergic Defect

Catecholamines in Autistic Disorder: Effects of Amisulpride and Bromocriptine in a Controlled Crossover Study

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