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Pulsatile Prolactin Secretion in Hyperprolactinemia due to Presumed Pituitary Stalk Interruption

Division of Endocrinology, University of Texas Health Science Center San Antonio, Texas 78284–7877
The Divisions of Endocrinology and Metabolism University of Colorado Health Sciences Center Denver, Colorado 80262
Pathology University of Colorado Health Sciences Center Denver, Colorado 80262
Neurosurgery University of Colorado Health Sciences Center Denver, Colorado 80262

Address requests for reprints to: Dr. M. H. Samuels, Department of Medicine, Division of Endocrinology, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, Texas 78284–7877.

PRL, like other anterior pituitary hormones, is normally secreted in a pulsatile fashion. However, it is not known whether such pulses depend on dopamine and/or other hypothalamic factors. This question can be addressed by investigating patients with large pituitary mass lesions, since such patients often have hyperprolactinemia due to disruption of normal hypothalamic input to the pituitary gland. Six such patients (5 with non-PRL-secreting tumors and 1 with a craniopharyngioma) and 11 healthy control subjects had PRL levels measured every 15 min over 24 h. PRL pulses were located by cluster analysis. All patients had PRL pulses of normal frequency, but increased amplitude. Circadian variation in PRL pulse amplitude, present in healthy women, was abolished in tumor patients. These results imply that normal pituitary levels of dopamine do not control the generation of PRL pulses. Instead, PRL pulses may arise from the pituitary gland, with pulse amplitude and circadian rhythm modulation by dopamine and other hypothalamic factors. Alternatively, the mild hyperprolactinemia associated with large hypothalamic-pituitary tumors may represent partial impairment of dopamine secretion, with sufficient pituitary dopamine levels to maintain normal PRL pulse frequency.

^* This work was supported in part by Adult GCRC Grant M01–RR–00051 and NIH Grants DK–36843–03 (to M.H.S.), CA–47411–01, and DK–36843 (to E.C.R.).

Received April 18, 1991.

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