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Results for “hyperprolactinemia”

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PubMed1994

Effect of the slow-release formulation of somatuline (BIM 23014) on estrogen-induced hyperprolactinemia and lactotroph hyperplasia in the female rat.

Somatuline, in common with other SRIH analogues, exerts antiproliferative and antisecretory activities on various tumors. Our purpose was to test the effectiveness of a slow-release formulation of somatuline on lactotroph hyperplasia and PRL hypersecretion induced by estrogens (17 beta E2) in rats. Female rats were primed with 17 beta E2 for 6 weeks before receiving somatuline (2 mg/kg) intramuscular injections every 10 days for one month. The mean anterior pituitary weight was 11.22 +/- 0.32 mg (mean +/- SEM) in non-estrogenized rats, 29.62 +/- 1.63 mg in 17 beta E2-primed rats and 23.58 +/- 1.26 mg in 17 beta E2-primed somatuline-treated rats. Mean plasma PRL level was 5.63 +/- 0.97 ng/ml, 182.37 +/- 27.55 ng/ml and 113.89 +/- 15.07 ng/ml in the same groups respectively. Thus, the 17 beta E2-induced pituitary enlargement and hyperprolactinemia were 20% and 38% lower respectively when animals were treated with somatuline during the last month of estrogenization. The 17 beta E2-induced increase in PRL cell density was also reduced by somatuline treatment. We conclude that the slow-release formulation of somatuline impedes 17 beta E2-induced hyperprolactinemia and pituitary enlargement concomittantly, at least in part by acting on lactotroph proliferation.

Animals↗

PubMed1989

Defective natural killer cell activity in puerperal hyperprolactinemia.

Prolactin (PRL) influences immune reactivity in animals and in humans and both T-cell abnormalities and reduced natural killer (NK) cell activity have been reported in women with pathological hyperprolactinemia. To investigate further the possible interactions between PRL and the immune system in humans, we analysed T-cell phenotypes and NK cell activity in 15 women with physiological hyperprolactinemia of the puerperium and in 45 age-matched healthy normal cycling women. Puerperal women displayed a normal T-cell phenotype but a significant reduction in the number of Leu-7+ and Leu-11+ cells, associated with a decreased NK cell activity, as measured against K-562 target cells. There was a significant inverse correlation between the raised serum PRL levels and both the number of Leu-7+ cells and NK cell activity. These data confirm an important immunoregulatory role for PRL in humans and suggest a direct inhibitory effect of the chronically raised PRL concentrations on the maturation of NK cells.

Female↗

PubMed1982

Normal LHRH neuronal function and hyperprolactinemia in old pseudopregnant Fischer 344 rats.

The relative contributions of LHRH neuronal function and hyperprolactinemia to the maintenance of the repeated pseudopregnant (PP) state in old Fischer 344 rats were examined. LHRH concentrations within 8 microdissected regions of the preoptico-tuberal pathway were not different between normally cycling 4-5 and 10-11 months old rats and PP 22-23 months old rats. LHRH concentrations were significantly decreased in the median eminence and serum LH was increased 2 weeks after ovariectomy in all 3 age groups. Ovariectomy had no significant effect on LHRH concentrations in any of the other brain regions examined in these three age-groups. Serum prolactin levels were elevated 4-fold in old PP rats when compared to younger animals and these old PP rats failed to exhibit the normally observed decline in serum prolactin in response to ovariectomy. Daily treatment for 10 days with the dopamine agonist, CB-154, reinitiated normal ovarian cycles in 7 of 7 old PP rats while vehicle treatment was ineffective in altering the PP state. The data suggest that persistent hyperprolactinemia rather than impaired LH secretory mechanisms is primarily responsible for the PP state in old Fischer 344 rats.

Age Factors↗

PubMed1982

Partial hypopituitarism and hyperprolactinemia: successful induction of ovulation with bromocriptine and human menopausal gonadotropins.

The case of a patient who developed partial hypopituitarism (hypogonadotropism and growth hormone deficiency) following transphenoidal removal of a prolactinoma is described. Hypogonadotropism persisted despite restoration of normoprolactinemia with bromocriptine therapy. Successful induction of ovulation with human menopausal gonadotropin (hMG) and bromocriptine suppression of the hyperprolactinemia was carried out, resulting in a pregnancy. The pros and cons of operative and nonoperative management of hyperprolactinemia are discussed.

Adult↗

PubMed1984

Effects of short-term hyperprolactinemia on the endocrine reproductive system in male rabbits.

We have systematically studied the effects of short-term hyperprolactinemia on reproductive function in male rabbits. Purified ovine prolactin (PRL) was administered intravenously, as bolus injections or by constant infusion, to unanesthetized animals bearing two chronically implanted Silastic catheters; blood samples were obtained via the second catheter. Short-term hyperprolactinemia did not modify serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations in either castrated or intact rabbits. However, in spite of no changes in LH and FSH, short-term PRL administration lowered the serum testosterone (T) in intact animals. Furthermore, while PRL had no effect on the LH and FSH response to gonadotropin-releasing hormone, it did inhibit the testicular secretion of T in response to the increased endogenous LH. PRL also inhibited human chorionic gonadotropin-stimulated T secretion by the testes. All of these studies indicate that PRL interferes with the testicular response to LH. The fact that LH and FSH did not rise in response to the lowered T in intact animals suggested that PRL also altered the steroid feedback control of LH and FSH secretion. To assess this, PRL or saline was repeatedly injected after castration. PRL prevented the postcastration rise in LH and FSH. These studies indicate that PRL acts at at least two sites in the reproductive system in rabbits: (1) directly at a gonadal level by interfering with gonadotropin action and (2) at a hypothalamic-pituitary central level by preventing the expected rise in gonadotropins in response to low gonadal steroids.

Animals↗

PubMed1985

Hyperprolactinemia in primary adrenocortical insufficiency.

A patient with primary adrenocortical deficiency presented with galactorrhea and hyperprolactinemia, in addition to the usual characteristic symptoms of adrenal insufficiency. With steroid replacement therapy, PRL levels returned to normal, with resumption of normal ovulatory cycles; and the patient became pregnant. Primary adrenocortical deficiency should be considered as one of the very rare causes in the differential diagnosis of hyperprolactinemia.

Abdomen↗

PubMed1983

Gonadotropin secretion during prolonged hyperprolactinemia: basal secretion and the stimulatory feedback effect of estrogen.

Inoculation of cyclic female rats with the prolactin (Prl)/growth hormone-secreting pituitary tumor, MtT.W15, resulted in a cessation of estrous cyclicity within 5--10 days. Associated with this acyclicity was a persistently low serum concentration of estradiol and marked increases in both circulating Prl and progesterone. At Day 26 of acyclicity, basal serum luteinizing hormone (LH) values measured in samples taken every 20 min from 0900--1100 h were significantly reduced when compared to cyclic, nontumor animals on diestrus Day 2. There was no difference in basal follicle-stimulating hormone (FSH) concentrations. In a separate group of acyclic, tumor-bearing females 42--56 days after transplantation, a single s.c. injection of 20 micrograms estradiol benzoate (EB) at 1030 h elicited significant increases in both serum LH and FSH values between 1700 and 1830 h on the next day. The magnitude of the LH surge was reduced and that of FSH was increased in tumor-bearing animals when compared to cyclic, nontumor females given a similar EB injection on diestrus Day 1. These results demonstrate that chronic hyperprolactinemia is associated with inhibition of basal LH secretion and ovarian estrogen production and an increase in circulating progesterone concentrations. Nevertheless, the stimulatory feedback effects of estrogen on LH and FSH release are still present and functioning in acyclic female rats under chronically hyperprolactinemic conditions. These data suggest that the cessation of regular ovulatory cycles associated with hyperprolactinemia may be due to a deficiency of LH and/or estrogen secretion, but not to a lack of central nervous system response to the stimulatory feedback action of estrogen.

Animals↗

PubMed1985

Long-term bromocriptine therapy may restore the inhibitory control of prolactin release in some patients with pathological hyperprolactinemia.

While bromocriptine is effective in controlling hyperprolactinemia, it is not known if bromocriptine therapy can restore the abnormal regulation of prolactin (PRL) release found in patients with pathological hyperprolactinemia. We report 15 hyperprolactinemic patients treated for a mean duration of 5.5 +/- 0.6 years (mean +/- SE) in whom stimulation tests to assess PRL control mechanisms [thyrotropin releasing hormone (TRH) and metoclopramide] were performed before and at least one month after withdrawal of bromocriptine therapy. The basal PRL level after withdrawal of bromocriptine therapy was significantly lower (p less than 0.001) than that before therapy. All patients had blunted PRL stimulatory responses to TRH and metoclopramide (% delta 16.0 +/- 5.6%) before treatment. After withdrawal of bromocriptine, PRL responses to stimulatory tests were significantly improved in seven patients (termed 'responders', % delta 376 +/- 55%) but remained unchanged in eight patients (termed 'non-responders', % delta 9.2 +/- 3.0%). Basal PRL levels were significantly lower (p less than 0.01) in responders (290 +/- 35 mIU/l) than in non-responders (10360 +/- 6790 mIU/l). Four of the responders have maintained normoprolactinemia and normal stimulated PRL responses for 15 months to three years following cessation of bromocriptine therapy and appear to be in remission. Favourable factors amongst the responders were the female sex, absence of a macroadenoma, and a pre-treatment PRL level below 3000 mlU/l. PRL stimulation tests performed before therapy could not predict which patients would respond. No relationship was found between duration of therapy, or age at presentation, and improvement after bromocriptine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

PubMed1981

Hyperprolactinemia counteracts the testosterone-induced inhibition of the preoptic area dopamine turnover.

The present study was undertake to determine the effects of hyperprolactinemia on dopamine (DA) concentrations and turnover rates in the medial basal hypothalamus (MBH) and the preoptic area-suprachiasmatic nucleus region (POA-SCN) in castrated and castrated, testosterone(T) implanted male rats. Subcutaneous implants, which raised serum T levels to those found in intact rats, decreased serum LH to basal levels but did not alter DA turnover in the MBH. Anterior pituitary (AP) transplants under the renal capsule increased serum prolactin to 60-110 ng/ml, and accelerated DA turnover by nearly 2-fold in the MBH of both castrated and castrated, T-implanted rats without influencing serum LH levels. While T implants caused a decrease in the POA-SCN DA turnover, high serum prolactin levels produced by AP implants in castrated rats were ineffective in altering POA-SCN DA turnover. However, in the presence of physiological levels of T, these elevated serum prolactin levels not only blocked the T-induced decrease in POA-SCN DA turnover, but further augmented DA turnover over that observed inthe castrated or castrated, T-implanted rats. These results indicate that (i) for acceleration of the MBHDA turnover by prolactin T priming is not essential and it appears to occur at serum prolactin levels which fdo not depress serum LH levels, and (ii) the stimulatory effects of prolactin on the POA-SCN DA turnover are dependent upon the presence of circulating T. Since these synergistic effects of prolactin and T on the POS-SCN DA turnover are not involved in the regulation of gonadotropin secretion, their participation in attenuation of male sexual behavior associated with hyperprolactinemia is discussed.

Animals↗

PubMed1978

Effect of hyperprolactinemia on pituitary-adrenal function.

Three patients with hyperprolactinemia (2 with pituitary tumors and 1 with a hypothalamic disturbance) underwent evaluation of their hypothalamic-pituitary-adrenal axis using ACTH, metyrapone and in one case repetitive insulin tolerance tests. With the exception of a suggestion of a slight increase in adrenal responsiveness to pharmacological doses of ACTH in one of the patients, there was no alteration in the adrenal responsiveness of the 3 patients evaluated. We conclude that hyperprolactinemia probably does not systematically modify the responsiveness of the hypothalamic-pituitary-adrenal axis.

Adenoma, Chromophobe↗

PubMed1985

Delayed puberty and hypoplastic uterus associated with hyperprolactinemia: successful treatment with bromocriptine.

A 15-year-old girl referred because of primary amenorrhea was found to have a hypoplastic uterus and persistent hyperprolactinemia (72-110 ng/ml). The gonadotrophin-dependent pubertal signs, i.e. breast and vulvar development, were significantly retarded (Tanner stage 2-3) while sexual hair was well developed; bone age was 13 years. The endocrinological evaluation revealed gonadotrophin secretion (LH-basal: 0.85-1.25; peak after LH-RH: 10.4 mIU/ml; FSH-basal: 1.63-2.5; peak: 8.2 mIU/ml) and E2 levels (26-68 pg/ml) which were appropriate for Tanner stage 3. The high basal levels of PRL were nonresponsive to either stimulatory (TRH) or inhibitory (nomifensine) agents. CT scan of the brain suggested the presence of a pituitary microadenoma. Following therapy with bromocriptine (2.5 mg/day) plasma PRL levels dropped to normal (5-6.8 ng/ml) with an accompanying catch-up of pubertal development and linear growth and a marked increase in size of the uterus as documented by repeated ultrasonographic examinations. Menarche occurred 5 months after initiation of therapy, followed by regular menses thereafter. Repeated CT scan of the brain showed a decrease in the density and size of the still persisting lesion. This patient demonstrates that hyperprolactinemia can cause delayed puberty with a particular inhibitory effect on uterine growth and development.

Adenoma↗

PubMed1981

Hyperprolactinemia in chronic renal failure: impaired responsiveness to stimulation and suppression. Normalization after transplantation.

(PRL) secretion was investigated in 12 undialyzed patients with chronic renal failure (CRF), 30 hemodialyzed patients (HD), 19 renal transplant (RT) recipients and 17 controls. Basal PRL levels in CRF and HD patients were higher than in controls and RT subjects. Plasma PRL values were higher in CRF than in HD patients. In the HD group, plasma PRL concentrations were significantly higher in men with reduced sexual potency than in those in which it was normal. After TRH stimulation in CRF and HD the PRL response was considerably less and the time of peak delayed with respect to the controls. In RT subjects PRL did not return towards baseline after 120 min. After bromocriptine, plasma PRL suppression in CFR and HD patients ws lower than in controls and RT subjects. These findings suggest that some factor which accumulates in uremia, is only partially removed by hemodialysis, and might be responsible for the hyperprolactinemia and might also interfere with the binding of TRH and bromocriptine to their respective pituitary receptors. Although a pituitary defect seems to be prevalent, a concomitant hypothalamic disorder cannot be excluded. Hyperprolactinemia seems to play a role in the sexual disturbances showed by some HD men. Whatever the alterations responsible for the impaired PRL regulation in uremia are, they are reversed by successful renal transplant.

Adolescent↗

PubMed1984

Hyperprolactinemia and sexual disturbances among uremic women on hemodialysis.

The investigation of a sample of 99 women on maintenance hemodialysis has shown the presence of sexual disturbances to a great extent: the rate of sexual intercourse and the ability to reach orgasm were significantly lower than in age-matched control women. 80% declared a reduction in their sexual desire and the frequency of intercourse was also lower as compared to the period prior to dialysis. Ageing decreased the sexual activity in both the ill and healthy population, but in uremic patients the sexual activity ended at an earlier age. The patients with hyperprolactinemia reported lower frequencies of intercourse and lower percentages of orgasm than normoprolactinemic ones. The incidence of sexual dysfunction and the role of hyperprolactinemia in this respect were similar to those which are found among male patients on hemodialysis.

Adult↗

PubMed1985

Central opioid receptor activity in patients affected by puerperal, idiopathic and tumoral hyperprolactinemia.

The aim of our study was to evaluate the activity of opioid receptors involved in the regulation of prolactin secretion in different kinds of hyperprolactinemic states (puerperal, idiopathic and tumoral subjects). Prolactin plasma level changes were measured after the acute administration of a met-enkephalin synthetic analogue. FK 33-824, and placebo. The prolactin-releasing effect of this drug, evident in control subjects, was blunted in patients affected by idiopathic hyperprolactinemia, and absent in puerperal and tumoral patients. These results indicate that hyperprolactinemia affects the activity of central opioid receptors, with the most evident effects in patients with highest prolactin plasma levels.

Adenoma↗

PubMed1982

Influence of sulpiride-induced hyperprolactinemia on baboon menstrual cycles: a longitudinal study.

The influence of sulpiride-induced hyperprolactinemia on the hypothalamic-pituitary-ovarian function of the baboon (Papio cynocephalus) was investigated. Plasma levels of prolactin, LH, FSH, estrone, estradiol, 17-hydroxyprogesterone, progesterone and 20 alpha-dihydroprogesterone in control and consecutive treatment cycles (sulpiride i.m. injections 100 mg/day) were determined serially. The hormonal changes indicate that the ovary is the most sensitive site to the direct inhibitory action of sulpiride-induced hyperprolactinemia.

Animals↗

PubMed1984

Hyperprolactinemia, distress, and hostility.

The scores of 14 women with hyperprolactinemia on the Symptom Rating Test and the Symptom Questionnaire were compared with those of nonpsychotic women attending a psychiatric clinic, women attending a family practice clinic, and female nonpatient employees. The scores of the hyperprolactinemic women were similar to those of the psychiatric patients. Hyperprolactinemic patients were significantly more hostile, depressed, and anxious and had more feelings of inadequacy than family practice patients and nonpatient employees. The authors recommend measuring the serum prolactin levels of women with depression, hostility, anxiety, and symptoms or signs suggestive of hyperprolactinemia.

Adult↗

PubMed1977

Effects of experimentally-induced chronic hyperprolactinemia on testosterone and gonadotropin levels in male rats and mice.

We have examined testicular and pituitary function in inbred CD-F rats and DBA/2J mice with chronic hyperprolactinemia induced by grafting 4 anterior pituitaries from adult females of the same strain under the kidney capsule. Eight rats were given pituitary isografts and 9 were sham-operated; blood samples were collected at 4-7 week intervals, and the animals were killed 6 months later. One month after surgery, PRL levels in grafted rats were elevated (348 +/- 15 vs. 94 +/- 11 ng/ml; P less than 0.001), LH levels were depressed (16 +/- 3 vs. 59 +/- 9 ng/ml; P less than 0.001), but T levels were not affected (1.0 +/- 0.1 vs. 1.1 +/- 0.2 ng/ml). The elevated PRL levels in grafted animals did not decline during the subsequent 5 months, while LH levels increased slightly, and T levels remained indistinguishable from those in the controls. At the time of autopsy, FSH levels were reduced in grafted rats (230 +/- 40 vs. 501 +/- 108 ng/ml; P less than 0.05). Multiple pituitary isografts did not affect the weight of the testes or the ventral prostate, but increased the weight of the seminal vesicles (P less than 0.001). In 11 mice examined 5.5 months after receiving pituitary isografts, plasma PRL levels were dramatically elevated (330 +/- 35 vs. 27 +/- 2 ng/ml; P less than 0.001), but plasma T levels and testicular weight were not different from those observed in 12 sham-operated controls. The weight of the seminal vesicles in grafted mice was increased (P less than 0.01). In both rats and mice, chronic hyperprolactinemia did not affect plasma testosterone levels or testes weight and increased seminal vesicle weight.

Adrenal Glands↗

PubMed1981

Effects of chronic hyperprolactinemia in mice on plasma gonadotropin concentrations and testicular human chorionic gonadotropin binding sites.

Effects of artificially induced hyperprolactinemia in male DBA/2 mice were studied by transplanting four pituitary glands under the kidney capsules. After 52--57 days the animals were sacrificed, and tissue and plasma samples were obtained. Plasma concentrations of FSH and LH were significantly higher in pituitary-grafted mice than in sham-operated controls. Testicular LH/human chorionic gonadotropin (hCG) binding, measured via use of [125I]iodo-hCG, was significantly depressed both on a per milligram protein and per testes basis in hyperprolactinemic mice. Coincident with decreased hCG binding was a significantly diminished ability of decapsulated testes to produce testosterone in response to hCG in vitro. However, testosterone production by unstimulated hyperprolactinemic mouse testes was normal. Significantly increased body, seminal vesicle, and adrenal weights were also present in hyperprolactinemic mice. The data indicate that hyperprolactinemia in mice is associated with decreased testicular LH/hCG binding and a concomitant decrease in the responsiveness to hCG in vitro. These actions may be mediated by increased plasma LH concentrations.

Animals↗