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PubMed2003

Hyperprolactinemia and sexual function in men: a short review.

Erectile dysfunction (ED), generally associated with reduced sexual desire and sometimes with orgasmic or ejaculatory dysfunction, is the major revealing symptom of hyperprolactinemia (HPRL) in men, a condition that should not be neglected since many cases result from pituitary tumors, likely to result in serious complications. It is generally believed that the mechanism of the prolactin (PRL)-induced sexual dysfunctions is a decrease in testosterone secretion. In fact, serum testosterone is normal in many hyperprolactinemic males and there are also testosterone-independent mechanisms, probably mainly set at the level of the brain's neurotransmitter systems. Systematic determinations of serum PRL found very low prevalences of marked HPRL (>35 ng/ml) in ED patients (0.76% in a compilation of over 3200 patients) as well as of pituitary adenomas (0.4%). In addition, the association of HPRL with ED may have been coincidental in some of these cases, since 10% of the HPRLs diagnosed by the usual immunological assays are composed of macroprolactins, which are biologically inactive or little active variants of PRL. Their identification requires a PRL chromatography that is restricted to some specialized laboratories. There is presently no consensus with regards to the screening for HPRL in ED: systematic determination of serum PRL may be justified since HPRL is a serious but reversible disease, while there is presently no reliable clinical, psychometric or hormonal criteria (including serum testosterone level) allowing to restrict its determination to certain categories of the ED patients without risk of neglecting some HPRLs. In case of consistent HPRL, searching for a hypothalamic or pituitary tumor is mandatory. Dopamine-agonist therapy is the first choice treatment for the PRL-induced sexual dysfunctions. Additional sexual counselling may be necessary for certain patients.

Erectile Dysfunction↗

PubMed1995

Identification of macroprolactin in a patient with asymptomatic hyperprolactinemia as a stable PRL-IgG complex.

We characterize the molecular form of PRL in a female patient with asymptomatic, idiopathic hyperprolactinemia. Size exclusion chromatography revealed that PRL was present exclusively in the form of macroprolactin (> 200 kD mol wt). By immunoaffinity purification, Western blot analysis, and binding studies the molecule was identified as a PRL-IgG complex of extremely high stability. Sequence analysis revealed no mutations in the protein coding region of the hPRL gene using hPRL cDNA amplified from the patient's peripheral blood lymphocytes. In spite of full bioactivity in vitro, as determined by Nb2 bioassay, the complex apparently lacks bioactivity in vivo. Its high molecular weight may reduce its access to target organs in the periphery as well as centrally.

Adult↗

PubMed2006

Hyperprolactinemia of pregnancy is not associated with increased in vivo platelet activity and shortened in vitro bleeding times.

The aim of the study is to investigate whether platelet activity is increased by hyperprolactinemia during pregnancy as reflected by beta-thromboglobulin level. Forty-eight healthy, pregnant, and 30 healthy, non-pregnant women were investigated with respect to platelet count, collagen/ADP and collagen/epinephrine closure times, beta-thromboglobulin and prolactin levels. The comparison of the variables between the two groups was made by Mann-Whitney U test. The correlation analyses were performed by Spearman's rank correlation test. Our results revealed that platelet counts, collagen/ADP and collagen/epinephrine closure times and beta-thromboglobulin showed no statistically significant differences between pregnant and non-pregnant women. We found no significant correlation between prolactin and collagen/ADP closure time (r = 0.175), between prolactin and collagen/epinephrine closure time (r = -0.112) and between prolactin and beta-thromboglobulin (r = 0.220) in pregnant women. Our findings suggest that platelet activity is comparable during pregnant and non-pregnant states and there is no significant effect of prolactin on platelet function in vivo as reflected by beta-thromboglobulin level.

Adenosine Diphosphate↗

PubMed1987

Catecholamines and pituitary function. VI. Effect of different dopamine doses on TRH-induced prolactin release in women with pathological hyperprolactinemia.

The present study was designed to examine the effect of low-dose dopamine (DA) infusion rates (0.02 and 0.1 microgram/kg X min) on both basal and TRH-stimulated prolactin release in normal and hyperprolactinemic individuals. Sixteen normally menstruating women in the early follicular phase of a cycle and 23 hyperprolactinemic patients were studied. 0.1 microgram/kg X min DA was infused in 8 normal women and 15 patients with pathological hyperprolactinemia, while 8 normal controls and 8 patients received 0.02 microgram/kg X min DA TRH (200 micrograms, i.v.) was administered alone and at the 180th min of the 5-hour DA infusion in all controls and patients. A significant reduction in serum PRL levels, which was similar in normal women (-59.5 +/- 4.0%, mean +/- SE) and hyperprolactinemic patients (-48.2 +/- 5.5) was observed in response to 0.1 microgram/kg X min DA. In normal cycling women DA infusion significantly (P less than 0.02) reduced the PRL response to TRH with respect to the basal TRH test (delta PRL 45.0 +/- 7.0 vs. 77.9 +/- 15.4 ng/ml). On the contrary, the PRL response to TRH was significantly higher during 0.1 microgram/kg X min DA than in basal conditions in hyperprolactinemic patients, both in absolute (delta PRL 91.8 +/- 17.6 vs. 38.4 +/- 6.8, P less than 0.03) and per cent (198.5 +/- 67.6 vs. 32.1 +/- 7.5, P less than 0.02) values. A normal PRL response to TRH, arbitrarily defined as an increase greater than 100% of baseline, was restored in 11 out of 15 previously unresponsive hyperprolactinemic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Dopamine↗

PubMed1985

Hyperprolactinemia inhibits development of Leydig cell tumors in aging Fischer rats.

In inbred CDF (Fischer 344) male rats autopsied at the age of 18-24 months, testicular tumors were present in 24 of 36 control animals but in none of 28 males rendered hyperprolactinemic by transplantation of anterior pituitaries from adult females under the renal capsules. In another experiment, microscopically detectable Leydig cell adenomas were present in each of 11 control animals at the age of 14.5 months but in none of 11 males in which hyperprolactinemia was induced by treatment with diethylstilbestrol. Development of testicular tumors had initially little effect on basal and hCG-stimulated plasma testosterone and androstenedione levels but eventually led to atrophy of the seminal vesicles. Incubated tumor tissue produced large quantities of progesterone and responded to hCG in vitro by an increase in progesterone but not testosterone secretion. Daily sperm production and epididymal sperm reserves were significantly reduced already during early stages of Leydig cell tumor development. We propose that hyperprolactin prevents development of Leydig cell tumors by suppression of plasma LH levels and suggest that age-related reductions in gametogenic and steroidogenic functions of the testes in Fischer rats are due to development of Leydig cell tumors rather than to aging per se.

Age Factors↗

PubMed2004

A prospective study of hyperprolactinemia in children and adolescents treated with atypical antipsychotic agents.

OBJECTIVE: Few studies have prospectively compared the change of prolactin levels in children and adolescents associated with the use of atypical antipsychotic agents. In our study, we present preliminary data of an ongoing study, which compares changes in prolactin levels in children and adolescents after treatment to risperidone versus olanzapine versus quetiapine. We hypothesized: (1) risperidone would be associated with hyperprolactinemia most frequently, and (2) postpubertal females may be at higher risk of prolactin elevation and associated adverse effects. METHODS: Prolactin levels were obtained at baseline and after a mean of 11.2 weeks (SD = 2.2; range, 4-15 weeks) from 40 subjects (mean age, 13.4 years; SD = 3.4; range, 5-18 years) who were started on risperidone (n = 21), olanzapine (n = 13), or quetiapine (n = 6). End-point prolactin levels were compared using a Kruskal-Wallis test. RESULTS: End-point prolactin levels were significantly higher with risperidone, compared to olanzapine (p = 0.027) or quetiapine (p = 0.008). With the Bonferroni correction, the latter remains significant. Twenty-five percent of our subjects experienced sexual side effects at end point, independent of prolactin levels and antipsychotic agents. CONCLUSION: Risperidone significantly increased prolactin levels in children and adolescents. The duration of this prolactin elevation, and its long-term effects in children and adolescents, are unknown.

Adolescent↗

PubMed1987

Effects of hyperprolactinemia on the control of luteinizing hormone and follicle-stimulating hormone secretion in the male rat.

Experiments were conducted to determine the effects of acute hyperprolactinemia (hyperPRL) on the control of luteinizing hormone and follicle-stimulating hormone secretion in male rats. Exposure to elevated levels of prolactin from the time of castration (1 mg ovine prolactin 2 X daily) greatly attenuated the post-castration rise in LH observed 3 days after castration. By 7 days after castration, LH concentrations in the prolactin-treated animals approached the levels observed in control animals. HyperPRL had no effect on the postcastration rise in FSH. Pituitary responsiveness to gonadotropin hormone-releasing hormone (GnRH), as assessed by LH responses to an i.v. bolus of 25 ng GnRH, was only minimally effected by hperPRL at 3 and 7 days postcastration. LH responses were similar at all time points after GnRH in control and prolactin-treated animals, except for the peak LH responses, which were significantly smaller in the prolactin-treated animals. The effects of hyperPRL were examined further by exposing hemipituitaries in vitro from male rats to 6-min pulses of GnRH (5 ng/ml) every 30 min for 4 h. HyperPRL had no effect on basal LH release in vitro, on GnRH-stimulated LH release, or on pituitary LH concentrations in hemipituitaries from animals that were intact, 3 days postcastration, or 7 days postcastration. However, net GnRH-stimulated release of FSH was significantly higher by pituitaries from hyperprolactinemic, castrated males. To assess indirectly the effects of hyperPRL on GnRH release, males were subjected to electrical stimulation of the arcuate nucleus/median eminence (ARC/ME) 3 days postcastration. The presence of elevated levels of prolactin not only suppressed basal LH secretion but reduced the LH responses to electrical stimulation by 50% when compared to the LH responses in control castrated males. These results suggest that acute hyperPRL suppresses LH secretion but not FSH secretion. Although pituitary responsiveness is somewhat attenuated in hyperprolactinemic males, as assessed in vivo, it is normal when pituitaries are exposed to adequate amounts of GnRH in vitro. Thus, the effects of hyperPRL on pituitary responsiveness appear to be minimal, especially if the pituitary is exposed to an adequate GnRH stimulus. The suppression of basal LH secretion in vivo most likely reflects inadequate endogenous GnRH secretion. The greatly reduced LH responses after electrical stimulation in hyperprolactinemic males exposed to prolactin suggest further that hyperPRL suppresses GnRH secretion.

Animals↗

PubMed1989

Effect of hyperprolactinemia on luteinizing hormone and prolactin secretion assessed using the reverse hemolytic plaque assay.

Hyperprolactinemia (hyperPRL) frequently suppresses luteinizing hormone (LH) and endogenous rat prolactin (rPRL) secretion under a variety of experimental circumstances. Several lines of evidence suggest that elevated prolactin (PRL) may act at the hypothalamic-pituitary axis to inhibit pituitary hormone secretion. The goal of this study was to determine whether hyperPRL, achieved by administration of ovine PRL (oPRL), influences LH and rPRL secretion as assessed by the reverse hemolytic plaque assay. Young Sprague-Dawley rats were ovariectomized on Day 0 and were treated with oPRL (4 mg/kg body weight, 3 times/day) beginning at 0900 h on Day 4. They were killed at 1000 h on Day 6, anterior pituitaries were collected, and cells were dispersed and prepared for the reverse hemolytic plaque assay. We analyzed mean plaque area by using a computerized image analysis system and determined the percentage of plaque-forming cells by counting the number of plaques compared to the total number of cells. HyperPRL decreases the percentage of LH plaque-forming cells under basal conditions. Although the mean LH plaque area was the same in vehicle-treated and oPRL-treated rats under basal and gonadotropin-releasing hormone-stimulated conditions, hyperPRL altered the frequency distribution of different-sized plaques under basal conditions. It appears that hyperPRL shifts the distribution of different-sized plaques such that there are more small plaques and no plaques of the largest size classes. Basal and thyrotropin-releasing hormone-induced rPRL release from single lactotropes, as measured by mean plaque area and the percentage of plaque-forming cells, is lower in lactotropes from hyperPRL rats than in controls after 1 h, but not 2 h, of incubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Prolactin dynamics in a patient with isolated ACTH deficiency accompanied by hyperprolactinemia.

Case of isolated ACTH deficiency accompanied by hyperprolactinemia was reported. Prolactin (PRL) secretory dynamics were evaluated by several stimulation (thyrotropin-releasing hormone [TRH], sulpiride) and suppression (L-dopa) tests. Before glucocorticoid replacement therapy, both TRH and sulpiride administration resulted in PRL hyper-responsiveness. The sulpiride-induced PRL increase was higher than that induced by TRH. L-dopa administration resulted in normal PRL suppression. Following glucocorticoid replacement therapy, the elevated basal PRL level returned to normal, and PRL hyper-responsiveness to TRH or sulpiride also returned to normal. These data suggest that the elevation of basal PRL level and PRL hyper-responsiveness observed in this patient is caused by glucocorticoid deficiency.

Adrenocorticotropic Hormone↗

PubMed1992

Hyperprolactinemia in systemic lupus erythematosus: association with disease activity.

This study was designed to determine the prevalence and clinical significance of hyperprolactinemia in systemic lupus erythematosus (SLE) and other rheumatic diseases. Basal levels of prolactin were determined in 130 nonselected sera from patients with rheumatic diseases including 45 with SLE, 31 with rheumatoid arthritis, 23 with osteoarthritis, 18 with fibromyalgia, and 13 with polymyalgia rheumatica. Serum samples of 28 healthy subjects were used as normal controls. Serum prolactin was measured by radioimmunoassay. ANA, anti-DNA, RNP, Sm, Ro, La, and anticardiolipin antibodies were determined by standard techniques. Elevated serum levels of prolactin (PRL greater than 20 ng/ml) were found in a subset of SLE patients. In addition, a direct correlation with clinical disease and serological (ANA) activity was also found. These findings suggest a potential role for this immunoregulatory hormone in SLE pathogenesis.

Adult↗

PubMedDate not supplied

Effects of oestrogen-induced hyperprolactinemia on the rat prostate.

Exposure of intact rats to increasing doses of oestradiol-17 beta in the presence of a constant amount of exogenous androgen caused a dose-related increase in the concentration of zinc in the lateral lobes and a decrease in the levels of ventral lobe prolactin binding. These changes occurred concomitantly with a dose-dependent increase in plasma prolactin levels, and could not be obtained in hypophysectomized rats given the same steroid treatment. In the intact animals a dose-dependent decrease in the responsiveness of the prostaglandin E1-dependent adenylyl cyclase in the ventral lobe was observed, an effect which has earlier been shown to be prolactin mediated. The results indicate that oestrogen has indirect effects on specific parameters of prostate function by inducing a relative hyperprolactinemia. This model may be useful in studying effects of chronically and physiologically elevated levels of endogenous prolactin on the rat prostate.

Adenylyl Cyclases↗

PubMed1996

Effectiveness of shakuyaku-kanzo-to in neuroleptic-induced hyperprolactinemia: a preliminary report.

We investigated the efficacy of Shakuyaku-kanzo-to (TJ-68) in neuroleptic-induced hyperprolactinemia in 11 treated schizophrenic patients. The mean plasma prolactin level decreased significantly from 28.9 +/- 14.5 ng/mL at baseline to 22.0 +/- 15.2 ng/mL at 4 weeks. Potassium levels did not change significantly. Neither the exacerbation of psychosis nor other adverse effects occurred.

Adult↗

PubMed1988

Effects of human chorionic gonadotropin, androgens, adrenocorticotropin hormone, dexamethasone and hyperprolactinemia on plasma sex steroid-binding protein.

This presentation reports the effects of androgens, glucocorticoids and some pituitary hormones on plasma sex steroid-binding protein (SBP). The latter was measured by a solid phase method after desteroidation of the plasma. An hCG test (1500 I.U. every other day X 7) was given to 60 boys. In the children with a normal testosterone (T) rise, plasma SBP decreased (% of basal values) either significantly (38.3 +/- 9.3%, group A; n = 29), or moderately (13.4 +/- 4.4%, group B; n = 9) or did not change (-1.6 +/- 6.4%, group C; n = 10). In the 3 infants tested at an age when SBP normally rise sharply, hCG partially prevented this rise. The administration of either fluoxymesterone (10 mg/m2 for 10 days) or depot-T (4 I.M. injections of 100 mg/m2 every 2 weeks) induced a significant drop (about 2-fold) in plasma SBP in a control group of infants or children, but did not change SBP in 3 infants with the androgen insensitivity syndrome. A single injection of 0.25 mg of ACTH did not significantly alter SBP levels. In contrast, at the end of a 3-day ACTH test (0.5 mg/m2 12 hourly X 6) SBP levels had significantly decreased (mean 35% fall) with no age or sex differences, and with no correlation with the cortisol levels reached. However, the lowering effect of ACTH on SBP levels is likely mediated by glucocorticoids, since its effect was reproduced by high doses (8 mg/day for 3 days) of dexamethasone given at once or after 3 days of treatment at lower dose (20 micrograms/kg BW). It would appear that the depressive effect of ACTH and/or dexamethasone is observed for a threshold dose of glucocorticoids (greater than 5-fold physiological levels) and a certain time (greater than or equal to 3 days) of exposure. The mechanism by which androgens and glucocorticoids lower SBP levels in vivo is not yet understood. From recent experiments, showing that both stimulate the secretion of SBP in hepatoma cells in vitro, it would appear that both hormones may alter SBP metabolism. In a selected population of hyperprolactinemic women, with normal weight and no hirsutism, plasma SBP levels were found in the normal female range. The discrepancy with previous studies in the literature may be explained by differences in the degree of hyperprolactinemia and/or associated hyperandrogenim. This study further documents the multifactorial and intricated hormonal influences involved in the regulation of plasma SBP in vivo.

Adrenocorticotropic Hormone↗

PubMed1998

Emotional aspects of hyperprolactinemia.

Patients with hyperprolactinemia often present with emotional difficulties. These occasionally persist even after successful treatment. Insight into the roots of their diseased state makes a difference in the handling of all cases, but becomes crucial in the not-so-rare situations in which the normalization of hormonal levels is not followed by a feeling of cure. This chapter attempts to provide details, discuss and situate in context the following blocks of pertinent information: (1) prolactin acts upon the central nervous system and variations in its concentrations do affect mood, emotions and behavior; (2) most actions of prolactin are directed to metabolical and behavioral adaptation to pregnancy and the care of the young; (3) even in the absence of pregnancy prolactin secretion responds to environmental stimuli under specific conditions. Whether adaptive, as in the case of surrogate maternity, or pathological, as in the case of pseudopregnancy, prolactin responds to a perceived need to take care of a child; (4) the facts that the clinical onset of prolactinomas often follows life-events and that these tumors occur preferentially in women brought up under specific conditions suggest the possibility that psychological factors may predispose to prolactinomas; (5) dealing with individual cases requires the perception that the relations between prolactin, emotions and feelings are circular, i.e., prolactin affects the brain and mood but, on the other hand, personality traits and environmental factors may stimulate the secretion of prolactin and may play a role in the genesis of the disease.

Affective Symptoms↗

PubMed1986

Normal lactotroph sensitivity to graded low-dose dopamine infusions in pathological hyperprolactinemia.

The question as to whether there is lactotroph resistance to dopamine (DA) in pathological hyperprolactinemia (PHP) is unresolved. Previous studies utilizing low-dose DA infusions to study lactotroph function have not considered the diurnal changes in prolactin (PRL) secretion that occur in normals but which are lost in PHP. As PRL levels show a fall in the hours after waking, studies performed during this time of day will falsely show a greater fall of PRL in normals than in PHP patients. The aim was to readdress the issue of lactotroph sensitivity using a study designed to minimize the problem arising from diurnal PRL changes. Eight normal subjects, 17 patients with PHP, and 6 hyperprolactinemic patients with nonfunctioning pituitary tumors (NFTs) were studied with three graded doses of DA - (0.01, 0.05, and 0.5 micrograms/kg X min) - by relating the changes induced by each dose to the maximal spontaneous fall in PRL that occurred during a 3-hour control saline study. The mean +/- SE maximal fall in PRL during control saline infusion to 46.0 +/- 4.1% of basal in normal subjects was significantly greater (p less than 0.001) than the fall in patients with PHP (88.0 +/- 1.0%) or NFTs (87.5 +/- 2.6%). The apparent fall in PRL was significantly greater in normals during the two lower infusion doses, but not at the highest dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

GABAergic biochemical parameters of the tuberoinfundibular neurons following chronic hyperprolactinemia.

The effect of chronic hyperprolactinemia was studied on (a) GABA concentration in the pituitary anterior lobe; (b) GABA biosynthesis enzyme, glutamate decarboxylase (GAD) activity in the hypothalamic median eminence, and (c) GABA degradation enzyme GABA-transaminase (GABA-T) activity at both levels. In male rats bearing the prolactin-secreting tumor MtTF4 for 1 month or treated for 5 days with estradiol benzoate, the plasma prolactin concentration was markedly increased (between 4- and 10-fold basal values). In both cases, GABA concentration was significantly increased (40-60%) in the anterior pituitary lobe. A slight reduction (20-30%) in GABA-T activity was observed in the anterior lobe while no change in GAD or GABA-T activity was measured in the median eminence. These results are discussed in relationship to a possible feedback input of prolactin on the tuberoinfundibular GABAergic system.

4-Aminobutyrate Transaminase↗

PubMed1994

Enhanced tuberoinfundibular dopaminergic neuron activity in thyroidectomized, ovariectomized and estrogen-treated rats with hyperprolactinemia.

The involvement of the tuberoinfundibular dopaminergic (TIDA) neurons in the genesis of hyperprolactinemia in female thyroidectomized rats treated with estrogen was the focus of this study. Rats that were ovariectomized (3 weeks), thyroidectomized (2 weeks) and treated with estrogen for 6 days had a 5- to 10-fold increase in serum prolactin (PRL) levels, while the rats receiving the same treatments but without estrogen had lower PRL levels. The activity of TIDA neurons, using dihydroxyphenylacetic acid (DOPAC) concentration or the DOPAC/dopamine (DA) ratio in the median eminence (ME) as an index, was increased and decreased in estrogen-treated and untreated rats, respectively. The increases in serum PRL level and the activity of TIDA neurons were dependent on the duration of thyroidectomy and could both be lowered by daily injection of thyroid hormone (20 or 100 micrograms/kg b.w. thyroxine, i.p.) for 12 days in a dose-dependent manner. Using dihydroxyphenylalanine (DOPA) accumulation in the ME as another index, we also found an increased DOPA/DA ratio in estrogen-treated hypothyroid rats, which effect could be reversed by replacement of thyroid hormone. Furthermore, treatments with bromocryptine (3 mg/kg b.w./day, s.c.) for 3 days or with cysteamine (100 mg/kg b.w., s.c.) at 26, 15 and 2 h before the rats were sacrificed lowered both serum PRL level and TIDA neuron activity. Since PRL can exert a short-loop feedback control on its own secretion, these results indicate that the increased serum PRL levels in estrogen-treated hypothyroid female rats should be the cause, but not the result, of the increased activity of TIDA neurons.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1981

Nomifensine test does not differentiate hyperprolactinemia associated with and without radiologic abnormalities in the sella turcica.

A group of 17 hyperprolactinemic women was given 200 mg of nomifensine orally to evaluate its diagnostic potential to discriminate between tumors and nontumorous hyperprolactinemia. The nomifensine suppressive effect on prolactin serum levels was not significantly different between patients with or without enlargement of the sella turcica. A control group of 5 women with normal prolactin levels exhibited a nomifensine suppressive effect below 65% of the baseline prolactin level, which was significantly different from that in the hyperprolactinemic group. In conclusion it is confirmed that the nomifensine test provides no value in the early diagnosis of the prolactinoma.

Adenoma↗