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PubMed2005

[The diagnosis of hyperprolactinemia in clinical practice].

Prolactin is a pituitary hormone that plays pivotal role in a variety of reproductive functions. Hyperprolactinemia is a common condition that can result from a number of causes; including use of medications and hypothyroidism, as well as pituitary disorders. Depending on the cause and consequences of hyperprolactinemia, selected patients require specific treatment. The underlying cause of hyperprolactinemia, sex, age and reproductive status must be considered. Management of this condition depends heavily on the cause and on the effects it has on the patient. The definition of the hyperprolactinemia is not uniformed, and in various clinical settings various criteria of this status are used. In the identification of hyperprolactinemia not only simple measurements of the prolactin serum level are used, the dynamic tests with the use of dopamine antagonists have a special role as well. Neither the measurement of the serum prolactin level, nor dynamic tests with dopamine antagonists are able to determine the presence of macroprolactin molecules in the serum, and this can lead clinicians to establish the false diagnosis of hyperprolactinemia.

Diagnosis, Differential↗

PubMed1987

[Clinical evaluation of the prolactin secreting capacity for the diagnosis of occult hyperprolactinemia].

To clarify the diagnostic criteria of occulted or transient hyperprolactinemia, the resting prolactin level and the prolactin secreting capacity of normal women, which were tested with a 500 micrograms of TRH injection, were compared with those of patients with occulted hyperprolactinemia. Results revealed that: resting levels of prolactin in normal women were 13.4 +/- 4.4 ng/ml (mean +/- S.D.) in the follicular phase and 13.4 +/- 5.6 ng/ml in the luteal phase, which overlapped those of occulted hyperprolactinemia. the prolactin secreting capacity of occulted hyperprolactinemia was significantly greater than that of the normal women. These results indicated that it was impossible to distinguish the occulted hyperprolactinemia from the normal by the measuring the resting prolactin level, but possible by the evaluating the prolactin secreting capacity. If the serum prolactin was more than 150 ng/ml at 15 min. after TRH administration, occulted hyperprolactinemia was strongly suggested.

Circadian Rhythm↗

PubMed1988

Effects of chronic sulpiride-induced hyperprolactinemia on menstrual cycles of normal women.

We investigated the influence of chronic (27-65 days) sulpiride-induced hyperprolactinemia on the menstrual cycles of four normal women. The hyperprolactinemia (206.4 ng/mL, the average of the mean values of each subject obtained by sulpiride treatment) suppressed the LH surge and the secretion of plasma estradiol-17 beta and progesterone to their basal levels. The results suggest that the endocrine changes in normal women with sulpiride-induced hyperprolactinemia are similar to those in women with spontaneous hyperprolactinemia. Sulpiride-induced hyperprolactinemia may be useful as a model for studying spontaneous hyperprolactinemia.

Adult↗

PubMed1988

Electron microscopical morphometry of pituitary adenomas. Comparison of tumours in acromegaly and hyperprolactinemia.

By electron microscopical morphometry (point counting method) 4 groups of adenomas were compared in order to identify the source of prolactin in hyperprolactinemia. The 4 types of adenomas were characterized by the following features: Group I: acromegaly without hyperprolactinemia (GH positive and PRL negative on the immunohistochemical level); Group II: acromegaly with hyperprolactinemia and/or galactorrhea (GH positive and PRL positive on the immunohistochemical level); Group III: adenomas with hyperprolactinemia without acromegaly (GH negative and PRL positive on the immunohistochemical level); Group IV: adenomas with hyperprolactinemia without acromegaly (GH and PRL negative on the immunohistochemical level). Morphometry was performed in order to analyse the relative amount of the following cellular structures: nuclei, nucleoli, rough endoplasmic reticulum, Golgi fields, immature secretory granules, mature secretory granules, lysosomes, mitochondria, unorganized cytoplasm, and cellular membranes. Significant differences (Student t-test, Wilcoxon test; 2 p less than 0.05) were found for the following compartments: rough endoplasmic reticulum and Golgi fields in group III had significantly larger volumes than in group IV. The volume of secretory granules of group II and group IV was larger than of group III. The volume of mitochondria of group IV was larger than in group I, and it was larger in group I and group III than in group II. Despite these differences a distinctive morphometrical pattern of the different subgroups could not be established. The quantitative data are valuable for interpretation of high or low functional activity but not for differential diagnoses. Therefore, if only the source of PRL in hyperprolactinemia has to be identified, immunocytochemistry is the best and simpler method.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

PubMed1998

[Antibodies against prolactin in patients with systemic lupus erythematosus and hyperprolactinemia].

We investigated patients with lupus erythematosus to detect the presence of hyperprolactinemia and to determine it's origin. From the seric specimens obtained in 225 patients with LES, we found 37 (14.5%) with hyperprolactinemia and they were trated with polyethylenglicol, in 11 of 37 patients (29.7%) had a high significance of prolactin precipitation (PRL). The test in gel filtration shown the big-big PRL (Molecular weight > 100 kDa) was the predominant form from PRL seric in these patients and no woman had clinic effects of hyperprolactinemia as galactorrhea and/or amenorrhea. The big-big PRL essence was due to an antibody, with it was found like a immune complex (Ig-PRL). This evidence suggest the patients with LES and hyperprolactinemia have a very high incidence of macroprolactinemia relationated to antibodies anti-PRL, and in spite of the hyperprolactinemia not have clinical effects like amenorrhea and/or galactorrhea, and it is other cause to explain the high incidence of hyperprolactinemia in patients with LES.

Autoantibodies↗

PubMed1978

Alteration of feedback mechanism of estrogen on gonadotropin by sulpiride-induced hyperprolactinemia.

Four normally cycling women received an iv injection of 20 mg Premarin (conjugated estrogens equivalent to 20 mg estrone sulfate) on the seventh day of two consecutive cycles; the second experiment was performed under sulpiride-induced hyperprolactinemia (mean PRL level = 906 microU MRC standard 71/222 per ml; significantly 7.8 times greater than mean control level of 115 microU MRC standard 71/222 per ml, P less than 0.001). In comparison to the control experiment, sulpiride-induced hyperprolactinemia prevented the occurrence of any gonadotropin peak within the 84 h of estrogen administration; the negative feedback effect of estrogen on gonadotropin secretion was maintained and was even potentiated. These alterations of feedback mechanisms of estrogen were considered to be related to hyperprolactinemia itself rather than to sulpiride. Five other normally cycling women received iv injections of 100 microgram LRH on the 22nd day of a cycle under sulpiride-induced hyperprolactinemia since the onset of menstruation. Their mean LH response was somewhat greater (although not statistically significant) and their mean FSH response was considerably greater (P less than 0.001 at all times) than those of a control group of 10 women tested in their luteal phase. The results of these LRH tests under sulpiride-induced hyperprolactinemia give some support to the concept that hyperprolactinemia interferes at the hypothalamic or higher level with cyclic release of indogenous LRH.

Adolescent↗

PubMed2003

Role of testicular interstitial macrophages in regulating testosterone release in hyperprolactinemia.

Hyperprolactinemia-induced hypogonadism has been linked to a dysfunction of the hypothalamus-pituitary-testis axis. The direct inhibitory effects of prolactin on the testicular release of testosterone have also been demonstrated, though their mechanisms remain unclear. Incubation of rat testicular interstitial cells (TICs) with prolactin stimulated the release of testosterone. TICs from rats with anterior pituitary-grafting-induced hyperprolactinemia release lower amounts of testosterone than controls. However, Leydig cells isolated from anterior pituitary-grafted rats release a greater amount of testosterone. These paradoxical observations have remained unexplained. This study examined the roles of testicular interstitial macrophages and of their product, tumor necrosis factor-alpha (TNF-alpha), in regulating Leydig cells under condition of hyperprolactinemia. Hyperprolactinemia was induced by grafting two anterior pituitary glands of rats under the renal capsule. Control animals were grafted with rat cortex tissue. The rats were sacrificed 6 weeks later. TICs and macrophages, and Leydig cells were isolated for in vitro incubation and drugs challenge. Testosterone released by testicular interstitial or Leydig cells was measured by radioimmunoassay. TNF-alpha concentration in the medium of TICs or macrophages was measured by enzyme-linked immunosorbent assay (ELISA). A dose-dependent stimulation of TNF-alpha secretion in the medium of TICs or macrophages by the prolactin challenge was observed. Higher amounts of TNF-alpha were released by TICs in the anterior pituitary-grafted rats than in the control group. In contrast, the release of TNF-alpha by testicular interstitial macrophages isolated from the anterior pituitary- and cortex-grafted groups was quantitatively similar. Challenge with human chorionic gonadotropin did not modify the TNF-alpha release by testicular interstitial macrophages in either group. Challenge of Leydig cells with TNF-alpha inhibited their release of testosterone stimulated by human chorionic gonadotropin, but not their basal testosterone release. These different patterns of testosterone release in TICs versus Leydig cells cultures in anterior pituitary-grafted rats may be due to the influence of testicular interstitial macrophages. These observations correlate with in vivo conditions, where prolactin increases the release of TNF-alpha by testicular interstitial macrophages, which, in turn, decreases the human chorionic gonadotropin-stimulated release of testosterone by Leydig cells. In summary, hyperprolactinemia-induced hypogonadism involves a mechanism of prolactin-originated, macrophage-mediated inhibitory regulation of testosterone release by Leydig cells. TNF-alpha, one of the cytokines secreted by macrophages, may play a key role in this mechanism.

Animals↗

PubMed1991

Effects of clomiphene citrate and leuprolide acetate on luteal-phase hyperprolactinemia during ovarian stimulation with menopausal gonadotropins.

Hyperprolactinemia, a known modulator of reproductive function, occurs commonly in women undergoing ovarian stimulation with human menopausal gonadotropins (hMG). Clomiphene citrate (CC) and gonadotropin releasing hormone analogues (GnRHa), when administered during the luteal phase, attenuate the hyperprolactinemic response to hMG. We asked whether follicular-phase administration of CC and GnRHa, as employed clinically in women undergoing ovarian stimulation for in vitro fertilization or gamete intrafallopian transfer, would alter the incidence and severity of hMG-induced luteal-phase hyperprolactinemia. Seventy-five percent of all patients had at least one luteal prolactin level greater than 25 ng/ml, and 40% had mean luteal-phase prolactin levels greater than 25 ng/ml. The incidence of hyperprolactinemia was similar in pregnant and nonpregnant cycles. The incidence of hyperprolactinemia was similar for both the GnRH agonist-treated group and those given clomiphene citrate. The increase in mean luteal prolactin levels over the follicular-phase baseline level was significantly greater in the CC-treated group (P = 0.03). This was due to the significant suppression of follicular-phase baseline prolactin levels in patients receiving CC. We conclude that neither CC nor GnRHa administration in the follicular phase prevents luteal-phase hyperprolactinemia in women undergoing ovarian stimulation with hMG.

Clomiphene↗

PubMed1998

Hormonal replacement therapy in menopausal women with a history of hyperprolactinemia.

Hyperprolactinemia is involved in almost 30% of infertility problems. At the onset of menopause, prolactin levels often decrease; however, no data are available regarding the course of hyperprolactinemia after menopause with hormonal replacement therapy (HRT). A retrospective study was undertaken in our department to evaluate the potential role of estrogens in women with a history of hyperprolactinemia. Twenty-two patients, with hyperprolactinemia before menopause, were followed-up. Group I included 11 patients who withdrew bromocriptine treatment when menopause was confirmed. These patients were placed on HRT with no other medication administered. HRT was a combination of percutaneous estradiol gel and an oral progestin. Group II included 7 women treated by bromocriptine before menopause and after menopause concomitantly with HRT. Group III included 4 patients who did not receive HRT or other treatments once menopause was diagnosed. The mean serum prolactin level was unchanged in Group I (22.8+/-21.7 before and 22.8+/-16.1 ng/ml after HRT) while it increased but not significantly from 8.1+/-5.2 to 16.0+/-11.7 ng/ml in Group II. The mean duration of HRT was 42.8+/-23.8 (7-81) and 37.3+/-31.0 (6-99) months in Group I and II respectively. In Group III patients, PRL levels decreased spontaneously from 61.2+/-39.8 to 33.0+/-34.7 ng/ml. In conclusion, in this population of menopausal patients with a history of moderate hyperprolactinemia, HRT did not seem to affect plasma prolactin levels.

Adenoma↗

PubMed1990

Hyperprolactinemia preferentially inhibits erectile function in adrenalectomized male rats.

To determine if the inhibitory effects of hyperprolactinemia on sexual arousal and serum LH levels could be dissociated from those on erectile function, copulatory behavior was examined in pituitary-grafted, adrenalectomized male rats that had been castrated and given 20mm subcutaneous testosterone implants. Whereas transplantation of three pituitaries under the kidney capsules inhibited mounting rates in intact animals, pituitary grafting did not significantly reduce mounting rates in the adrenalectomized group beyond the effect of adrenalectomy alone. In contrast, the effects of pituitary grafting on erectile function were enhanced in the adrenalectomized animals. Hyperprolactinemia also caused a significant reduction in serum LH, but only in the intact animals. These results suggest that: 1. the effects of hyperprolactinemia on erectile function occur independently from those on sexual arousal, and 2. the inhibitory effects of hyperprolactinemia on sexual arousal are linked to the effects of hyperprolactinemia on LH release.

Adrenalectomy↗

PubMed1977

Hyperprolactinemia and hypogonadism in the human female.

Prolactin is a mammotropic hormone essential for the initiation of lactation. It also influences ovarian function; during hyperprolactinemia hypogonadism occurs. This is true for pathological forms of hyperprolactinemia but also for the early puerperium when there is physiological hyperprolactinemia. Amenorrhea is a better parameter of hyperprolactinemia than galactorrhea. The mechanisms by which prolactin disrupts ovarian function are not as yet fully understood; it probably alters hypothalamic neurotransmitter content through a direct feedback mechanism resulting in a decrease of Gn-RH. However, the direct effect of prolactin-producing pituitary tumors on the capacity of the gonadotrophs or a direct interference of prolactin at the gonadal level are also possibilities. Hyperprolactinemia can be treated very effectively with bromocriptine and this drug appears to have become the favorite form of treatment. In the case of obvious tumors hypophysectomy is indicated. When there are smaller tumors irradiation of the pituitary gland previous to bromocriptine treatment may prevent expansion of the gland during subsequent pregnancy.

Amenorrhea↗

PubMed2005

The dopamine receptor D2 genotype is associated with hyperprolactinemia.

OBJECTIVE: To evaluate patients with hyperprolactinemia for the presence of dopamine receptor D2 polymorphisms. DESIGN: Case-control study. SETTING: Academic research environment. PATIENT(S): Women and men with pathologic hyperprolactinemia and healthy controls. INTERVENTION(S): DNA extraction of peripheral blood, polymerase chain reaction, single-strand conformation polymorphism, DNA sequencing, and restriction digest. MAIN OUTCOME MEASURE(S): Two polymorphisms in exon 7 of the dopamine receptor D2 (DRD2) gene. Polymorphism 1 involves nucleotide 3420 (C to T, 313 His), and polymorphism 2 involves nucleotide 3438 (C to T, 319 Pro). RESULT(S): The frequency of DRD2 polymorphism 1 alleles was increased in subjects with hyperprolactinemia. Analysis of the DRD2 genotypes demonstrates an odds ratio of 6.77 (2.39, 19.14; 95% confidence interval) for the polymorphism 1 homozygous state in hyperprolactinemia. CONCLUSION(S): A genetic predisposition to hyperprolactinemia is suggested by an excess homozygosity for polymorphism 1 in exon 7 of the DRD2 gene. Previous studies of lactotrophs from prolactinomas have found normal DRD2 receptors but differing isoform density. Homozygosity of polymorphism 1 may influence the distribution of the DRD2 isoforms on the lactotroph. Other potential mechanisms include an association with a molecular defect in a postreceptor signaling mechanism, such as a somatic inactivating mutation in a G1 protein, which could result in autonomous function of the lactotroph. Mutations could also result in different receptor-G protein interactions, such as a Gs instead of Gi, and result in autonomous lactotroph function.

Alleles↗

PubMed1989

The incidence of transient hyperprolactinemia in gonadotropin-stimulated cycles for in vitro fertilization and its effect on pregnancy outcome.

The incidence of transient hyperprolactinemia and its impact on in vitro fertilization (IVF) were determined in 151 euprolactinemic women with tubal infertility undergoing an identical gonadotropin stimulation for IVF. Prolactin (PRL) levels were measured on the morning of cycle day 3, days of human chorionic gonadotropin (hCG) administration, and peak estradiol (E2), and in the midluteal phase. Women were divided into high (H: peak E2 greater than 1,000 pg/mL, n = 51), intermediate (I:peak E2: 500 to 800 pg/mL, n = 50), or low (L:peak E2 less than 400 pg/mL, n = 50) E2 response groups. There was no difference in the incidence of hyperprolactinemia on cycle day 3 between the response groups (H:16%, I: 12%, and L:8%). However, high responders had a higher incidence of hyperprolactinemia than intermediate or low responders on all other study days. The incidence of hyperprolactinemia was greater than baseline (cycle day 3) only in the high responders on the day of peak E2. Serum prolactin was strongly correlated with peak E2 (r = 0.41). There were no differences in the number of preovulatory oocytes retrieved or fertilized or the pregnancy rates between hyperprolactinemic and euprolactinemic patients in each response group or when all hyperprolactinemic and euprolactinemic patients, regardless of E2 response, were compared. Transient hyperprolactinemia during gonadotropin stimulation for IVF occurs and correlates with E2 response but has no impact on IVF outcome.

Adult↗

PubMed2002

Hyperprolactinemia: etiology, diagnosis, and management.

Hyperprolactinemia is the most common endocrine disorder of the hypothalamic-pituitary axis. A prolactinoma is the most common cause of chronic hyperprolactinemia once pregnancy, primary hypothyroidism, and drugs that elevate serum prolactin levels have been excluded. Patients can present with hypogonadism, infertility, galactorrhea, osteopenia, and mass effects of the tumor. When hyperprolactinemia is confirmed, a cause for the disorder needs to be sought. This involves a careful history and examination, followed by laboratory tests and diagnostic imaging of the sella turcica. The goals of treatment are to normalize prolactin levels, restore gonadal function, and reduce the effects of chronic hyperprolactinemia. Dopamine agonists are the treatment of choice for the majority of patients. Transsphenoidal surgery is usually reserved for patients who are intolerant of or resistant to dopamine agonists or when hyperprolactinemia is caused by non-prolactin-secreting tumors compressing the pituitary stalk. Cabergoline has been shown to be more effective and better tolerated than bromocriptine. However, there are more data on the safety of the latter drug during pregnancy and bromocriptine, therefore, remains the treatment of choice in hyperprolactinemic women wishing to conceive.

Bromocriptine↗

PubMed2001

Treatment of risperidone-induced hyperprolactinemia with a dopamine agonist in children.

BACKGROUND: Risperidone, a potent antagonist of both serotonergic (5HT2A) and dopaminergic D2 receptors is associated with hyperprolactinemia in adults and children. Chronically elevated prolactin levels in children with prolactinomas may be associated with arrested growth and development resulting in either delayed puberty or short stature. These possibilities stress the importance of developing a safe and effective approach to drug-induced hyperprolactinemia in youth. We report the successful treatment of risperidone-induced hyperprolactinemia with cabergoline in youth. METHODS: We undertook a retrospective case review of four children with risperidone-induced hyperprolactinemia treated with cabergoline. RESULTS: Four males (age 6-11 years) with Diagnostic and Statistical Manual of Mental Disorders (fourth edition) bipolar disorder or psychoses, with risperidone-induced elevations in serum prolactin levels (57.5-129 ng/mL, normal 5-15 ng/mL), were treated with cabergoline (mean dose 2.13 +/- 0.09 mg/week). When serum prolactin levels normalized in all four subjects (mean 11.2 +/- 10.9 ng/mL), the cabergoline dose was reduced to 1 mg/week in three of four subjects. The mean duration of therapy with cabergoline was 523.5 +/- 129.7 days, and the mean duration of therapy with risperidone was 788.5 +/- 162.5 days. Cabergoline was well tolerated without adverse effects. CONCLUSIONS: Cabergoline may be useful for the treatment of risperidone-induced hyperprolactinemia in youth; however, further research is needed.

Age Factors↗

PubMed2006

Macroprolactinemia in a patient with infertility and hyperprolactinemia.

A significant number of patients with hyperprolactinemia have macroprolactinemia, a condition characterized by the preponderance of big-big prolactin with normal levels of free prolactin. As macroprolactin does not have biologic activity, such patients do not require further investigations or treatment for hyperprolactinemia. The case of a patient with hyperprolactinemia diagnosed during investigation of secondary infertility is presented. She was treated for over 2 years with dopamine agonists, with which her prolactin level normalized, but she remained infertile. Subsequent investigations demonstrated that she suffered from macroprolactinemia, not true hyperprolactinemia. The patient is currently not on dopamine agonist therapy, and although her total prolactin levels remain significantly elevated, her free prolactin levels have been in the normal range. Physicians should familiarize themselves with this entity and consider testing for it in patients with hyperprolactinemia to avoid an inappropriate diagnosis and unnecessary treatment.

Adult↗

PubMed1988

[Pathophysiology of hyperprolactinemia in breast cancer].

To characterize the prolactin secretion in human breast cancer, plasma prolactin levels were measured in 514 patients with breast cancer in long term follow-up studies. In hyperprolactinemic patients suppression and stimulation tests were performed and the 24-h secretion profile was recorded. Tissue extracts and sera of hyperprolactinemic breast cancer patients were incubated with cultured pituitary cells in vitro to detect a prolactin releasing activity in these specimens. 44% of breast cancer patients developed hyperprolactinemia in the course of the disease. In 35% of measurements hyperprolactinemia was induced by non tumor related causes, e.g. prolactin-stimulating drugs, surgery, uremia, prolactinoma. Excluding such influences on the prolactin level, hyperprolactinemia over 1,000 mU/l was almost only found in patients with progressive metastatic disease. In these patients hyperprolactinemia was associated with tumor load, but not correlated to BSR, CEA or prognostic factors. Hyperprolactinemia in breast cancer was not of paraneoplastic origin. No prolactin-releasing activity was detected in tumor tissue and sera of hyperprolactinemic breast cancer patients.

Breast↗

PubMed2003

Resolution of risperidone-induced hyperprolactinemia with substitution of quetiapine.

OBJECTIVE: To report a case of risperidone-induced hyperprolactinemia that was successfully managed with quetiapine. CASE SUMMARY: A 30-year-old white woman with schizoaffective disorder, depressive type, and comorbid alcohol and cocaine abuse was treated successfully for her psychotic symptoms with risperidone until she developed adverse effects consistent with hyperprolactinemia. This was confirmed by laboratory blood tests, as her prolactin level was 186.9 ng/mL (normal for nonpregnant women 2.8-29.2). The woman had experienced similar effects in the past, which had led to noncompliance and subsequent psychotic relapse. Normalization of prolactin levels and associated adverse effects were achieved upon switching to quetiapine. No psychotic symptoms reoccurred. DISCUSSION: Dopamine type 2 (D(2)) receptor blockade in the mesolimbic tract is thought to mediate the therapeutic effects of antipsychotics. This action in the tuberoinfundibular system produces prolactin level elevation. Risperidone has a relatively higher affinity for the D(2) receptor in comparison with other atypical antipsychotics, which may explain why it is associated with a higher incidence of hyperprolactinemia. Quetiapine, which has one of the lowest D(2) receptor affinities, is not known to increase prolactin levels to any significant degree. This pharmacologic property allows quetiapine to be a reasonable treatment option for patients who develop risperidone-induced hyperprolactinemia. CONCLUSIONS: Quetiapine may be a suitable substitute when a patient taking risperidone develops hyperprolactinemia.

Adult↗