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[Hyperprolactinemia and primary amenorrhea].

Six patients with primary amenorrhea and hyperprolactinemia are presented. The patients had normal secondary characteristics and normal body proportions. In four patients a tumour of the hypophysis was diagnosed radiologically, while in two patients the cause of hyperprolactinemia remained unknown. The gonadotropin concentration in the serum was normal. Reaction to Gn-RH was the same as that in women with the normal cycle in the follicular phase. In all the patients with function of the thyroid was normal. Primary amenorrhea was found in 14.6% of women with a disturbed cycle and hyperprolactinemia. In all the patients the administration of bromocryptin normalized prolactin concentrations, induced ovulation, and four patients became pregnant.

Amenorrhea↗

PubMed2006

Drug-induced hyperprolactinemia.

Hyperprolactinemia is the most common biochemical abnormality currently encountered in clinical endocrinology. Hyperprolactinemic syndromes are a diverse group of disorders that are common in both men and women. Once the diagnosis of hyperprolactinemia has been established, the patient should be screened for the numerous causes of hormone hypersecretion. Hence, an accurate medical history is extremely important for the clinician to find out the most frequent causes of hypersecretion of prolactin (e.g., drugs). Clinicians should be aware of the possibility of prolactin elevation and associated problems with any drug that has the potential to cause hyperprolactinemia, particularly in patients who have other factors that might stimulate prolactin release.

Journal Article↗

PubMed1987

[Transient hyperprolactinemia during ovulation induction with gonadotropin releasing hormone (GnRH) pulsatile administration].

Seven clomiphene-resistant normoprolactinemic anovulatory patients were treated with GnRH pulsatile administration (total 15 treatment cycles). Several problems with GnRH pulse therapy were raised through 6 unsuccessful cases. In 5 cases (10/15 treatment cycles), transient hyperprolactinemia (50-100 ng/ml) appeared immediately after the initiation of the treatment and persisted for 6-10 days. Follicle maturation and ovulation was not induced in these cases. Frequent blood sampling failed to demonstrate GnRH-induced LH secretion in 3 cases. Synchronous secretion of PRL with LH was observed when serum PRL levels were low, but not in situations with elevated serum PRL levels. The lack of GnRH-induced LH secretion indicates the down-regulation of the pituitary with increased frequency of GnRH pulses due to intrinsic and exogenous GnRH. The synchrony of LH and PRL suggests the contribution of GnRH-mediated PRL releasing factor (PRF) through a paracrine system between gonadotrophs and lactotrophs. Transient hyperprolactinemia observed in the current study might be attributable to a relative increase in GnRH to a GnRH-associated peptide (GAP), a constituent of GnRH prohormone and possessing an intrinsic effect of PRL suppression, by exogenously administered GnRH, causing overwhelming superiority of GnRH-mediated PRF. Transient hyperprolactinemia and regulation of the pituitary may hamper ovulation induction with GnRH pulse therapy when applied to cases with intact hypothalamic-pituitary axis.

Anovulation↗

PubMed1978

[Drug therapy of hyperprolactinemia and acromegaly].

Hyperprolactinemia can be treated medically. Thus all patients with a normal sella turcica and those patients with only slight enlargement of the sella turcica can be treated medically with the dopaminagonist bromocriptine. This treatment is also indicated in paitents with postoperative persisting hyperprolactinemia. In contrast to hyperprolactinemia medical therapy of acromegaly is still in the experimental stage, through the dopaminagonist bromocriptine induces a decrease of growth hormone levels and improvement of the disease in many patients with acromegaly.

Acromegaly↗

PubMed1982

[Pathologic hyperprolactinemia. I. Positive diagnosis and etiology].

Hyperprolactinemia is common and mainly encountered in premenopausal women. The most prevalent causes are drugs (estrogens, neuroleptics), hypothalamic and pituitary disorders (functional abnormalities, intrasellar adenomas, suprasellar lesions) and hypothyroidism. Although the typical picture is the amenorrhea-galactorrhea syndrome, hyperprolactinemia may be revealed by many other features, including obesity, hirsutism and sterility. When plain roentgenograms show a normal sella, neither dynamic tests nor polytommography can lead to unequivocal diagnosis of a tumor. Computerized tomography scanning is now the most reliable investigation in patients with hyperprolactinemia resulting from an obvious or suspected tumor.

Adenoma↗

PubMed1983

[Dopaminergic agents in the treatment of hyperprolactinemia].

The treatment of hyperprolactinemia with dopaminergic agents is directly correlated with the improvement of the knowledge about hypothalamic control of prolactin secretion. Since 1963 it is wellknown that the hypothalamus acts on this activity of the pituitary gland with a tonic inhibition. A prolactin inhibiting factor (PIF) was suspected for this control and the tubero-infundibular dopaminergic system was considered to modulate the secretion of PIF. In fact a lot of experience demonstrated a direct control of dopamine on pituitary gland itself (fig. 1). Ergot alkaloids are the most useful dopaminergic drugs. They derive from 6 methyl 9 ergoline (fig. 2) and, in the main group of 12 ergocryptine molecules, alpha-ergocryptine and ergocornine are the most potent (fig. 3). Bromocryptine (2 alpha-bromoergocryptine, BEC) is a compound (fig. 4) with a magnification of the effect on prolactin secretion and loss of uterotonic and vasoconstrictive effects. This drug acts directly on normal pituitary cells and on adenomas in vitro. The inhibition of secretion is first seen, followed by inhibition of synthesis. Transplanted tumors (MtTW15) are sensible to ergocornine but not to BEC. The oral administration of the drug is followed by an increase in serum concentration (fig. 5) maximum at 3 hours. The decrease of prolactin is progressive and prolonged until the 7th hour. Some similarities between the structure of dopamine and bromocryptine may explain the effect of the drug (fig. 6). Hyperprolactinemia constitutes a frequent clinical syndrome with amenorrhea-galactorrhea and sterility. The cause is a pituitary tumor composed of prolactin secreting cells. All the clinical and biological manifestations are due to high prolactin secretion and the surgical ablation of the adenoma is followed by complete cure. This result is obtained frequently in microadenomas. The medical treatment of hyperprolactinemia with BEC was initiated in 71 by Lutterbeck. Since that time a lot of clinical experiences give the same kind of results: Improvement in 100% of galactorrhea, 90% of amenorrhea and 80% of fertility. These results are now wellknown and the secondary effects of the drug are quite limited. The development of pregnancy in a patient suspected of a pituitary adenoma is a major problem which is now clearly solved. In a survey of the literature Nillius found 146 patients in this situation with only 5.6% of complication. Our experience with 18 patients is confirmative. Moreover we found after delivery a decrease of serum prolactin (fig. 7).(ABSTRACT TRUNCATED AT 400 WORDS)

Bromocriptine↗

PubMed1984

Hyperprolactinemia: comparison of thyrotropic-releasing hormone and tomography.

A group of 95 women with unexplained hyperprolactinemia (over 20 ng/mL) underwent radiologic examination of the sella turcica with hypocycloidal polytomography (N = 58), computed axial tomography (N = 8), or both (N = 29). All patients also underwent a thyrotropin-releasing hormone (TRH) stimulation test, with serum prolactin (PRL) measurement before and 20 and 30 minutes after a 500-micrograms intravenous bolus of TRH. Their PRL responses were compared with those of two control groups, nine normal women in the follicular phase of the menstrual cycle, and 13 women in the first five months of gestation with pregnancy-related hyperprolactinemia. Both control groups exhibited PRL increases with 95% confidence limits at least 200% above baseline levels. In all, 12 patients from the study group also had a normal PRL response (more than a 200% increase) to TRH, and none of these women had tomographic findings consistent with a pituitary tumor. The remaining 83 women all had diminished or absent PRL increases after TRH administration; 46 (55%) of these patients had radiographic evidence of an adenoma, whereas 37 (45%) had no clear signs of a tumor on either polytomography or computed axial tomography. No patient with a baseline PRL level in excess of 60 ng/mL had a normal PRL response to TRH. The results of the study indicate that 1) in patients with PRL between 20 and 60 ng/mL, a normal TRH test can be relied upon to avoid the expense and radiation of tomography (computed axial tomography or polytomography), 2) there is no benefit to be obtained in performing a TRH test in patients with a baseline PRL level over 60 ng/mL, and 3) about 45% of patients with hyperprolactinemia and an abnormal TRH test have a normal computed tomography or polytomography. These patients may have a small adenoma, and thus warrant closer follow-up than patients with a normal TRH test.

Adenoma↗

PubMed1984

Hyperprolactinemia in women with paternal deprivation during childhood.

It was reported that most females with prolactinoma, idiopathic hyperprolactinemia, or euprolactinemic galactorrhea were reared either without their father or with an alcoholic, violent father. To gain further insight into this association, a group of sisters of patients with prolactinoma (generally exposed to the same environment as the patients') and a control group were studied. Women with paternal deprivation during childhood differed from the women who had normal childhoods in that they had: 1) higher mean serum prolactin concentration (14.7 versus 9.4 ng/mL; P less than .001); 2) higher incidence of hyperprolactinemia (12 of 50 versus three of 59; P less than .005); and 3) higher incidence of galactorrhea (14 of 50 versus seven of 59: P less than .03). These observations support the contention that paternal deprivation during childhood is associated, in a minority of women, with a predisposition to develop hyperprolactinemia and presumably, prolactinoma later in life. A hypothesis on the possible mechanisms of a casual relationship is presented.

Female↗

PubMed1980

[An endocrinological study of hyperprolactinemia and its treatment (author's transl)].

Twenty-six cases of women with pituitary adenoma and seven cases of women with functional hyperprolactinemia were studied to evaluate the effects of neurosurgery and Bromocriptine treatment. In the patients with pituitary adenoma, the mean serum PRL level was significantly higher than that in the functional cases. Among the patients with pituitary adenoma, the serum PRL levels were roughly correlated to the size of the tumors. Basal serum LH, FSH and 17 beta-estradiol levels were lower in the patients with pituitary macroadenoma than in those with microadenoma. Neurosurgery was performed on fourteen patients of pituitary adenoma. Of ten cases with visual disturbance, it was necessary to use Bromocriptine to reduce the serum PRL to the normal level after operation. In the treatment of sixteen patients with microadenoma, Bromocriptine alone was used for eight of them and surgery was performed on four. As a result, there was a significant lowering of the serum PRL level and induction of regular menses in ten patients. Regular menses were induced by means of Bromocriptine treatment in all of the patients with functional hyperprolactinemia. Our data indicate that neurosurgery, either selective or combined with Bromocriptine, can normalize PRL levels and induce regular menses in patients with hyperprolactinemia.

Adenoma↗

PubMed1983

Successful pregnancies in patients with hyperprolactinemia--clinical and endocrinological studies on mothers and babies.

To study the effect of pregnancy and lactation on the clinical course of patients with pituitary adenoma and the influence of maternal hyperprolactinemia and bromocriptine treatment on fetal and neonatal development, prolactin levels were serially determined and abnormalities of newborn babies were examined. Ninety-nine patients with hyperprolactinemic amenorrhea were treated by surgery, bromocriptine therapy, and a combination of them; thus 34 patients conceived and gave birth to 43 babies. Almost all patients progressed uneventfully except for 2 cases who manifested diabetes insipidus and acute visual impairment. After the end of lactation, prolactin levels declined to lower values than before attempting pregnancy, except in 3 patients. Furthermore, those diagnosed as functional hyperprolactinemia before pregnancy were not found to have developed microadenoma. These results suggest that there is little influence on growth and activity of tumor throughout pregnancy and lactation. All of the newborns were normal and their growth up to 2 years after birth showed no special abnormalities. It was therefore concluded that maternal hyperprolactinemia or bromocriptine therapy in early pregnancy do not cause any deleterious effect on fetal and neonatal development.

Adenoma↗

PubMed1980

Psychosomatic factors in patients with hyperprolactinemia and/or galactorrhea.

A biographic and clinical investigation of 101 patients with hyperprolactinemia and/or galactorrhea is reported. Fifty-one patients were reared without their fathers and 18 with an alcoholic, violent one. These situations were uncommon in the control population, and the differences were statistically significant. There was a high frequency of complaints of obesity, headaches, frigidity, lightheadedness, and fullness of the abdomen, limbs, or face. There was a significant temporal correlation of external events in the natural history with onset or worsening of the symptoms. It is concluded that exposure during childhood to an environment characterized by an absent or alcoholic, violent father conditions some women to develop hyperprolactinemia and/or galactorrhea later in life as a response to specific environmental changes. These conclusions apply similarly to patients with prolactinoma, idiopathic hyperprolactinemia, and euprolactinemic galactorrhea, suggesting a close relationship among the 3 entities.

Family Health↗

PubMed1981

Experimental hyperprolactinemia and hypoprolactinemia and human chorionic gonadotropin during early pregnancy.

The effect of experimental hyperprolactinemia and hypoprolactinemia on human chorionic gonadotropin (hCG) concentration was studied in 34 healthy volunteers between weeks 6 and 11 of normal pregnancy. Hyperprolactinemia was induced in 12 women with 150 mg of sulpiride daily for 2 weeks; treatment led to a mean plasma prolactin (PRL) rise from 14.6 to 84.1 microgram/liter after 1 week and to 83.0 microgram/liter after 2 weeks. Hypoprolactinemia was effected in 11 women wit 5.0 to 7.5 mg of bromocriptine, daily for 2 weeks; treatment decreased the mean plasma prolactin from 19.2 to 6.0 microgram/liter after 1 week and to 5.2 microgram/liter after 2 weeks. These PRL changes were significant (P less than .001) in comparison with the plasma PRL concentrations in the 11 control women. Hyperprolactinemia induced by the sulpiride treatment was accompanied by a significant decrease in hCG concentration, whereas no difference in hCG was seen between hypoprolactinemia and control groups. This may suggest a synergistic action of hCG and PRL, or a direct effect of sulpiride on hCG, but the final mechanism and biologic importance of the phenomenon remain to be investigated.

Adult↗

PubMed1981

The relation between oral contraceptive use and subsequent development of hyperprolactinemia.

Serum prolactin levels were determined in 123 patients who presented with menstrual irregularities and/or infertility of more than 1 year's duration. Sixty-three patients had hyperprolactinemia with serum prolactin levels of 26 to 843 ng/ml (normal 5 to 22 ng/ml); 44.4% of this group of patients received oral contraceptive for a period of 2 months to 7 years. Sixty patients were normoprolactinemic, with serum prolactin levels of 3 to 22 ng/ml; 33.4% of this group received oral contraceptives for a period of 6 months to 7 years. The age of presentation, onset of symptoms, age at which they started on oral contraceptives, and duration of use were tabulated. The data were analyzed using chi 2 test corrected for continuity. There was no significant difference in age at the time of evaluation between oral contraceptive users and nonusers with hyperprolactinemia. The relative odds developing hyperprolactinemia were 2.64 times greater among women who has used oral contraceptives for more than 1 year and 6.25 times greater if this use started before the age of 25.

Adolescent↗

PubMed1975

[The pulsatile LH fluctuation (spiking) dependent on the circulating prolactin. Studies during physiological (puerperium), functional pathological and TRH induced hyperprolactinemia].

The magnitude and frequency of episodic LH-fluctuations have been observed to change during the different phases of the menstrual cycle. A hypothalamic control center appears to be responsible for these variations. Disturbances of the hypothalamus often make themselves known through a lack of LH-episodes. Ahypothalamic derangement in women with functional amenorrhoea can result in a disregulation of gonadotropins as well as prolactin, thereby leading to hyperprolactinemia. One finds an inverse relationship between high prolactin secretion and cessation of or decreased pulsatile LH-secretion (spiking). LH-spiking was tested in physiological post partum, functional pathological and TRH-induced hyperprolactinemias. No LH-episodes were observed post partum after the end of HCG clearance although prolactin had returned to normal levels at 12 days p.p. The mode of LH-secretion in a group of functionally amenorrhoic patients was changed by a TRH-induced prolactin increase: the previously observed LH-spikes in these women could no longer be seen. Normal cycling women, however, were not affected. In patients with hyperprolactinemic anovulatory syndromes, prolactin suppressed LH-fluctuations reappeared after administration of 2-Bromo-alpha-ergocryptin. The inhibitory influence of hyperprolactinemia on the function of the gonadostat will be discussed. High plasma prolactin levels influence the cyclic and tonic hypothalamic function. Furthermore, prolactin appears to have a peripheral inhibitory influence on ovarian gonadotropin stimulation. Post partum anovulation and amenorrhoea can be caused by an antigonadotropic and antigonadic effect of prolactin.

Amenorrhea↗

PubMed1996

Node negative breast carcinoma: hyperprolactinemia and/or overexpression of p53 as an independent predictor of poor prognosis compared to newer and established prognosticators.

The purpose of this study was to investigate a prognostic indicator that can differentiate node negative breast cancer patients (N = 39, T2N0M0) with high risk and low risk for the development of recurrence or metastases. Preoperative plasma prolactin (PRL) was estimated by radioimmunoassay. The expression of PRL, p53, nm23, and c-erbB2 was investigated by immunohistochemical (IHC) localization; cathepsin D (CD, Enzyme Linked Sorbant Assay) and estrogen- and progesterone-receptors (ER and PR, Dextran coated charcoal method) were estimated in the tumor cytosols. The follow-up period was 2-6 years. Statistical comparisons were made between each marker for relapse-free survival (RFS) and overall survival (OS). Of the 39 patients, 18 had hyperprolactinemia (PRL > 20.0 ng/ml plasma), whereas overexpression of p53 was observed in 55% (17/31) tumors. These were independently and in combination associated with a reduced RFS and OS. The rest of the investigated markers did not show promising results. Hyperprolactinemia and/or overexpression of p53 were associated with aggressiveness of the tumor, early disease relapse or metastases, and poor OS in patients with node negative breast cancer. These two markers may enhance our ability to identify node negative breast cancer patients with aggressive tumors, for whom the use of adjuvant chemo and/or endocrine therapy is unequivocally justified.

Adult↗

PubMed2004

A case of Costello with parathyroid adenoma and hyperprolactinemia.

A 23-year-old female with Costello syndrome is presented. She had mental retardation, macrocephalia, "coarse" facial features, deep palmar and plantar creases, hyperkeratosis in palms and soles, hyperpigmentation, curly hair, and cutis laxa, which are among the diagnostic features of the syndrome, and a history of hyperprolactinemia since the age of 16. Her present complaint was weakness and widespread bone-pain. In routine biochemistry, she had an elevated calcium level of 11.1 (8.6-10.2) mg/dl and her DEXA evaluation was consistent with osteoporosis (vertebra and femur T score <-2.5). High PTH levels, 103 (8-78) pg/ml, suggested presence of a parathyroid adenoma. Tc-MIBI scintigraphy revealed two focuses of pathological uptake, one located inferior to left lobe of thyroid and the other in the superior left lobe of thyroid gland. After parathyroid adenomectomy, her serum calcium and PTH levels returned to normal values. This is the first case of parathyroid adenoma and hyperprolactinemia in the literature, reported in a patient with Costello syndrome.

Abnormalities, Multiple↗

PubMed1992

Premature death with bladder outlet obstruction and hyperprolactinemia in New Zealand black X New Zealand white mice treated with ethinyl estradiol and 17 beta-estradiol.

OBJECTIVE: To determine causes of death, estrogen toxicity, and hyperprolactinemia in a murine model of systemic lupus erythematosus (SLE). METHODS: Female New Zealand Black x New Zealand White (NZB x NZW) mice were implanted with ethinyl estradiol, 17 beta-estradiol, or empty capsules (controls). RESULTS: Estrogen-treated mice developed striking hyperprolactinemia and died prematurely with genitourinary complications. CONCLUSION: Implanted estrogens, including 17 beta-estradiol in a dose reported previously to stimulate SLE, contribute to premature death in NZB x NZW mice, through toxic effects. Estrogen therapy increases the level of prolactin, an immunostimulatory hormone.

Animals↗

PubMed1989

The influence of transient hyperprolactinemia on hormonal parameters, oocyte recovery, and fertilization rates in in vitro fertilization.

A detrimental effect of transient elevation of plasma prolactin (PRL) during in vitro fertilization (IVF) has not been proven; however, treatment with a dopamine agonist has been suggested. The present study was undertaken to determine if transient, midcycle hyperprolactinemia exerted a deleterious effect on the number of oocytes retrieved or on fertilization of oocytes in vitro. Fifty-three infertile patients with midcycle hyperprolactinemia (PRL greater than 20 micrograms/liter) during ovarian hyperstimulation for IVF were compared with 53 matched controls who remained normoprolactinemic. Mean (+/- SE) serum PRL levels on the day after hCG were significantly higher in the study group (29.5 +/- 1 micrograms/liter) than in the control (13.1 +/- 0.5 microgram/liter) (P less than 0.0005), whereas the mean estradiol (E2) concentrations on the same day were not significantly different (4822 +/- 287 and 4492 +/- 269 pmol/liters, respectively). Fertilization rates (72 +/- 4 and 70 +/- 4%, respectively) and the mean number of oocytes recovered (4.2 +/- 0.3 and 3.7 +/- 0.3, respectively) did not differ between the two groups. No correlation was observed between serum PRL and E2 levels, fertilization rates, or the number of oocytes retrieved in either group. Eleven patients with elevated PRL levels as a result of ovarian hyperstimulation were treated with 2.5 mg bromocriptine daily during the next IVF cycle. Serum PRL levels were significantly lower in the treated (5.6 +/- 1.8 micrograms/liter) than in the untreated cycles (35.6 +/- 3.1 micrograms/liter) (P less than 0.0005), whereas serum E2 concentrations did not differ.(ABSTRACT TRUNCATED AT 250 WORDS)

Bromocriptine↗