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Results for “Hyperprolactinemia”

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At least 19 recordsLinked to original sources

PubMed1989

Diagnosis of stress-related hyperprolactinemia. Evaluation of the hyperprolactinemia rest test.

It remains controversial whether two or three random estimations of prolactin (PRL) concentration obviate the need for special testing to rule out stress-related hyperprolactinemia. In order to clarify this issue, we measured PRL, cortisol, and growth hormone (GH) in serial blood samples obtained under resting conditions (HPR test) in 70 women who had had high PRL levels in two or more random blood samples. Twenty out of 70 women were found to have stress-related hyperprolactinemia, and 11 of the 20 would have been misdiagnosed by using only three random samples. Cortisol levels from the HPR test indicated stress-related pituitary adrenal reactivity in all groups, including the idiopathic (N = 30) and prolactinoma (N = 20) groups. However, PRL secretion in response to stress--a downward trend as a function of time--was evident only in the stress-related hyperprolactinemia group. These results suggest that a limited HPR test (ie, serial PRL determinations at 0, 30, and 60 min) is a valuable and simple measure to identify stress-related hyperprolactinemia in order to avoid diagnostic pitfalls and unnecessary treatment.

Adolescent↗

PubMed1979

[Adrenocortical function in hyperprolactinemia. The study of glucocorticoids, mineralocorticoids and androgens in chronic and acute hyperprolactinemias (author's transl)].

Glucocorticoids, mineralocorticoids, and adrenal androgens were studied in 3 groups of patients: control subjects (group I), hyperprolactinemic subjects (group II) and miscellaneous patients including chromophobe adenomas and normalized hyperprolactinemic subjects treated with Bromocriptine (group III). All the patients were studied in the basal state and under various conditions: Metyrapone, ACTH, TRH for glucocorticoids, ACTH, TRH, saline perfusion for mineralocorticoids, ACTH and TRH for androgens. It is concluded that: the adrenal secretion of glucocorticoids, mineralocorticoids and androgens is not altered under basal conditions in chronic hyperprolactinemia nor during dynamic tests in chronic hyperprolactinemia (prolactin adenoma) nor in acute hyperprolactinemia (induced by TRH).

Acute Disease↗

PubMed1989

Hachimijiogan treatment is effective in the management of infertile women with hyperprolactinemia or bromocriptine-resistant hyperprolactinemia.

Twenty-seven infertile women with hyperprolactinemia were treated with Hachimijiogan (5.0 to 10.0 g/day), Chinese herbal medicine. In 15 out of 18 patients, who were treated with Hachimijiogan, the serum prolactin levels dropped to 19.4 +/- 10.5 ng/ml during Hachimijiogan treatment, and the levels in 8 patients remained essentially unchanged during 6 months after the cessation of Hachimijiogan treatment. Three patients with 100 to 300 ng/ml did not drop to the level below 30 ng/ml. Four of 6 patients with amenorrhea ovulated. Eleven patients conceived and delivered normally. The hormonal profiles during or after pregnancy were normal. These results indicate that Hachimijiogan is a new safe treatment for hyperprolactinemic women.

Adult↗

PubMed1987

Suppression of pulsatile LH secretion, pituitary GnRH receptor content and pituitary responsiveness to GnRH by hyperprolactinemia in the male rat.

To assess whether gonadotropin-releasing hormone (GnRH) release from the hypothalamus might be altered by hyperprolactinemia in the male rat, we measured in chronically hyperprolactinemic rats the pituitary GnRH receptor content and described the pattern of luteinizing hormone (LH) release during the postcastration rise in gonadotropin secretion 24 and 72 h after gonadectomy. In intact rats, the effect of hyperprolactinemia was determined by describing the pattern of LH secretion, pituitary GnRH receptor content and assessment of pituitary responsiveness to small doses of GnRH (1.0 ng). In addition, to determine the role endogenous opioids might play in inhibiting GnRH release in hyperprolactinemic rats, we examined the effect of both a continuous infusion and a bolus injection of the opioid antagonist naloxone on the pattern of LH release. Chronic hyperprolactinemia was achieved by implanting 4 pituitaries under the kidney capsules 3-4 weeks before study. Acute hyperprolactinemia was achieved by injecting rats with 1 mg ovine prolactin every 12 h for 3 days. Control animals were untreated or were chronically hyperprolactinemic rats in which the hyperprolactinemia was transiently reversed by treatment for 3 days with the dopamine agonist 2-alpha-bromoergocryptine. The mean LH concentration was greatly decreased at 24 postcastration in chronically hyperprolactinemic rats relative to controls. This decrease was associated with a decrease in LH pulse height and pulse amplitude and pituitary GnRH receptor content, but not with an increase in the LH interpulse interval. In contrast, the decrease in mean LH concentrations in hyperprolactinemic animals at 72 h postcastration was primarily associated with a significantly longer LH interpulse interval than that observed in control animals. Chronic hyperprolactinemia in intact rats decreased the pituitary GnRH receptor content, in addition to decreasing the mean LH concentrations during pulsatile GnRH administration. Chronic hyperprolactinemia also inhibited LH release relative to controls during the continuous 4-hour infusion of naloxone and in response to a bolus injection of naloxone. However, in acutely hyperprolactinemic intact male rats a bolus injection of naloxone increase LH secretion 20 min later to levels similar to those obtained in control rats. In summary, these results indicate that chronic hyperprolactinemia decreased LH secretion by primarily decreasing GnRH secretion as suggested by a decrease in pituitary GnRH receptor content and a decrease in LH pulse frequency and pulse amplitude.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗

PubMed1991

[The effects of pregnancy on prolactin secretion in occulted hyperprolactinemia].

The changes in the maternal prolactin level during pregnancy and puerperium were studied in 14 patients with occulted hyperprolactinemia, 5 patients with functional hyperprolactinemia, and 135 women with normoprolactinemia. All of those with occulted hyperprolactinemia and functional hyperprolactinemia became pregnant through bromocriptine treatment. Higher prolactin levels were noted in occulted hyperprolactinemic patients from the first to second trimester of pregnancy, but in the third trimester prolactin levels fell to the normal control levels. This change completely resembled the change in functional hyperprolactinemic patients. Prolactin secreting capacities after puerperium returned to normal in 4 of the 5 patients with occulted hyperprolactinemia. These 4 became pregnant for the second time without any treatment. However, the other patient, whose prolactin secreting capacity was aggravated after the first puerperium, became pregnant the second time through bromocriptine treatment. These results indicate the following: 1) most cases of occulted hyperprolctinemia which may be due to functional lesions return to normal after pregnancy, 2) in rare cases of occulted hyperprolactinemia, prolactin secretion capacity is aggravated after the pregnancy, 3) it is important to observe the natural history of the patient in the treatment of occulted hyperprolactinemia.

Bromocriptine↗

PubMed1989

Luteal phase hyperprolactinemia during ovulation induction with human menopausal gonadotropins: incidence, recurrence, and effect on pregnancy rates.

Hyperprolactinemia may develop during ovulation induction with human menopausal gonadotropins and hCG (hMG/hCG). Because elevated serum prolactin (PRL) has several adverse effects on female reproductive function, this event has been implicated as a factor to explain the difference between ovulation and pregnancy rates in hMG/hCG treatment cycles. The incidence and severity of hyperprolactinemia in the luteal phase of hMG/hCG-stimulated cycles was investigated in a large series of patients. We analyzed 240 consecutive, ovulatory hMG/hCG cycles in 96 women from July 1984 to January 1986. All women had failed to conceive with clomiphene citrate, and had normal luteal phase PRL levels during unstimulated cycles. Daily serum total estrogens were determined during hMG administration. Serum progesterone and PRL were determined in the mid-luteal phase (7 days post-hCG administration). In 7.5% of the cycles, luteal phase PRL elevations were greater than 25 ng/mL. Only 2.5% of cycles had levels of PRL greater than 35 ng/mL. Hyperprolactinemia infrequently recurred in different cycles of the same patient (two of 16 patients, 12.5%). Cycles with hyperprolactinemia were found to have significantly higher preovulatory estrogen levels. Serum progesterone levels were not significantly decreased in cycles with elevated PRL. Pregnancy rates in cycles with and without hyperprolactinemia were similar (7.7 versus 11.1%, respectively; P greater than .05). We conclude that the development of luteal phase hyperprolactinemia during ovulation induction with hMG/hCG is an isolated event. High preovulatory estrogen levels may predispose to its development. Because hyperprolactinemia is uncommon and is usually mild, other factors must be responsible for the difference between ovulation and pregnancy rates using hMG/hCG.

Chorionic Gonadotropin↗

PubMed1989

Hyperprolactinemia and nonpuerperal mastitis (duct ectasia).

In 108 patients with nonpuerperal mastitis (inflammatory symptoms of duct ectasia), serum prolactin levels were determined before, during, and after treatment. Twenty-nine patients (26.8%) exhibited transiently elevated prolactin levels during the period of inflammation (mean +/- SD level, 42 +/- 22 micrograms/L) that returned to normal within 4 weeks. Twenty-two patients (20.4%) presented with more severe hyperprolactinemia (78 +/- 56 micrograms/L), and 15 were found to have pituitary microadenomas. In 11 cases, mastitis was the first symptom of hyperprolactinemia. A second group of 83 patients with known hyperprolactinemia and 83 normoprolactinemic controls were interviewed with regard to recent symptoms or past treatment of nonpuerperal mastitis. Sixteen hyperprolactinemic women (19.3%) and none of the controls reported that they had experienced mastitis. We conclude that duct ectasia is due in part to increased prolactin secretion. Thus, nonpuerperal mastitis may be a symptom of hyperprolactinemia. On the other hand, nonpuerperal mastitis may induce transient hyperprolactinemia (neurogenic hyperprolactinemia) of about 3 weeks' duration that is less pronounced than central hyperprolactinemia.

Adenoma↗

PubMed1992

Effects of hyperprolactinemia on prolactin and LH pulsatile pattern in female rats.

Prolactin (PRL) and luteinizing hormone (LH) secretions are very closely-related. To further understand these mechanisms, the pulsatile secretion pattern of both hormones in experimentally-induced hyperprolactinemia has been studied in adult female rats. Hyperprolactinemia was induced by the transplanting of two pituitary glands. Nine days after the transplant operation, rats were bled (75 or 100 microliters/7 min for 3 h). Serum samples were analyzed for prolactin and LH values by RIA. Hyperprolactinemia modifies pulsatile PRL secretion by increasing the absolute amplitude and duration of the peaks together with a decrease in their frequency. Also, the mean values of the hormone during the whole studied period were increased. Hyperprolactinemia was followed by an increase in the mean values of LH and in the absolute amplitude of the peaks. All these results suggest that hyperprolactinemia induced by pituitary grafting in adult female rats, is followed by a significant change in prolactin and LH pulsatility, which may explain, to some extent, the effects of hyperprolactinemia on reproduction.

Animals↗

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↗

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↗

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↗

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↗

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↗

PubMed1992

Gonadotropin-releasing hormone-associated peptide gene sequences in women with hyperprolactinemia.

OBJECTIVE: To determine if mutations in the structural gene for gonadotropin-releasing hormone (GnRH)-associated peptide are present in women with hyperprolactinemia. DESIGN: Patients with hyperprolactinemia and controls were studied retrospectively for GnRH-associated peptide gene mutations. SETTINGS: Patients seen in a clinical setting were studied at a medical school laboratory setting. PATIENTS: Fifteen women with hyperprolactinemia and two fertile controls with normal prolactin levels were studied. INTERVENTIONS: Genomic deoxyribonucleic acid (DNA) was extracted from each patient and subjected to Southern blot analysis and polymerase chain reaction (PCR). For Southern blot analysis, DNA was digested with EcoRI, XbaI, BglII, PstI, and BamHI and hybridized to two DNA probes for GnRH-associated peptide. Exons II to IV, which encode for the structural gene, were amplified by PCR. MAIN OUTCOME MEASURES: Fragment sizes from autoradiographs were compared among patients and controls. Amplified PCR products of exons II to IV of the GnRH-associated peptide were also compared. RESULTS: No large deletions, insertions, or polymorphisms were identified in women with hyperprolactinemia or controls by Southern blotting. Each of the exons was present and of normal size by PCR in the study patients and controls. CONCLUSIONS: No large deletions of the GnRH-associated peptide gene appear to be present in our patients with hyperprolactinemia. Small deletions, insertions, or point mutations are not excluded by this analysis.

Adolescent↗

PubMedDate not supplied

Hyperprolactinemia and 5-alpha-reductase activity.

A number of experimental data indicate that hyperprolactinemia inhibits the activity of 5-alpha-reductase; however, no information is available about the time required for this enzyme to re-activate after prolactinemia has returned to normal values. In the present study, five normal caucasian men, whose fertility had previously been proven, were given HCG (5000 IU/day by intramuscular route for three days) both in basal conditions and after sulpiride-induced hyperprolactinemia (dosage = 200 mg/day for ten days). In both conditions, the plasma levels of prolactin (PRL), testosterone (T), dihydro-testosterone (DHT), 17-beta-estradiol (E2), and dehydroepiandrosterone sulfate (DHAS) were monitored during the treatment with HCG and for an additional 24 hrs after HCG discontinuation. All hormones were assayed by RIA. Our results demonstrate that hyperprolactinemia causes a marked decrease (58%) of DHT, a less marked decrease (39%) of T, an increase (43%) of DHAS whereas only a small increase (2%) of E2 was observed. Steroids were shown to behave differently after the HCG tests performed in the two experimental conditions. In particular, the levels of DHT had a much more pronounced increased after HCG in the second test than in the first; in contrast, both DHAS and E2 had a less marked response after the second test. Our data, on the one hand, confirm that 5-alpha-reductase is inhibited by hyperprolactinemia; on the other hand, the hyperprolactinemia-induced block of this enzyme appears to be rapidly reversible because the enzyme is reactivated within 48-72 hrs after normalization of prolactin levels. (Normal values of prolactin were on the average achieved on the 4th day after sulpiride discontinuation).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

PubMed1989

Hyperprolactinemia decreases naloxone binding in the arcuate nucleus of ovariectomized rats.

Hyperprolactinemia suppresses endogenous prolactin (PRL) secretion and inhibits LH release in ovariectomized rats. Opiate peptides appear to mediate the suppressive effects of hyperprolactinemia on both endogenous PRL and LH secretion. A mechanism by which hyperprolactinemia may change the ability of opiates to influence PRL and LH is by altering the density of opiate receptors. We, therefore, examined the effect of hyperprolactinemia on the density of naloxone binding sites in hypothalamic regions that are important in the regulation of PRL and LH secretion. Female rats, ovariectomized for 4 days, were treated with ovine prolactin (oPRL) every 8 h for 2 days, and naloxone binding sites were measured using autoradiographic procedures. oPRL treatment suppressed the concentration of naloxone binding sites throughout the arcuate nucleus but had no effect in the median eminence, suprachiasmatic nucleus, and medial preoptic nucleus. There is evidence that the tuberoinfundibular dopaminergic neurons of the arcuate nucleus are directly influenced through opiate receptors. We propose that the observed decrease in the density of opiate receptors may occur on dopaminergic neurons. This theory provides an explanation for a mechanism for the suppression of endogenous PRL and LH by hyperprolactinemia: a decrease in opiate receptors will decrease opiate suppression of dopamine neurons allowing dopamine activity to increase. Increase in dopamine release are known to decrease PRL and LH secretion in ovariectomized rats. Alternatively, decreased naloxone binding may result from homologous down-regulation of receptors due to increased opiate activity. If opiate activity increases, it may directly inhibit LHRH neurons and may suppress the activity of inhibitory neurons leading to increased dopamine activity.

Animals↗

PubMed1990

Hyperprolactinemia and temporal lobe epilepsy in a woman: concomitant and persistent prolactin suppression and temporal lobe epilepsy relief.

It has been reported that hyperprolactinemia may be associated with increased temporal lobe activity. Coexisting hyperprolactinemia (97.5 +/- 3.2 ng/ml) related to a pituitary tumefaction (8 mm) and Temporal Lobe Epilepsy (TLE), were observed in a 37-year-old woman. Carbamazepin (CBZ) therapy induced a marked improvement in TLE symptoms and EEG recordings, but did not influence hyperprolactinemia and related symptoms. Long-lasting (27 months) normoprolactinemia (19.4 +/- 0.6 ng/ml) and TLE relief were achieved on a dopamine (DA) agonist medication, e.g. pergolide mesylate, 25-50 micrograms/day given over 8 months, and persisted as long as 27 months after drug withdrawal. Posttreatment CT scans showed progressive shrinkage of the pituitary tumor (2 mm) associated with an empty-sella. It is proposed that, whenever TLE and hyperprolactinemia coexist, therapy with a DA agonist such as pergolide mesylate, resulting in normoprolactinemia, may be beneficial in TLE control.

Adult↗