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PubMed1988

Transient hyperprolactinemia during cycle stimulation: influence on the endocrine response and fertilization rate of human oocytes and effects of bromocriptine treatment.

The effect of transient hyperprolactinemia and its treatment during cycle stimulation on the endocrine response and fertilization rate of human oocytes was studied. Fifty stimulated cycles were included in the study and divided into three groups: group I consisted of 18 cycles with serum prolactin (PRL) levels less than or equal to 25 ng/ml; group II contained 15 cycles, where patients developed PRL levels greater than 25 ng/ml; group III consisted of 17 cycles, where patients, who already developed hyperprolactinemia in a previous cycle, were treated by 3.75 mg bromocriptine daily. The serum estradiol (E2), progesterone (P) and PRL levels 1, 2, and 3 days before and at oocyte retrieval were evaluated. The E2 decrease at oocyte retrieval was significantly steeper in groups I and III. Follicular luteinization was more effective in groups I and III. The fertilization rate in groups I and III was significantly higher than in group II. High serum PRL levels seem to interfere in follicular and oocyte development. The treatment of transient hyperprolactinemia improved the patients' endocrine response and the fertilization rate of oocytes.

Adult↗

PubMed1989

Effectiveness of vaginal bromocriptine in treating women with hyperprolactinemia.

Treatment of hyperprolactinemia with oral bromocriptine has been associated with a high incidence of side effects. The authors recently demonstrated that, in normal women, the vaginal route of administration was an effective and safe alternative to oral bromocriptine. To evaluate the effectiveness of vaginal bromocriptine in treating women with hyperprolactinemia, the authors treated 15 hyperprolactinemic women with daily vaginal administration of 2.5 mg tablets of bromocriptine. Serum prolactin (PRL) levels and vital signs were measured daily for 6 days, then weekly for 4 weeks. Gastrointestinal side effects were limited to a single episode of mild nausea, and two cases of transient constipation. In all patients there was a dramatic initial reduction in PRL in response to a single 2.5 mg dose of bromocriptine. In 13 patients PRL levels were maintained within the normal range with daily administration of 2.5 mg, whereas in two patients, PRL levels remained higher than normal despite an increase in bromocriptine dose to 5 mg. These results suggest that short term use of vaginal bromocriptine is a safe and effective method of therapy for hyperprolactinemia.

Administration, Intravaginal↗

PubMed1997

Hyperprolactinemia in postmenopausal women.

OBJECTIVE: To study the clinical cause and course of hyperprolactinemia in postmenopausal women. DESIGN: Retrospective case-note study. SETTING: Tertiary care hospital. PATIENT(S): Six postmenopausal women with hyperprolactinemia. MAIN OUTCOME MEASURE(S): Clinical history and physical examination, serum levels of PRL, LH, FSH, computed tomography (CT) of the pituitary gland before and after treatment with bromocriptine. RESULT(S): At presentation, the mean age was 57.5 +/- 7.5 SD years. The mean level of PRL was 1,427 +/- 1,599 ng/mL (1,427 +/- 1,599 micrograms/L). All women suffered from secondary amenorrhea for a mean duration of 31.8 +/- 5.6 years. Five of six had galactorrhea at some time in the past. Pituitary imaging revealed a pituitary macroadenoma in four women, an enlarged sella suggestive of a pituitary macroadenoma in one woman, and a microadenoma in one. After treatment with bromocriptine, the PRL level decreased in all women to within normal limits. Five of six women developed hot flushes after the PRL level returned to normal. CONCLUSION(S): Most cases of hyperprolactinemia in postmenopausal women are due to macroadenoma rather than microadenoma, the common finding in younger women. The clinical course is suggestive of a prolonged disease that was not detected earlier, although clinical signs were present. These findings are suggestive of an enlargement of microadenomas to macroadenomas as time passes.

Adenoma↗

PubMed2003

Hyperprolactinemia and bone mineral density: the potential impact of antipsychotic agents.

The prevalence of schizophrenia is about 1% worldwide. Individuals with schizophrenia are at increased risk for osteoporosis and fractures for several reasons, including poor diet, lack of exercise, cigarette smoking, and polydipsia. Some antipsychotic medications may further increase the risk of fractures by causing dizziness, orthostatic hypotension, and falls. Studies in women with hyperprolactinemia resulting from pituitary tumors have demonstrated high rates of osteoporosis believed to result from hypoestrogenism. Similarly, hyperprolactinemia in men results in hypogonadism and bone loss. Preliminary surveys have indicated that schizophrenia patients also may have elevated rates of osteoporosis and pathological fractures, possibly resulting in part from the long-term administration of antipsychotic agents that produce hyperprolactinemia and secondarily lower estrogen and testosterone levels. This potential complication of treatment with certain antipsychotic agents requires careful study and could represent a serious public health problem.

Antipsychotic Agents↗

PubMed1986

Light and electron microscopical morphometry of pituitary adenomas in hyperprolactinemia.

Two highly differentiated acidophil prolactin-cell adenomas with hyperprolactinemia (group I), 8 large cell chromophobe adenomas with hyperprolactinemia (group II), and 2 small cell chromophobe adenomas (group III), one of which was combined with hyperprolactinemia, were studied immunohistologically. Morphometry was performed on the light- and electron microscopical level. The 11 active adenomas were immunohistologically positive for prolactin, the 12th adenoma with normal prolactin plasma level was negative for prolactin. Light microscopical morphometry displayed significantly more cells of smaller size in the "small cell chromophobe" adenomas, whereas the large cell chromophobe adenomas and the highly differentiated prolactin cell adenomas were not different. Ultrastructural morphometry demonstrated significant differences between highly differentiated prolactin cell adenomas (group I), and large cell chromophobe adenomas (group II). The latter contain smaller "relative volumes" of nucleoli and of secretory granules, whereas the rough endoplasmic reticulum, the Golgi fields and the nuclei were not different. Comparison of large cell chromophobe adenomas (group II), and small cell chromophobe adenomas (group III) revealed significantly larger relative volumes of nuclei and of mitochondria but smaller volumes of rough endoplasmic reticulum and of Golgi fields in the small cell chromophobe adenomas. Significant differences between the active and the inactive adenoma of small cell chromophobe type in the group III were not found. In spite of the low quantity of small cell chromophobe adenomas and of acidophil prolactin cell adenomas, our data demonstrate that there exist distinct and significant light microscopical and ultrastructural differences between the three adenoma types.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma, Acidophil↗

PubMed2005

[When and how should hyperprolactinemia be treated?].

Hyperprolactinemia affects the gonadotropic axis. Its results in women include amenorrhea, menstrual disorders and galactorrhea; in men, the frequency of macroadenomas tends to lead to problems related to sexual performance or tumor volume. Radioimmunoassays make diagnosis easy. Secondary causes of hyperprolactinemia, drug reactions in particular, must be ruled out before MRI exploration to look for a pituitary tumor. First-line treatment of prolactin adenomas is based on the use of dopaminergic agonists, especially cabergoline, because of their excellent efficacy and the risk of relapse following surgery. For patients who wish to become pregnant, the dopaminergic agonist must be continued during pregnancy for those with macroadenoma and withdrawn for women with microadenoma. When hyperprolactinemia is induced by anti-psychotic agents, treatment requires an in-depth assessment.

Dopamine Agonists↗

PubMed2001

Polycystic ovary syndrome and hyperprolactinemia.

Analysis of the evidence linking PCOS and hyperprolactinemia suggests that these conditions have independent origins. Elevated prolactin serum levels are documented in the early studies of patients with polycystic ovaries. However, recent investigators using serial serum sampling have excluded transient elevations of prolactin and have shown a less frequent association of these disorders. Treatment of individuals with both PCOS and hyperprolactinemia is distinct from the management of the individual with only one of these conditions. Upon evaluating the therapeutic alternatives for dysfunctional uterine bleeding and hirsutism in these patients, the effect of exogenous estrogen and progesterone on the secretion of prolactin must be considered. The addition of a dopamine agonist (e.g., bromocriptine or cabergoline) to a regimen of clomiphene citrate must also be considered as ovulation induction options for these women. Finally, future discoveries about the relationship between PCOS and hyperprolactinemia will require a better understanding of how the hypothalamus regulates the pituitary secretion of LH and prolactin.

Female↗

PubMed2004

Hyperprolactinemia in Sjogren's syndrome: a patient subset or a disease manifestation?

OBJECTIVE: To investigate the prevalence of hyperprolactinemia in patients with primary Sjogren's syndrome (SS), its clinical significance and its implication to our understanding of the disease pathogenesis. MATERIALS AND METHODS: Forty-nine patients with primary SS (44 females and five males) age range 37-66 years were included in this study. All patients underwent clinical assessment for disease manifestations in addition to laboratory assessment for serum prolactin, sex hormones and immunological profile. Fifty healthy subjects (44 females and six males) of matched age were studied as control group. RESULTS: The mean prolactin serum level was significantly higher in SS patients compared to the control group (P < 0.01). This significant difference was persistent after subgrouping the patients and the controls based on their menstrual history. Hyperprolactinemia (>20 ng/ml) was prevalent in 16.3% of SS patients. There was no correlation between serum prolactin levels and hormonal status, autoantibodies as well as systemic manifestations of the disease. CONCLUSION: Patients with primary SS have moderately increased levels of prolactin. Hyperprolactinemia reflects disease pathology rather than being present in a subset of patients. The presence of elevated prolactin levels was not associated with hormonal status, clinical or immunological manifestations of primary SS.

Adult↗

PubMed2002

[True and false hyperprolactinemia: how to discriminate one from the other in infertility management?].

Serum prolactin measurement is usually performed in infertility evaluation, even if there's no specific clinical presentation of hyperprolactinemia. High levels of prolactin are noted in 20 to 30% of menstrual abnormalities and in about 10% of regular menses. It is of importance to determine whether hyperprolactinemia is related to pituitary adenoma, drug administration, general diseases, or circulating large forms of prolactin, in order to avoid heavy, expensive, time consuming and unnecessary clinical investigations or therapeutic actions. We must first to confirm the biological diagnosis of hyperprolactinemia with few repeated plasmatic measurements, and, later, if necessary use TRH-metoclopramide test and/or pituitary magnetic resonance imaging.

Female↗

PubMedDate not supplied

Atypical polypoid adenomyoma in a patient with hyperprolactinemia.

We report a case of an atypical polypoid adenomyoma in a patient with hyperprolactinemia. A 23-year-old Japanese woman was admitted complaining of atypical genital bleeding. Specula examination revealed a walnut-size polypoid mass extruding from the cervix. The patient was oligomenorrheac, and endocrine analysis showed hyperprolactinemia. Transvaginal ultrasonography and magnetic resonance imaging revealed an endometrial polypoid mass (4 x 3 x 3 cm) arising from the lower segment of the uterine corpus. The pathologic diagnosis of the tumor after polypectomy was atypical polypoid adenomyoma. It is suggested that ovarian dysfunction caused by hyperprolactinemia may be involved in the pathogenesis of atypical polypoid adenomyoma in the present case.

Adenomyoma↗

PubMed1987

Absence of suppressive effect of somatostatin on prolactin levels in patients with hyperprolactinemia.

The effect of somatostatin (SRIF: 10 micrograms/min during 120 min) on serum prolactin (PRL) levels was studied in eleven patients with hyperprolactinemia of varying causes: 2 patients with acromegaly; 2 with primary hypothyroidism; 4 with prolactinoma and 3 with drug (sulpiride) induced hyperprolactinemia. During SRIF infusion, no significant change in PRL levels was observed in any of the 4 groups studied except in one female patient with a prolactinoma. The biological activity of SRIF was demonstrated by the significant inhibition (P less than 0.05) of insulin levels seen in all 11 patients (52% fall in relation to basal) without simultaneous modification of glycemia. These data suggest that SRIF does not decrease PRL secretion in most patients with hyperprolactinemia.

Acromegaly↗

PubMed1986

Hyperprolactinemia associated with chronic renal failure in the rat.

Patients with CRF exhibit hyperprolactinemia and resistance to the prolactin-suppressive effects of dopamine. In order to explore the pathogenetic mechanisms involved, an animal model of CRF was developed in the adult male rat bearing an indwelling right atrial catheter by performing a two stage 5/6 nephrectomy (NX). Following NX, serum creatinine levels rose to a value of 1.36 +/- 0.2 mg/dl at 8 weeks as compared to sham-operated controls (0.31 +/- 0.1, P less than 0.01). There was a parallel increase in plasma prolactin levels in NX animals with values significantly greater than in controls by 8 weeks (49 +/- 11 vs 17 +/- 2 ng/ml, P less than 0.02). At 8 weeks, the plasma prolactin responses to metoclopramide (500 micrograms/kg, iv) were similar in unanesthetized NX and sham-operated control animals. The prolactin-suppressive effects of an iv dopamine infusion (6 micrograms/kg/min X 30 min) was also similar in the two groups (46 +/- 8% vs 40 +/- 10% suppression). The responses of lactotrophs in vitro were compared in NX and control animals at 8 weeks. Basal prolactin release during 4 h was similar in the two groups as were the suppressive responses to dopamine and bromocriptine. The results indicate that the rat with CRF, like human develops hyperprolactinemia. In contrast to the human, however, responses to dopaminergic agonists and antagonists in vivo and in vitro are unimpaired, indicating that hyperprolactinemia in rats with CRF occurs on a non-dopaminergic basis.

Animals↗

PubMed2000

Effect of chronic hyperprolactinemia on daily changes of glutamate and aspartate concentrations in the median eminence and different hypothalamic areas of male rats.

The 24h changes of glutamate (GLU) and aspartate (ASP) were studied in the median eminence (ME) and hypothalamic areas. It was analyzed whether prolactin may change their daily patterns. The hypothalamic concentration of these amino acids was measured by high-performance liquid chromatography (HPLC) with fluorometric detection. Plasma prolactin levels increased over the 24h light-dark cycle after pituitary grafting compared to controls, and its circadian rhythm was disrupted. In controls, aspartate and glutamate in the hypothalamic areas studied followed a specific daily variation or showed no rhythmicity. In the median eminence, hyperprolactinemia seem to phase advance the aspartate or glutamate peaks from 16:00 to 12:00. In the mediobasal hypothalamus, hyperprolactinemia altered daily changes of aspartate and significantly decreased its concentration. Also, it seems to delay the nocturnal glutamate peak compared to controls. In the posterior hypothalamus, hyperprolactinemia did not change aspartate and glutamate concentrations and their daily changes, although it increased the glutamine concentration. These data show the existence of 24h changes of amino acid concentration in three of the hypothalamic regions studied. Increased plasma prolactin levels differentially affected these patterns depending on the hypothalamic area analyzed.

Animals↗

PubMed2002

Relapse of hyperprolactinemia after transsphenoidal surgery for microprolactinoma: lessons from long-term follow-up.

OBJECTIVE: The long-term results of transsphenoidal surgery for microprolactinoma, with particular reference to the question of permanence of relapse of hyperprolactinemia after biochemical cure, are examined. METHODS: Patients whose operations were performed in the city of Glasgow, Scotland, by one neurosurgeon (GMT) have been followed up for between 15 and 21 years after surgery was performed. RESULTS: Of a cohort of 44 patients with confirmed microprolactinoma at the time of surgery, 8 patients (18.2%) who experienced recurrent hyperprolactinemia postoperatively continued to be monitored. Selective hypophysectomy resulted in normal prolactin levels in all patients initially. Relapse occurred at 2 to 10 years (mean, 5.3 yr) postoperatively, but was permanent in only two patients (4.5%). Of the remaining six patients (13.6%), four (9.1%) became normoprolactinemic after 6 or 7 years' recurrence, and two (4.5%) are now only marginally hyperprolactinemic (prolactin >500 but <700 mU/L) at 15 and 18 years after transsphenoidal hypophysectomy. CONCLUSION: The recurrence of hyperprolactinemia after transsphenoidal surgery for microprolactinoma is not necessarily a permanent feature and does not inevitably indicate operative failure.

Adult↗

PubMed2003

Hyperprolactinemia in patients on antipsychotic drugs causes ADP-stimulated platelet activation that might explain the increased risk for venous thromboembolism: pilot study.

Recently, an increased risk of venous thromboembolism in patients on antipsychotic drugs has been reported, but the molecular etiology is still unknown. Most antipsychotic drugs act as dopamine antagonists, and some of them cause hyperprolactinemia. Hyperprolactinemia has recently been found to cause increased platelet activation via potentiating ADP effects on human platelets. We assessed prolactin values as well as ADP-stimulated and thrombin receptor activator 6-stimulated expression of the platelet activation marker P-selectin in 20 consecutive patients under therapy with antipsychotic drugs. We detected a significant correlation between prolactin values and ADP-stimulated P-selectin expression on platelets in patients on antipsychotic drugs, revealing a significant higher platelet stimulation in hyperprolactinemic patients on antipsychotic drugs than in normoprolactinemic controls. Therefore, hyperprolactinemia might be the yet unknown acquired risk factor in patients on antipsychotic drugs explaining the increased risk for venous thromboembolism in these patients.

Adolescent↗

PubMedDate not supplied

Effects of experimental hyperprolactinemia and clomiphene on pituitary responsiveness to LHRH and TRH in men.

The effect of clomiphene citrate during sulpiride-induced hyperprolactinemia on pituitary function was tested in 8 healthy men, who ingested 100 mg of clomiphene, 150 mg of sulpiride or 100 mg of clomiphene + 150 mg of sulpiride daily for 7 days. Clomiphene treatment increased FSH and LH plasma concentrations and this increase was unaffected by sulpiride-induced hyperprolactinemia. Sulpiride intake alone did not alter serum gonadotropin concentrations. A reduced LH response to LHRH during sulpiride intake was seen, whereas the FSH response was unchanged. The prolactin response to TRH was unaffected during the combined sulpiride + clomiphene ingestion. Sulpiride treatment did not change the basal and/or clomiphene-stimulated gonadotropin secretion in healthy men. Thus, oligozoospermic men using psychotropic drugs and/or with hyperprolactinemia may be suitable candidates for clomiphene treatment.

Adult↗

PubMedDate not supplied

Effect of chronic hyperprolactinemia induced by sulpiride on plasma dehydroepiandrosterone (DHA) in normal men.

In order to elucidate the relationship between plasma dehydroepiandrosterone (DHA) and sulpiride-induced hyperprolactinemia (of 60 day duration) in normal men, five normal men (aged 27-46) were administered daily 300 mg of sulpiride orally for 60 days to induce hyperprolactinemia. Plasma levels of prolactin, DHA and cortisol were measured by radioimmunoassay before sulpiride treatment, at day 14 and day 60 after initiation of the treatment. Plasma levels of prolactin after the administration rose significantly (P less than 0.001) to 71.6-95.3 ng/ml in four out of the five subjects compared with those of the controls. In the same four subjects the mean DHA values in plasma were elevated significantly (P less than 0.05) to 877 +/- 160 ng/dl from the mean baseline values (669 +/- 91 ng/dl). The elevated values remained during sulpiride treatment. Plasma levels of cortisol did not change significantly during sulpiride administration in all subjects. Our results suggest that sulpiride-induced hyperprolactinemia sustained at least 14-60 days in normal men stimulates the adrenal cortex to secrete DHA.

Administration, Oral↗

PubMed2001

Effects of hyperprolactinemia on rat prostate growth: evidence of androgeno-dependence.

The effects of the polypeptide hormone prolactin (PRL) in the development and regulation of benign prostate hyperplasia (BPH) and also in prostate cancer are not very well characterized. This study examines the action of PRL, either alone or in association with androgens [testosterone (T) or dihydrotestosterone (DHT)], in the rat prostate gland. The effects of PRL and androgens were investigated after 30 and 60 days in control, castrated, castrated with a substitutive implant of T or DHT, and sham-operated Wistar rats. To enhance PRL release, we induced hyperprolactinemia by administering chronic injections of sulpiride (40 mg. kg(-1). day(-1)). Chronic hyperprolactinemia induces enlargement and inflammation of the lateral rat prostate without any histological changes on ventral and dorsal lobes. We also demonstrate that hyperprolactinemia induces Bcl-2 overexpression in the lateral rat prostate and that this could inhibit the level of apoptosis. The in vivo model established here is a useful in vivo approach for studying the hormonal regulation of normal and pathological prostate development.

Animals↗