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Results for “hyperprolactinemia”

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PubMed1982

Breast tumors in patients with hyperprolactinemia.

The histology of breast lumps in five patients with hyperprolactinemia showed benign mammary dysplasia with vacuolation of acinar and duct lining cells. In two cases, foci of lobular development resembling lactating breast tissue were also noted. In the past, focal secretory change has been considered to be idiopathic, but these cases indicate a possible association with hyperprolactinemia. Among other causes hyperprolactinemia may be a manifestation of occult pituitary adenoma. Therefore it is suggested that patients with benign breast nodules showing focal secretory change should be screened for clinical and laboratory evidence of hyperprolactinemia. Although it is accepted that in mice and rats prolactin plays an important role in chemically induced mammary tumorigenesis, a consensus has not been reached with regard to its role in man.

Adult↗

PubMed1983

Hypothalamic and limbic GABA concentrations and turnover rates and glutamate concentrations following induction of hyperprolactinemia in ovariectomized rats.

Hyperprolactinemia was induced by transplantation of pituitaries of donor rats under the kidney capsule of ovariectomized recipient rats. This results in a permanently increased serum prolactin and temporarily suppressed luteinizing hormone (LH) levels. Concentrations of gamma-aminobutyric acid (GABA) and glutamate as well as turnover rates of GABA were determined in micropunches of the nucleus accumbens (ACB), medial preoptic area (MPO), anterior and posterior part of the mediobasal hypothalamus (AMBH and PMBH) and in the mediocortical amygdala (AMY). GABA concentration in the ACB and MPO were reduced in hyperprolactinemic rats. This was significant at day 8. At days 4 to 21 following pituitary transplantation glutamate concentrations were also significantly reduced in the AMY. The most conspicuous changes in GABA turnover rates were observed in the ACB and MPO. In the former structure hyperprolactinemia reduced GABA turnover, while in the latter high prolactin levels increased GABA turnover at day 4. It is concluded that the suppressive effect of hyperprolactinemia on blood LH levels may involve a preoptic GABAergic component and possibly a glutamatergic mechanism in the AMY. Alternatively, the AMY and the ACB may be involved in eliciting the many behavioral effects associated with hyperprolactinemia.

Animals↗

PubMed1985

Influence of chronic hyperprolactinemia induced by sulpiride on the hypothalamo-pituitary-testicular axis in normal men.

For elucidation of the effects of hyperprolactinemia on the hypothalamic-pituitary-testicular axis, five healthy men were exposed to sulpiride (300 mg/day by mouth); four among the five maintained hyperprolactinemia (71.6 to 95.3 ng/ml) for 78 days. Clomiphene citrate (CC), luteinizing hormone (LH)-releasing hormone, and human chorionic gonadotropin tests were performed before and after sulpiride treatment. The CC test, given as a measure of hypothalamic function, was carried out in each of the five volunteers before sulpiride treatment (control) and on days 14 (2 weeks) and 60 (2 months) of sulpiride administration. Each value of plasma LH stimulated by CC was integrated and expressed as a ratio of the integrated value obtained after administering CC at 2 weeks and 2 months to that from each control experiment. The mean ratio in the four subjects at 2 months (mean +/- standard deviation, 0.769 +/- 0.121) was significantly lower than that at 2 weeks (0.942 +/- 0.073; P less than 0.05) and before sulpiride treatment (1.000; P less than 0.01). Impairment of LH responses to CC by 2-month long sulpiride-induced hyperprolactinemia suggests that chronic hyperprolactinemia in men partly suppresses LH secretion by its inhibitory action on the hypothalamus.

Adult↗

PubMed1981

[Oral steroid contraception in hyperprolactinemia (author's transl)].

A study on the statistical correlation between oral contraceptives and similar mixtures of steroids and the development and maintenance of hyperprolactinemia is presented. 91 cases with hyperprolactinemia-amenorrhoea were compared to a group of 91 women with amenorrhoea and normal prolactinemia. Matched pairs regarding duration of amenorrhoea, parity, gonadal function and thyroid function were used. It was shown that oral contraceptives and similar combination of estrogen and progesterone do not increase the relative risk for functional or adenomatous hyperprolactinemia. There were no evidence that existing adenomas were deteriorating during oral contraception. However, two cases with pituitary adenoma following long-term high dosage estrogen therapy was found. The presented results show that low dosage steroid medications do not increase the risk for the development or maintenance of hyperprolactinemia.

Adenoma↗

PubMed2003

Hyperprolactinemia and schizophrenia: mechanisms and clinical aspects.

The association between elevated prolactin levels and conventional antipsychotics is well-established. The novel antipsychotic, risperidone, has also been shown to elevate prolactin levels. Patients undergoing treatment with these medications are at high risk for developing hyperprolactinemia, which is associated with decreased bone mineral density, osteoporosis, menstrual disruptions and infertility, galactorrhea, breast cancer, cardiovascular disorders, and sexual impairment. Patients treated with conventional antipsychotics and risperidone should be routinely screened for hyperprolactinemia, and monitored for known sequelae. Optimally, patients with hyperprolactinemia secondary to antipsychotic drug treatment should be switched to a prolactin-sparing antipsychotic. This review will briefly highlight the regulation and function of prolactin secretion, discuss clinical effects of antipsychotic-induced hyperprolactinemia, and suggest a course of treatment.

Journal Article↗

PubMed1983

Effects on male sex behavior and preoptic dopamine neurons of hyperprolactinemia induced by MtTW15 pituitary tumors.

We have earlier reported that dopamine (DA) activity in the preoptic anterior hypothalamic (POA-AH) region of castrated rats is inhibited by testosterone and accelerated by PRL. These results suggested that dopaminergic neurons may play an important role in male copulatory behavior, particularly in the attenuation of sex behavior reported to be associated with hyperprolactinemia. We have now examined the effects of severe hyperprolactinemia on the POA-AH DA activity in association with any modifications of copulatory behavior. Sexually experienced adult male rats were castrated and implanted sc with Silastic implants containing testosterone to maintain serum testosterone levels in the range found in intact rats. Hyperprolactinemia was induced by inoculation of minced MtTW15 PRL secreting pituitary tumor fragments. Copulatory behavior was assessed at weekly intervals in hyperprolactinemic and control rats. During the period of tumor growth serum PRL levels increased logarithmically. Whereas sexual activity continued to improve in control rats, there was a marked decrease in several important parameters of copulatory behavior in hyperprolactinemic rats. The most dramatic decrease occurred in the percentage of tumor-bearing rats ejaculating which decreased progressively to zero at 6 weeks after tumor inoculation. Ejaculation frequency decreased and ejaculation latency increased in tumor-bearing rats before the complete disappearance of ejaculatory behavior. The deficits in copulatory behavior of hyperprolactinemic rats were accompanied in parallel studies by significant depletions of DA concentrations in the POA-AH. Further, neuronal activity, as evidenced by the turnover rates measured by rate of loss of DA after tyrosine hydroxylase inhibition with alpha-methyl paratyrosine, was markedly augmented in the POA-AH of hyperprolactinemic rats as compared to control animals. These findings disclose a close association between the acceleration in POA-AH DA activity and the attenuation of copulatory behavior induced by hyperprolactinemia and suggest the probability of an underlying role of the POA-AH DA neurons in male sex behavior normally induced by testosterone.

Animals↗

PubMed1984

Human menopausal gonadotropin/human chorionic gonadotropin-induced ovarian hyperstimulation with transient hyperprolactinemia: steroidogenesis enhanced during bromocriptine therapy in monkeys.

To examine the role of gonadotropin-induced hyperprolactinemia on reproductive function, 17 euprolactinemic ovulatory monkeys were given extended fixed dose regimens of human menopausal gonadotropin (hMG) (12 days), followed by hCG the next day, and some animals then received bromocriptine. All animals were given hMG/hCG from day 3 (D3) until D14, with hCG on D15; those in group I (n = 12) received no further therapy, while those in group II (n = 5) received bromocriptine (0.25 mg/kg X day, im) daily from the day of hCG administration until menses. Ovarian hyperstimulation developed to various degrees in all animals. Based on serum estradiol (E2) levels, 13 were high responders (E2, greater than 1000 pg/ml), 2 were medium responders (E2, 500-1000 pg/ml), and 2 were low responders (E2, 150-500 pg/ml). In group I, transient hyperprolactinemia occurred in the luteal phases in 8 of the 12 animals compared to the follicular phase levels in the same animals (P less than 0.01). In group II, bromocriptine treatment in the luteal phase prevented hyperprolactinemia, but there was no change in the menstrual cycle or luteal phase lengths; however, significant luteal phase increases in progesterone (P less than 0.005) and E2 (P less than 0.02) secretion occurred during bromocriptine therapy. Deliberate hMG/hCG studies in euprolactinemic women seem indicated to learn whether women so treated experience estrogen-progesterone-induced hyperprolactinemia like that in monkeys and, if so, to determine its consequences on the reproductive process.

Animals↗

PubMedDate not supplied

Reversible thioridazine-induced magnetic resonance imaging-documented pituitary enlargement associated with hyperprolactinemia.

OBJECTIVE: To document a case of reversible thioridazine-induced pituitary enlargement associated with hyperprolactinemia in a patient with schizophrenia. METHODS: We describe a 19-year-old woman with paranoid schizophrenia who was taking thioridazine (a phenothiazine), in whom hyperprolactinemia, galactorrhea, oligomenorrhea, and a reversible anatomic pituitary abnormality developed. Serial magnetic resonance imaging (MRI) studies were used to assess the status of the pituitary gland during various pharmaceutical therapies. RESULTS: Laboratory evaluation revealed increased serum prolactin (PRL) levels that ranged from 76 to 135 mg/L. Results of thyroid function tests were normal, and gonadotropins and estradiol levels were low, consistent with hyperprolactinemia. MRI revealed asymmetric enlargement of the right side of the pituitary gland. Discontinuing the thioridazine therapy resulted in normalization of the serum PRL and resolution of the pituitary abnormality. Subsequent worsening of the patient's psychiatric condition necessitated a course of electroconvulsive therapy and initiation of treatment with clozapine, a D4 dopamine receptor antagonist. At 1-year follow-up, at which time the patient was maintained on clozapine and was not taking thioridazine, both serum PRL levels and MRI findings remained normal. CONCLUSION: Our patient was shown to have asymmetric pituitary enlargement associated with thioridazine-induced hyperprolactinemia, which reversed when use of the drug was discontinued. In patients with serum PRL levels in excess of 100 mg/L during antipsychotic drug therapy, evaluation for a prolactinoma is warranted.

Journal Article↗

PubMedDate not supplied

Tumor-grade hyperprolactinemia induced by multiple medications in the setting of renal failure.

OBJECTIVE: To describe a patient with galactorrhea and severe hyperprolactinemia in whom workup revealed a nontumoral mechanism. METHODS: We present the medical history of a woman with long-standing diabetes in whom bilateral galactorrhea and hyperprolactinemia developed. In addition, the details of her clinical course and management are reviewed. RESULTS: A 33-year-old woman with diabetes, end-stage renal disease, and gastroparesis was admitted to the hospital because of intractable nausea and vomiting. Several months before admission, she had been noted to have galactorrhea and irregular menses. Routine medications included captopril, verapamil, furosemide, prochlorperazine, metoclopramide, cisapride, and Ortho-Novum. Laboratory evaluation showed normal thyroid function, increased serum prolactin levels (up to 1,197 ng/mL), and normal findings on magnetic resonance imaging of the pituitary. Electrophoresis of the patient's serum on a protein A Sepharose column showed no evidence of macro-prolactinemia. Orally administered medications were discontinued, and the patient was given total parenteral nutrition. These measures resulted in a decrease of 300 ng/mL in serum prolactin levels in 4 days. The prolactin levels eventually normalized after withdrawal of verapamil, prochlorperazine, and metoclopramide. CONCLUSION: A modest increase in serum prolactin level often can be produced by a variety of medications, but gross hyperprolactinemia of 200 ng/mL or higher usually raises suspicion of an underlying prolactin-secreting tumor. This case report demonstrates that conventional limits for nontumoral hyperprolactinemia can be exceeded by concurrent exposure to multiple lactotropic medications in the setting of renal failure.

Journal Article↗

PubMed2001

Effect of transitory hyperprolactinemia on in vitro fertilization of human oocytes.

OBJECTIVE: To examine the changes in plasma prolactin (PRL) during ovarian hyperstimulation (OH) and the influence of hyperprolactinemia on folliculogenesis, oocyte retrieval and in vitro fertilization (IVF) success rates and the usefulness of the metoclopramide (MCP) test in predicting the onset of hyperprolactinemia. STUDY DESIGN: Forty-nine cycles of OH were induced in 32 infertile women using follicle-stimulating hormone, human menopausal gonadotropin and human chorionic gonadotropin (GI) (n = 36), also in association with gonadotropin-releasing hormone (GII) (n = 13). The MCP test (10 mg, intravenously) was performed on fertile control women (control group, n = 9) and in GI (n = 21) and GII (n = 8) patients. RESULTS: Plasma PRL and estradiol levels increased during OH, reaching maximum levels on the day preceding oocyte retrieval in GI and GII. Since these two groups exhibited similar PRL curves, they were evaluated as a single group. Patients showing an increase in PRL of > 200% presented a greater number of follicles with a mean diameter > or = 12 mm and more mature oocytes and better IVF success rates than patients with a PRL increase < or = 200%. Oocyte retrieval did not differ between the groups. The MCP test showed hyperresponsiveness in the three groups studied, but no correlation was found between the PRL increase in this test and that during OH. CONCLUSION: Plasma PRL and estradiol levels increase during OH, while the MCP test cannot predict the onset of hyperprolactinemia. Transitory hyperprolactinemia seems to be associated with an increase in the numbers of follicles with a mean diameter > or = 12 mm and with more mature oocytes and better IVF success rates.

Adult↗

PubMed1985

Hyperprolactinemia and contraception: a prospective study.

The authors measured serum concentrations by single and multiple sampling techniques in 347 women before, during, and after treatment with either hormonal or barrier methods of contraception. The prolactin responses to an intramuscular injection of estrogen also were evaluated in control and selected study patients. The incidence of hyperprolactinemia in oral contraceptive users was higher than control subjects (12 versus 5%). Hyperprolactinemia was best assessed by multiple blood sampling, it is often transient and resolves spontaneously in about 50% of women. The estrogen provocation study suggests that some women who develop hyperprolactinemia while taking oral contraceptives are more sensitive to the effects of exogenous estrogen and may be at greater risk of developing pill-related menstrual aberrations and hyperprolactinemia.

Adolescent↗

PubMed1985

Hyperprolactinemia and associated pituitary prolactinomas.

The association between serum prolactin (PRL) and the presence of pituitary tumors as determined by third generation computed tomography scan was studied in hyperprolactinemic patients. Patient charts from a four-year period were reviewed to identify those patients with elevated PRL (greater than or equal to 25 ng/mL). All patients with hyperprolactinemia underwent computed tomography scan evaluation of the pituitary gland. Hyperprolactinemia was identified in 79 patients, mean PRL 59 +/- 6.1 ng/mL SEM. Pituitary tumors were identified in 35 of these patients, mean PRL 65 +/- 11.9 ng/mL. This level was not significantly different from the level in 43 patients with normal computed tomography scans (52 +/- 5.7 ng/mL). This review found that computed tomography scan identified pituitary tumors in 44% (35 of 79) of patients with hyperprolactinemia. The likelihood of finding a pituitary tumor did not correlate with the level of hyperprolactinemia. Computed tomography scan is indicated for the diagnosis of prolactinomas in all hyperprolactinemic patients regardless of the serum PRL level.

Adenoma↗

PubMed1985

Further evidence that big,big prolactin is preferentially secreted in women with hyperprolactinemia and normal ovarian function.

The heterogeneity of human serum prolactin (PRL) in 12 women with hyperprolactinemia and different derangements of the hypothalamic-pituitary-ovarian axis was studied. The patients were subdivided into three groups: four women with hyperprolactinemia and normal ovarian function (group I), four women with hyperprolactinemia associated with sporadic endometrial bleedings and a positive progestin test (group II), and four women with amenorrhea and a negative progestin test (group III). Gel filtration chromatography of serum samples from patients in group I revealed in three of them that most (80%) of their immunoreactive PRL eluted as big,big PRL (Mr greater than 100,000); whereas the rest of the patients, including those from groups II and III, exhibited a distribution pattern similar to that obtained in normal menstruating women. All PRL species had similar affinities for the antibody, as disclosed by the slopes generated in dose-response curves. These results indicate that ovarian function in hyperprolactinemia might be dependent upon PRL heterogeneity and suggest that big,big PRL may have, under in vivo conditions, a low degree of biologic activity.

Adult↗

PubMed1979

Hyperprolactinemia and primary amenorrhea.

Four women with primary amenorrhea and hyperprolactinemia are presented. These patients started thelarchal and pubarchal development but never had a spontaneous menses. Hypothyroidism was not demonstrable in these patients. The causes for hyperprolactinemia in these patients and the clinical follow-up are discussed. In the authors' experience, hyperprolactinemia is seen in about one third of women with normogonadotropic primary amenorrhea, and primary amenorrhea is seen in about 3% of women with hyperprolactinemia.

Adolescent↗

PubMed1983

[Hyperprolactinemia in chronic kidney failure patients].

The determination of the endocrine state of the patients with chronic renal insufficiency is of significance because of the endocrine sexual disorders often observed in those patients. According to literature data, hyperprolactinemia in combination with gonad dysfunction is often observed in the sera of those patients. Hyperprolactinemia was established, with the present study, in the examined 47 patients (18 females and 29 males) with chronic renal insufficiency, the normal physiological difference in prolactin level depending on sex, being eliminated in those patients. The hyperprolactinemia in the patients examined, as compared with the prolactin level in a control group of healthy subjects (10 females and 12 males) is statistically significant (p less than 0.01). Very likely that hyperprolactinemia in the patients with chronic renal insufficiency is complexly conditioned by the disturbed regulation and disturbed degradation and elimination.

Adult↗

PubMed2026

Macroprolactinemia as a diagnostic pitfall in hyperprolactinemia: a systematic review and quantitative synthesis.

CONTEXT: Macroprolactinemia is a well-recognized cause of hyperprolactinemia and an important diagnostic pitfall in endocrine practice. However, interpretation of published quantitative prolactin data remains sparse as studies vary in confirmation method, assay platform, polyethylene glycol (PEG) recovery cutoff, and reporting of prolactin measurement. EVIDENCE ACQUISITION: PubMed, Embase, Scopus, Web of Science, the Cochrane Library, and Google Scholar were systematically searched. Eligible studies reported macroprolactinemia-specific quantitative prolactin data in patients with confirmed macroprolactinemia defined by PEG precipitation, gel filtration chromatography (GFC), or both. Two reviewers independently performed study selection, data extraction, and quality assessment. Findings were summarized using study-level descriptive synthesis. The review was prospectively registered in PROSPERO and conducted in accordance with PRISMA 2020 guidelines. EVIDENCE SYNTHESIS: Forty-five studies encompassing 2853 macroprolactinemia cases from 21 413 screened patients with hyperprolactinemia across 22 countries were included. Among 33 studies eligible for primary quantitative analysis, the median study-level central total prolactin attributed to macroprolactinemia was 61.4 ng/mL ([IQR] 42.0-80.0; range 28.1-137.6), and the median study-level post-PEG monomeric prolactin was 11.7 ng/mL (IQR 8.3-13.2; range 4.0-17.0)). The median study-level maximum total prolactin was 264.5 ng/mL (IQR 97.0-425.5; range 81.8-663.0); extreme elevations were attributable to coexisting prolactinomas. CONCLUSION: In confirmed macroprolactinemia, total prolactin elevation is typically moderate, and post-PEG monomeric prolactin is usually within or near the normal range. The post-PEG monomeric prolactin value, rather than percent recovery alone, is the most informative parameter for distinguishing isolated macroprolactinemia from coexisting true hyperprolactinemia. These quantitative benchmarks may help clinicians to avoid unnecessary investigation or treatment.

Humans↗

PubMed2000

Pharmacological effects of the lipidosterolic extract of Serenoa repens (Permixon) on rat prostate hyperplasia induced by hyperprolactinemia: comparison with finasteride.

BACKGROUND: The growth of the prostate gland is mainly dependent on androgens. Other hormones, like prolactin (PRL), also influence prostate development. Our purpose was to analyze and compare the effects of two drugs (5alpha-reductase inhibitor) used in the therapy of benign prostatic hyperplasia: lipidosterolic extract of Serenoa repens (LSESR), and finasteride in an in vivo model of rat prostate hyperplasia induced by hyperprolactinemia. METHODS: Hyperprolactinemia was induced by 30 daily injections of sulpiride. Wistar rats received daily gavages of LSESR or finasteride. We used the following groups: control, castrated, castrated with a substitute testosterone (T), or 5alpha-dihydrotestosterone (DHT) implant. RESULTS: Hyperprolactinemia increases the wet weight and induces hyperplasia in the lateral prostate (LP). Unlike finasteride, LSESR significantly reduced LP growth and hyperplasia in castrated, DHT-implanted, and sulpiride-treated rats. CONCLUSIONS: Finasteride was only capable of inhibiting the effect of androgens on rat prostate enlargement. LSESR inhibited not only the androgenic but also the trophic effect of PRL in rat LP hyperplasia.

Androgen Antagonists↗

PubMedDate not supplied

Effects of chronic sulpiride-induced hyperprolactinemia on plasma testosterone and its responses to hCG in normal men.

To elucidate the effects of sulpiride-induced (300 mg daily) long-term (64 days) hyperprolactinemia on basal and hCG-stimulated plasma testosterone (T), hCG was given to five normal men five times at 2-week intervals (before sulpiride administration and at 2, 4, 6 and 8 weeks). Mean integrated hCG responses of plasma T did not change significantly as compared with baseline. However, mean (+/- SEM) basal plasma levels of T decreased significantly (P less than 0.05) from 1011 +/- 148 ng/dl to 852 +/- 13 at 2 weeks, 520 +/- 53 at 4 weeks, 572 +/- 137 at 6 weeks and 554 +/- 140 at 8 weeks. These results suggest that sulpiride-induced hyperprolactinemia (73.8 ng/ml, the average of mean values obtained at 2, 4, 6 and 8 weeks) for 64 days does not suppress secretion of T in response to hCG in spite of a decrease in basal plasma T concentrations. It is unlikely that the low concentrations of plasma T are due to direct effects of hyperprolactinemia on the testis.

Adult↗