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Results for “hyperprolactinemia”

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PubMed1992

Effect of hyperprolactinemia on the androgen response to an oral glucose load.

OBJECTIVE: To investigate the effect of hyperprolactinemia on the androgen response to an oral glucose load in patients with normal and abnormal carbohydrate metabolism. DESIGN: Sixty-three women underwent a 75-g oral glucose tolerance test (OGTT) at approximately 6 weeks' postpartum. SETTING: University hospital setting. PATIENTS: Patients with a previous history of gestational diabetes. MAIN OUTCOME MEASURE: Adrenal and ovarian androgen response to oral glucose load. RESULTS: Results were stratified by the result of the OGTT (patients with impaired glucose tolerance or diabetes as a single group and patients with a normal OGTT as a separate group) and prolactin (PRL) level. All androgens decreased significantly over the 2-hour test in all groups except dehydroepiandrosterone sulfate (DHEAS) in the patients with both elevated PRL and abnormal glucose tolerance. CONCLUSION: Hyperprolactinemia and insulin resistance may act synergistically in the adrenal to alter DHEAS suppression and may result in chronically elevated circulating DHEAS levels.

Adult↗

PubMed1988

Bone density and reproductive hormones in patients with neuroleptic-induced hyperprolactinemia.

To study the prevalence of osteoporosis and hyperandrogenism in neuroleptic-induced hyperprolactinemia, the authors evaluated 10 patients. Three were amenorrheic, while seven had oligomenorrhea. Nine patients had galactorrhea. The Ferriman-Gallway hirsutism score was 12 +/- 2. Vaginal smear maturation value was 53 +/- 8. Bone density, measured by dual photon absorptionometry in the spine, femoral neck, Ward's triangle, and trochanteric region, was 98 +/- 1.5, 92.7 +/- 3, 88.5 +/- 4.2, and 92.6 +/- 3.3 percentile of controls matched for age, sex, weight, and ethnicity, respectively. Serum prolactin, follicle-stimulating hormone (FSH), luteinizing hormone (LH), dehydroepiandrosterone sulfate (DHEAS), total testosterone, and free testosterone were 82 +/- 10 ng/ml, 8.5 +/- 1.1 mIU/ml, 11.1 +/- 2.6 mIU/ml, 4695 +/- 594 ng/ml, 90 +/- 17 ng%, and 2.36% +/- 0.3%, respectively. Serum thyroid-stimulating hormone (TSH) and free thyroxine index were normal. Bone density strongly correlated with vaginal maturation value (r = 0.904, P less than 0.01). It is concluded that (1) neuroleptic-induced hyperprolactinemia is associated with hirsutism and androgen excess primarily of adrenal origin and (2) a subset of these patients is at an increased risk of developing osteoporosis. It may be possible to identify patients at risk of osteoporosis by examining vaginal smears for maturation value. Early detection and management are imperative in this group of patients.

Adult↗

PubMed1989

Bromocriptine inhibition of anesthesia-induced hyperprolactinemia: effect on serum and follicular fluid hormones, oocyte fertilization, and embryo cleavage rates during in vitro fertilization.

Thirty-two patients undergoing in vitro fertilization (IVF) were given bromocriptine either 1 or 12 hours before anesthesia or received no drug to determine what effect suppression of transient, anesthesia-induced hyperprolactinemia would have on peripheral and follicular fluid hormones, fertilization and cleavage rates, and pregnancy. Thirty minutes after anesthesia, there was a 120-ng/mL rise in serum prolactin (PRL) in control patients versus an insignificant change in women given bromocriptine. Levels of PRL in follicular fluid were significantly less, and estradiol (E2) levels were higher (P less than 0.05) in all bromocriptine-treated patients compared with controls, whereas follicular fluid levels of progesterone (P), inhibin activity, and midluteal serum P were unaffected. Although fertilization and pregnancy rates were similar, a greater proportion of fertilized oocytes from bromocriptine-treated patients advanced to cleaving embryos compared with controls (95% versus 63%, respectively; P less than 0.001). We conclude that bromocriptine, given before anesthesia, can suppress transient, anesthesia-induced hyperprolactinemia and dramatically alter follicular fluid concentrations of PRL and E2. Although these changes in hormonal milieu affected neither oocyte fertilization nor pregnancy rate in our IVF patients, they seemed to have a positive influence on embryonic development after IVF.

Adult↗

PubMed1999

Nonfunctioning pituitary macroadenoma presenting with mild hyperprolactinemia and amenorrhea.

OBJECTIVE: To describe a patient with a clinically nonfunctioning pituitary macroadenoma who presented with mild hyperprolactinemia and amenorrhea. DESIGN: Case report. SETTING: Tertiary care medical facility. PATIENT(S): A 44-year-old woman with a 6-month history of amenorrhea. INTERVENTION(S): Pituitary testing, magnetic resonance imaging of the sella turcica, and transsphenoidal surgery. MAIN OUTCOME MEASURE(S): Pituitary function testing, magnetic resonance imaging, and return of menstrual cycles. RESULT(S): Baseline laboratory data revealed a serum prolactin level of 34 ng/mL (normal range, 3-20 ng/mL), normal thyroid function test results, and an FSH level of 6.7 mIU/mL. A second fasting prolactin level was 48 ng/mL. Magnetic resonance imaging of the sella turcica revealed a pituitary macroadenoma measuring 1.4 x 3.2 cm. Further testing of baseline pituitary function revealed normal findings. The patient underwent an uncomplicated transsphenoidal resection of the pituitary tumor and maintained normal pituitary function. Pathologic evaluation revealed a pituitary adenoma that stained positive for FSH and focally for the alpha subunit. The adenoma stained negative for GH, prolactin, ACTH, LH, and TSH. CONCLUSION(S): This patient had a nonsecreting gonadotroph macroadenoma that resulted in hypogonadotropic hypogonadism along with mild hyperprolactinemia, presumably secondary to interruption of normal transport down the pituitary stalk.

Adenoma↗

PubMed1989

Hyperprolactinemia and impotence: why, when and how to investigate.

The contribution of hyperprolactinemia to erectile disorders has not been clarified. Modest elevations of serum prolactin occur after administration of drugs that by themselves affect erectile function. Prolactinomas produce marked elevations of the hormone and invariably are accompanied by hypogonadotropic hypogonadism. Among 1,236 consecutive impotent patients investigated at our center 5.3% had serum levels of prolactin greater than normal. Only 34 of the 66 hyperprolactinemic patients were available for analysis. The etiology of the hyperprolactinemia in this group was pituitary adenoma in 14.7%, drug-induced in 29%, chronic renal failure in 6%, laboratory error in 2.9% and idiopathic in 47.1%. Medical management has a high degree of success but simply lowering the levels of prolactin is not invariably accompanied by restoration of function.

Adenoma↗

PubMed1999

Effects of hyperprolactinemia on calcitonin secretion in male rats.

The role of prolactin (PRL) in calcitonin (CT) release by the thyroid C cell in male rats was studied. Anterior pituitary (AP)-grafted male rats were characterized by hyperprolactinemia. Brain cortex (CX)-grafted male rats were used as control animals. AP- and CX-grafted rats were infused intravenously with CaCl2 and bled from the jugular catheter at 0, 30, 60, and 120 minutes following the CaCl2 challenge. Rat thyroid gland was incubated with or without 3-isobutyl-1-methylxanthine (IBMX) at 37 degrees C for 30 minutes. Thyroid C cells were incubated in culture medium at 37 degrees C for 60 minutes. Cyclic adenosine 3',5'-monophosphate (cAMP) in rat thyroid tissues following incubation with IBMX was extracted by 65% ethanol. AP-grafted rats had higher plasma levels of PRL and CT compared with CX-grafted rats. Both the release of CT and accumulation of cAMP in thyroid glands were higher in AP-grafted versus CX-grafted rats. Direct administration of ovine PRL (oPRL) on the thyroid glands did not increase CT secretion in vitro. Thyroid C cells of AP-grafted rats secreted more CT compared with CX-grafted rat cells. These results suggest that hyperprolactinemia increases the release of CT by thyroid C cells in rats through a cAMP-dependent pathway caused by an indirect effect of PRL.

Animals↗

PubMed2003

Efficacy and safety of daily intake of apomorphine SL in men affected by erectile dysfunction and mild hyperprolactinemia: a prospective, open-label, pilot study.

OBJECTIVES: To evaluate the efficacy of the "daily" use of apomorphine SL compared with the "on demand" administration of the drug in patients with mild to moderate erectile dysfunction (ED) and mild hyperprolactinemia who were nonresponders to apomorphine administered "on demand." METHODS: In this open-label prospective study, 34 patients with mild-to-moderate ED and mild hyperprolactinemia were screened. The subjects answered the International Index of Erectile Function (IIEF) questionnaire and underwent follicle-stimulating hormone, luteinizing hormone, testosterone, free testosterone, and prolactin plasma testing, and Doppler sonography at the 2-week screening period to define the ED severity and etiology, at the end of a 4-week "as required" dose-escalation regimen of 2 mg/3 mg apomorphine SL, and at the end of a 4-week period of daily administration of the drug to assess the efficacy of each treatment modality. RESULTS: Twenty patients (age range 27 to 46 years) were included in the study. Eighteen subjects completed the 4-week "as required" drug intake period, and three (16.7%) benefited from this modality of treatment (P <0.05). Fifteen nonresponder patients participated in the 4-week daily apomorphine SL use, and 13 (86%) reported satisfaction with the treatment (P <0.05). The 3-mg daily administration was more effective than the 2-mg daily administration for erectile function (P <0.02) but not for other sexual domains scored with IIEF. Adverse events were of mild or moderate severity, either during the "as required" drug intake (4 patients) or during daily use (3 subjects) and were mainly nausea, dizziness, or headache. CONCLUSIONS: Data from the clinical evaluation of symptomatic apomorphine SL use have always shown a poor success rate, probably because it is used "as sildenafil." Using apomorphine SL as a treatment of ED, we observed a significant improvement in both subjective and objective aspects scored with the IIEF. The increase of prolactin could influence the erective mechanisms, and it cannot be excluded that a subgroup of men with ED may have an impairment of central dopaminergic function. Moreover, additional studies need to define the daily use of apomorphine SL in large subgroups of men on the basis of ED etiology and severity.

Adult↗

PubMed1997

[Macroprolactinemia, a variety of hyperprolactinemia. Apropos of 5 cases].

Macroprolactinemia, due to increased circulating levels of large molecular weight forms of prolactin, results in elevated level of immuno-reactive prolactin. The big variants have only weak biological activity; thus macroprolactinemia appears as a case of hyperprolactinemia without clinical significance as demonstrated by the five patients described. The diagnosis is based upon chromatography which separates the hormone and its variants. This disorder produces a pitfall in the diagnostic evaluation of hyperprolactinemia.

Adult↗

PubMed1999

Establishment of reference values for endocrine tests. II: Hyperprolactinemia.

BACKGROUND: In patients with hyperprolactinemia, the thyrotropin-releasing hormone (TRH) stimulation test is widely applied to distinguish prolactinoma from other causes of hyperprolactinemia. In the present study, we established reference values for the plasma concentration of prolactin (PRL) and its response to TRH. METHODS: Basal PRL and the PRL response to 400 micrograms TRH i.v. was determined in 50 subjects recruited from the general population, equally distributed according to sex and age between 20 and 69 years. PRL was determined by a fluoroimmunometric assay. Reference values are given as the observed range. RESULTS: Plasma concentrations of PRL were 4.0-25 micrograms/l (median: 10.0 micrograms/l) in women and 0.5-19.0 micrograms/l (median: 8.5 micrograms/l) in men (p = 0.11). The peak PRL concentration after stimulation with TRH was slightly higher in women (median: 51 micrograms/l) than in men (median: 41 micrograms/l; p = 0.04) and was reached at t = 20 min in all subjects. The relative increase in plasma PRL (median: 440%) did not show a statistically significant effect of age or sex. In 12 subjects (24%), the relative increase in plasma PRL was lower than 250%, which has traditionally been considered the minimum cutoff for a normal response. There were no effects of smoking and alcohol, but regular ingestion of liquorice was associated with lower basal (p = 0.03) and lower stimulated (p = 0.05) plasma concentrations of PRL. CONCLUSIONS: The present study provides reference values for basal and TRH-stimulated plasma concentrations of PRL.

Adult↗

PubMed1999

Neuroleptic-induced hyperprolactinemia.

Neuroleptic-induced hyperprolactinemia (NIHP) has been a 'cost' of traditional antipsychotic therapy. Because all of the traditional neuroleptics are capable of elevating serum prolactin, clinicians have had to accept the implications of NIHP along with the antipsychotic's efficacy. Accordingly, the clinical consequences of NIHP have received limited attention. With the introduction of some of the new, more highly selective mesolimbic and mesocortical dopamine-blocking, prolactin-sparing antipsychotic drugs, NIHP may now be prevented or minimized. Given this possibility, it becomes more important than ever that clinicians understand both the short- and long-term consequences of hyperprolactinemia and current management approaches.

Antipsychotic Agents↗

PubMed1997

Marked hyperprolactinemia caused by carotid aneurysm.

BACKGROUND: Pituitary dysfunction caused by intracranial aneurysms is rare. We report a patient with the unique feature of hyperprolactinemia to a degree previously seen only with prolactin-secreting tumours. METHOD: Case report. RESULT: A 42-year-old woman had a galactorrhea, left-sided headache, reduced vision in the left eye and a left temporal hemianopsia. Serum prolactin was elevated (365 micrograms/L). Cranial computed tomography (CT) revealed a suprasellar mass, which carotid angiography showed to be a left internal carotid artery aneurysm. At craniotomy, this aneurysm and a smaller one of the ophthalmic artery were repaired, and the patient's vision returned to normal. The prolactin level fell to normal. Follow-up CT showed no evidence of pituitary adenoma or hypothalamic lesion. CONCLUSIONS: Carotid aneurysm can cause reversible pituitary dysfunction. A prolactin level > 300 micrograms/L is not a reliable cut-off for distinguishing prolactin-secreting adenomas from other causes of elevated prolactin. A co-existing prolactinoma was felt to be ruled out by both a normal CT scan and normal prolactin levels following aneurysm repair. Patients with marked hyperprolactinemia should be considered for angiography or MRI to rule out carotid aneurysm, since the consequences of pituitary exploration in this setting are potentially grave.

Adult↗

PubMed2006

Drug Insight: prolactin-receptor antagonists, a novel approach to treatment of unresolved systemic and local hyperprolactinemia?

Prolactin is a polypeptide hormone whose major biological actions are related to normal lactation and reproduction. Abnormally high prolactin levels, referred to as hyperprolactinemia, can result in various reproductive disorders. Currently, therapeutic management of hyperprolactinemia relies on dopamine agonists, since dopamine is the primary physiological suppressor of pituitary prolactin production. Epidemiologic studies have shown that prolactin levels in the high-normal range, as well as medications that interfere with dopamine action (e.g. certain antipsychotic drugs), might correlate with increased breast cancer risk. In addition to circulating prolactin, it is now well established that prolactin is also produced locally within various tissues, including breast and prostate. Increasing evidence, mainly from animal studies at present, suggests that excess locally produced prolactin may promote the growth of breast and prostate tumors via an autocrine or paracrine mechanism. These findings have renewed the interest in finding alternative strategies to suppress prolactin actions when dopamine agonists are ineffective. Our studies of the relationship between prolactin structure and function have resulted in the development of pure prolactin-receptor antagonists. These molecules prevent endogenous prolactin from exerting its actions via a competitive mechanism for receptor binding. In this review, we discuss the possible future therapeutic utility of this novel class of compounds.

Animals↗

PubMed2001

Severe erectile dysfunction is a marker for hyperprolactinemia.

The need for routine prolactin (PRL) measurement in the initial evaluation of erectile dysfunction (ED) has been questioned because of the low rate of hyperprolactinemia (HP) in these men and the costs involved. In addition, it is widely thought that sexual desire problems are a good clinical marker for HP and/or low testosterone in men with ED. Within a 15-month period, 844 consecutive PRL and sexual hormone determinations were conducted in men at the Kingston General Hospital. Of these patients, 138 were comprehensively evaluated at the first visit for ED and completed the International Index of Erectile Function (IIEF). In the 138 patients, 2.2% had severe hyperprolactinemia (>35 ng/ml), within the range of 1-5% previously reported. No correlation between initial prolactin value and the sexual desire domain or the erectile function domain (EFD) of the IIEF was found for this population. However, all cases of severe HP were found to occur in men who scored less than 10 in the EFD of the IIEF. Low libido is widely accepted as a marker of HP. In this study, HP was found in patients not reporting major problems with a desire disorder. Clinically significant HP may be reliably found with routine biochemical evaluation and in this series was not detected in patients with EFD scores above 10. A routine PRL measurement is inexpensive and early detection of a serious and treatable disease may afford greater therapeutic success.

Adult↗

PubMed1988

Coincidence of gonadal dysgenesis and hyperprolactinemia.

It is reported about 4 female patients aged from 3 to 31 years (average age 18 years) with gonadal dysgenesis and hyperprolactinemia. Beside one all these females were not treated with synthetic sexual steroids. In 3 of the 4 patients both hyperprolactinemic and hypergonadotropic serum levels were observed. In one case the gonadotropic serum levels were normal. A stimulation test with GnRH-TRH or arginine-GnRH-TRH, respectively, was performed. In patients with gonadal dysgenesis a change on the area of hypothalamo-hypophyseal axis is supposed to cause the hyperprolactinemia.

Adolescent↗

PubMed1994

Calcium and prolactin secretion in humans: effects of the channel blocker, verapamil, in the spontaneous and drug-induced hyperprolactinemia.

The effects of the intravenous administration of a calcium channel blocker, verapamil (0.0833 mg/min for 2-3 h after a 5 mg bolus) on prolactin (PRL) and thyrotropin (TSH) circulating levels were assessed in 7 normal subjects and in 17 patients with hyperprolactinemia (11 with prolactinoma and 6 sulpriride-induced). In the normal group a non-significant increase in PRL levels occurred (mean +/- SEM = 11.7 +/- 2.9 micrograms/l verapamil vs. 8.5 +/- 1.4 micrograms/l saline). In this control group the peak response of PRL and TSH to TRH (thyrotrophin releasing hormone) during verapamil or saline was also determined: PRL = 112.0 +/- 27.0 micrograms/l on verapamil vs. 53.6 micrograms/l on saline, p = 0.02; TSH 7.1 +/- 0.7 microU/l on verapamil vs. 9.0 +/- 0.6 mU/l on saline, p = 0.01. In the hyperprolactinemic subjects verapamil induced opposite effects on PRL levels, the prolactinoma group exhibiting an increase in the mean values (168.5 +/- 22.3 micrograms/l vs. 150.8 +/- 23.6 micrograms/l on saline, p = 0.04) whereas in the sulpiride-induced there was a reduction in the mean PRL levels (61.1 +/- 13.8 micrograms/l vs. 78.5 +/- 19.3 micrograms/l on saline, p = 0.002). In both groups of hyperprolactinemic patients no effects on TSH levels were observed. The authors discuss the possibility that the divergent effects of verapamil in hyperprolactinemia of different etiologies could be related to the balance between dopamine and calcium channel effects on hypothalamus and/or pituitary.

Adult↗

PubMed1989

Hyperprolactinemia in hepatic encephalopathy may result from impaired central dopaminergic neurotransmission.

Ten patients with liver disease and hepatic encephalopathy (HE) and eight normal controls were studied. Five of the 10 HE patients had hyperprolactinemia. The administration of L-dopa produced a decrease of serum prolactin in all. Prior administration of Carbidopa, a peripheral decarboxylase inhibitor, did not change the prolactin suppression by L-dopa in the normal controls or in the patients with normal baseline prolactin levels. In the hyperprolactinemic group, Carbidopa significantly inhibited the response to L-dopa. Impaired central neurotransmission, at least involving the hypothalamic-pituitary dopaminergic system, may underlie the hyperprolactinemia in HE.

Adult↗

PubMedDate not supplied

Bromocriptine for infertile males with mild hyperprolactinemia: hormonal and spermatogenic effects.

To clarify the influence of hyperprolactinemia on spermatogenesis and steroidogenesis in infertile male patients, the serum prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol concentrations were and the effect of bromocriptine treatment on spermatogenesis was examined. A total of 1234 patients were evaluated and 147 men had hyperprolactinemia. Of these, only 30 had PRL concentrations more than twice the upper limit of normal and most of them had a little excess over the upper limit. For 10 of these 30, serum hormone concentrations were measured and semen was analyzed before and after bromocriptine administration. No relationship between the PRL and other hormone concentrations was found. No changes were noted in the LH, FSH, testosterone, or estradiol concentrations, or in the sperm density and motility after treatment. The mean PRL decreased from 26.5 +/- 4.5 to 1.4 +/- 1.8 ng/mL. In infertile men who are mildly hyperprolactinemic, bromocriptine administration does not improve semen analysis, although it does normalize the PRL.

Bromocriptine↗

PubMed1990

Hyperprolactinemia in a patient with a pituitary and an ovarian dermoid tumor: case report.

A patient with galactorrhea, amenorrhea, and hyperprolactinemia caused by a dermoid tumor of the pituitary gland is presented. The patient had a prior history of an ovarian dermoid tumor. The pathology of dermoid tumors is discussed along with the management of pituitary tumor-associated hyperprolactinemia. This is the first reported case of an intracranial and an ovarian dermoid tumor occurring in the same patient.

Adult↗