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PubMed1984

Hyperprolactinemia in Cushing's disease and Nelson's syndrome.

In an attempt to clarify the pathogenesis of hyperprolactinemia associated with Cushing's disease, PRL secretion was evaluated in 42 patients with hyperadrenocorticism (Cushing's disease, 26; and adrenocortical adenoma, 16) and in 10 patients with Nelson's syndrome. Mild hyperprolactinemia was found in 6 patients with Cushing's disease (23%) and in 5 patients with Nelson's syndrome (50%). In contrast, basal plasma levels of PRL were normal in all of the patients with Cushing's syndrome secondary to adrenocortical adenoma. Injection of TRH unequivocally induced PRL release; however, the responses were blunted in patients with Cushing's disease and in those with Nelson's syndrome who had hyperprolactinemia. Short term administration of dexamethasone, on the other hand, failed to alter PRL secretion in these patients. In 5 patients with Cushing's disease, plasma levels of PRL were reevaluated when they developed a typical clinical picture of Nelson's syndrome after bilateral adrenalectomy. Four patients had a definite increase in PRL levels. Immunohistochemistry of pituitary adenomas surgically removed from 7 patients with Cushing's disease or Nelson's syndrome demonstrated, in 4 of them, the presence of PRL-containing cells as well as ACTH-containing cells. Two of these patients had hyperprolactinemia, which was corrected by the removal of pituitary tumors. These results suggest that hyperprolactinemia is not a fortuitous occurrence in patients with Cushing's disease and could be explained by the concomitant production and secretion of PRL from corticotroph adenomas.

Adenoma↗

PubMed1984

Effects of metoclopramide-induced hyperprolactinemia during early follicular development on human ovarian function.

Nine healthy women, aged 25 to 36 yr, were treated with metoclopramide (MC) (10 mg orally three times daily) from the first to the sixth day of their cycle (treatment A) for two successive cycles (n = 18) and six of these women later received MC from -3 to the fifth day of the menstrual cycle (treatment B) during one or two cycles (n = 10), to investigate the effects of hyperprolactinemia during the early phase of ovarian follicular growth. Comparisons were performed with control cycles in the same women. The treatment cycles were characterized by low serum concentrations of LH during the early follicular phase and at midcycle, low early follicular phase serum testosterone (T) levels and high luteal phase T and free T index values, with no significant differences between A and B treatment modalities. We classified the treatment cycles into two categories, seriously disturbed and normal or only slightly disturbed, on the basis of ultrasonographic findings and midcycle estradiol (E2) and luteal phase progesterone (P) concentrations. Folliculogenesis was seriously disturbed in 11 of the 28 treatment cycles (39%). During these cycles, midcycle serum LH and the LH to FSH ratio were lowered, luteal phase LH and FSH increased, midcycle E2 and luteal phase P and the P to E2 ratio decreased, luteal phase T and the free T index and androstenedione increased, and luteal phase 5 alpha-dihydrotestosterone decreased. During the early follicular phase and at midcycle the ratios of T to E2 and androstenedione to E2 were increased, and at midcycle and during the luteal phase of the cycle the ratio of T to 5 alpha-dihydrotestosterone was increased. These changes in steroid hormones were probably of ovarian origin since the serum concentrations of dehydroepiandrosterone sulfate and sex hormone-binding globulin were similar in seriously disturbed and control cycles. Four of the nine study subjects were hyperprolactinemia sensitive (disturbed folliculogenesis) and five hyperprolactinemia resistant (no disturbance in folliculogenesis). During the control cycles the hyperprolactinemia-sensitive women had significantly higher serum concentrations of T than the other women. The present observations indicate that hyperprolactinemia may impair the development of the ovarian follicles during their recruitment period, especially in women with relatively high serum T levels.

Adult↗

PubMed1983

Prolactin and thyroid-stimulating hormone responses to thyrotropin-releasing hormone in cases of hyperprolactinemia with normal and abnormal sella tomograms.

An intravenous bolus of 500 micrograms of thyrotropin-releasing hormone (TRH) was used to test prolactin and thyroid-stimulating hormone (TSH) responses in normoprolactinemic patients and in hyperprolactinemic patients with normal and abnormal sella turcica. The prolactin response showed a mean increment of 64.1 +/- 46.3 ng/ml in normoprolactinemic women. In patients with hyperprolactinemia, the mean increment was 14.1 +/- 22.4 ng/ml and 13.8 +/- 33.1 ng/ml for patients with normal and abnormal sella, respectively. The difference in the prolactin response between the normoprolactinemic patients and either group of hyperprolactinemic patients is significant (P less than 0.005). The mean baseline TSH in normoprolactinemic patients is significantly higher than in patients with hyperprolactinemia with normal and abnormal sella. The mean increment of TSH after TRH stimulation is significantly higher in normoprolactinemic patients than in either group of patients with hyperprolactinemia (P less than 0.005). These results suggest an inhibitory action of hypothalamic dopamine on the response of both prolactin and TSH to TRH in patients with hyperprolactinemia. The hypothalamic dopamine mechanism might also be the factor leading to suppression of baseline TSH levels in hyperprolactinemic patients. In addition, these results suggest that patients with hyperprolactinemia, with or without changes in the sella turcica, might have various degrees of the same pathology affecting the lactotropes.

Adult↗

PubMed1995

Plasma levels of parathyroid hormone-related peptide are elevated in hyperprolactinemia and correlated to bone density status.

Osteopenia is an important clinical manifestation of hyperprolactinemia. Bone loss in these patients has mainly been attributed to concomitant deficiency of gonadal hormones rather than to hyperprolactinemia per se. Parathyroid hormone-related peptide (PTHrP) is expressed in human mammary tissue, and elevated circulating PTHrP levels as well as concomitant hypercalcemia have been described during lactation. We sought to determine circulating PTHrP levels in patients with long-standing hyperprolactinemia and whether PTHrP may exert possible systemic effects on bone and mineral metabolism. We studied 45 patients (30 women and 15 men) with persisting hyperprolactinemia 6 +/- 4 years (mean +/- SD) after trans-sphenoidal surgery for prolactin-producing pituitary adenomas. PTHrP levels in 117 healthy controls were 10.6 +/- 7.3 pmol-eq/l (mean +/- SD). In hyperprolactinemic patients, plasma PTHrP was elevated to 30.3 +/- 13.4 pmol-eq/l (p < 0.001, n = 45), and in patients with humoral hypercalcemia of malignancy PTHrP levels were 52.9 +/- 29.6 (p < 0.001 to controls and hyperprolactinemic patients). Fifty-three percent of hyperprolactinemic patients (n = 24) had clearly elevated PTHrP levels (> 2 SD). Retrospective immunocytochemical studies of the removed pituitary adenomas from 19 patients generally showed a higher degree of immunoreactivity for PTHrP (1-34) in all but one case when compared with normal pituitary tissue. Patients with elevated circulating PTHrP levels showed in most instances strong immunoreactivity to PTHrP in 70-100% of tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗

PubMed1994

Hyperprolactinemia in male NZB/NZW (B/W) F1 mice: accelerated autoimmune disease with normal circulating testosterone.

It has been proposed that the immunostimulatory hormone, prolactin, is associated with flares of systemic lupus erythematosus (SLE). In autoimmune female NZB/NZW F1 (B/W) mice with accelerated lupus-like disease, hyperprolactinemia accelerated autoimmunity. The current study explored effects of moderate and severe hyperprolactinemia in male B/W mice, which have late-onset SLE. Autoimmune disease in B/W males was assessed by measurement of anti-DNA antibodies (anti-DNA), gp70-anti-gp70 immune complexes (gp70IC), IgM, IgG, and renal function. Serum testosterone concentrations were assayed serially. All mice were necropsied when moribund. Hyperprolactinemic B/W males were characterized by premature appearance of anti-DNA and gp70IC and elevation of IgM and IgG. Hyperprolactinemia accelerated mortality with vasculitis and renal disease compared to control mice. Serum testosterone concentrations were not suppressed. In male B/W mice, chronic hyperprolactinemia stimulated autoimmune disease activity; the deleterious effects of prolactin were not mediated through suppression of the immunoprotective hormone, testosterone. This observation supports the proposed association between elevated prolactin levels and exacerbations of SLE.

Animals↗

PubMed1999

Hyperprolactinemia due to big big prolactin is differently detected by commercially available immunoassays.

Macroprolactinemia, i.e. sustained hyperprolactinemia where the predominant circulating form of prolactin (PRL) is of large molecular weight, is a common phenomenon comprising up to one-fourth of all cases of hyperprolactinemia. We measured serum PRL levels by four different immunoassay systems (PROL-CTK, RIAgnost, Delfia, ACS 180) and by the Nb2 bioassay in patients with prolactinomas/idiopathic hyperprolactinemias in whom monomeric PRL was the major species of PRL (n=11, group 1) and in patients with macroprolactinemia (n=12, group 2). In group 1, the results obtained with the different immunoassays and with the Nb2 assay were highly correlated (r=0.945-0.982). On the other hand, big big-PRL (bb-PRL) was differently recognized by the immunoassays, since measured serum PRL values from each patient were highly variable in group 2. RIA-gnost Prolactin and Delfia Prolactin detected bb-PRL similarly and they were highly correlated with each other (r=0.937, p<0.0001). ACS 180 detected bb-PRL somewhat differently from the RIA-gnost and Delfia systems, but likewise most of the patients of group 2 had PRL values above normal. PROL-CTK was the method less influenced by the presence of bb-PRL since most of the subjects with macroprolactinemia had PRL levels either within the normal range or only marginally elevated. From the immunoassays tested, PROL-CTK was the system which was less correlated with the Nb2 bioassay in group 2 (r=0.252; NS). Our experience is that macroprolactinemia is an asymptomatic condition in most of the cases. Therefore, we suggest that the routine measurement of PRL should be done with methods that are only minimally affected by the presence of macroprolactin. Such an approach would obviate the use of extensive, frequently expensive and ultimately useless diagnostic tests that are needed to determine the cause of the hyperprolactinemia.

Adult↗

PubMed2003

Insulin sensitivity and hyperprolactinemia.

It has been shown that prolactin (PRL) induces glucose intolerance, hyperinsulinemia and insulin resistance in several animal species. In women with microprolactinomas, the sensitivity to insulin is lower in hyperprolactinemia than in normoprolactinemia. Thirty non-obese women with hyperprolactinemia and 30 healthy non-obese women were included into the study. Age, body weight (bw), height, body mass index (BMI), waist circumference, hip circumference and waist to hip ratio of both patients with hyperprolactinemia and control subjects were not different. Mean serum prolactin level was higher in hyperprolactinemic patients than in control group (84.5 +/- 51.1 ng/ml and 13.8 +/- 5.3 ng/ml respectively, p<0.002). Mean HOMA-(%B) index of hyperprolactinemic patients was higher than in control subjects (121 +/- 49 and 84 +/- 38, respectively, p<0.02). Mean HOMA-(%S) index was lower in hyperprolactinemic patients (56 +/- 39 and 105 +/- 55, respectively, p<0.006). Serum total testosterone, free testosterone, androstenedione, estradiol, cortisol, sex hormone binding globulin and DHEA-S levels in both hyperprolactinemic women and healthy subjects, statistically did not show any difference between the two groups. The present data indicate that hyperprolactinemia is associated with an insulin-resistant state. This resistant state may not be a result of obesity, androgenic hormones, and SHBG or pregnancy. It may be the result of serum free fatty acids (FFA) levels, decrement in the number of insulin receptors (by a down-regulation of insulin receptors) or post-binding defect in insulin action or more.

Adolescent↗

PubMed2005

Hyperprolactinemia affects spermiogenesis in adult male rats.

The mechanisms underlying the antifertility effects of hyperprolactinemia have yet to be established in an appropriate experimental model. Hyperprolactinemia is a known side effect of fluphenazine, a broad spectrum, long-acting phenothiazine known to be dopamine type-D2 receptor antagonist. In our earlier study in adult male rats, we reported that fluphenazine at a dose of 3 mg/kg/day suppressed serum FSH but not testosterone (T) through increasing dopamine (DA) metabolism in the pituitary gland, within 60 days. Fluphenazine treatment affected sperm quality and male rats treated with fluphenazine sired fewer litters. The effects of fluphenazine-induced hyperprolactinemia on sperm quality appeared to be related to reduced FSH. We now report that FSH suppression enhanced the uptake of acridine orange (AO), a DNA intercalating, fluorescent dye by the fluphenazine-treated caput epididymal sperms with concomitant reduction in the uptake of thiol-specific monobromobimane (mBBr) fluorescent dye in vitro, suggesting greater accessibility of DNA intercalating dye to sperm chromatin and reduction in free sperm protein thiols. The concomitant increase in AO and decrease in mBBr fluorescence was suggestive of loose chromatin packaging in caput epididymal sperms after treatment with fluphenazine at 3 mg/kg/day for 60 days. The suppression in levels of protamine (P1) in caput epididymal sperms suggested that chromatin hypocompaction was due to reduced deposition of protamines in sperm chromatin. Reduction in testicular levels of cyclic adenosyl 3', 5' monophosphate response element modulator (CREMtau) and P1 further suggested that reduced deposition was indeed due to reduced synthesis. The concomitant reduction in testicular levels of transition protein 1 (TP1) and transition protein 2 (TP2) also suggested that hypoprotamination was due to reduced synthesis of these proteins crucial for facilitating P1 deposition. The effect appeared to have occurred at the level of translation of CREMtau, since its transcript levels were unaffected whereas those of TP1, TP2 and P1 and protamine were upregulated. The study led to the view that the effects of FSH suppression were manifest on the posttranscriptional modifications of CREMtau, as also on transcript repression of TP1, TP2, P1, which do the RNA- binding proteins bring about. Reduction in FSH did not decrease ABP expression in the testis, which has recently been implicated in the expression of transition protein 1 in vitro. However, a significant reduction was evident after fluphenazine treatment, in the immunoexpression of testicular cAMP, the mediator of FSH effects in the Sertoli cells and putative mediator of ABP effects in the spermatids. The study suggests that fluphenazine-induced hyperprolactinemia suppressed FSH and affected a putative cAMP-dependent mechanism underlying posttranscriptional modification of spermatidal genes involved in chromatin condensation, presumably by reducing the availability/secretion of ABP, a paracrine regulator of spermiogenesis in vitro.

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↗

PubMed2004

Complete remission of hyperprolactinemia and erythrocytosis after hysterectomy for a uterine fibroid in a woman with a previous diagnosis of prolactin-secreting pituitary microadenoma.

A 44-year-old woman who had been suffering for 10 years from amenorrhea and hyperprolactinemia resistant to high doses of bromocriptine was hospitalized with erythrocytosis, normal serum erythropoietin (sEpo) levels, and hypertension. Erythrocytosis secondary to uterine myoma and a prolactin-secreting pituitary microadenoma were initially diagnosed. The hyperprolactinemia was bromocriptine resistant, despite gradual increase of the dosage to 30 mg/day. Both hyperprolactinemia and erythrocytosis unexpectedly regressed completely after the patient underwent hysterectomy for a uterine fibroid 9 months after the erythrocytosis was first disclosed. Given the well-known effects of prolactin on hematopoietic cells, we hypothesize that--in this very unusual case--the two main, apparently unrelated abnormalities (erythrocytosis with normal sEpo levels and hyperprolactinemia) may have been the clinical consequence of the functional redundancy and pleiotropy of the "pituitary" hormone prolactin, inappropriately secreted by a uterine fibroid for more than 10 years.

Adult↗

PubMed1989

Lack of effect of hyperprolactinemia on serotonin turnover in ovariectomized and ovariectomized estrogen-treated rats.

Hyperprolactinemia suppresses luteinizing hormone (LH) and prolactin (PRL) secretion under a variety of experimental conditions. The secretion of both of these hormones is regulated at the hypothalamic level by several neurotransmitters, including serotonin (5-HT). Therefore, we examined the effect of hyperprolactinemia on 5-HT neuronal activity in key hypothalamic areas that are rich in 5-HT terminals and which are known to regulate the release of LH and PRL. Young cycling virgin rats were ovariectomized (day 0). From days 11-16, animals were injected with ovine prolactin (oPRL, 4 mg/kg, s.c.) or vehicle every 8 h. On day 14, one-half of the oPRL- and vehicle-treated rats were implanted with 20-mm long Silastic capsules containing estradiol (180 micrograms/ml). On day 16, animals were killed at 08.00, 12.00 or 18.00 h or treated with pargyline (75 mg/kg) and killed 10 min later. Trunk blood was collected and serum was radioimmunoassayed for LH and endogenous rat PRL (rPRL). Brains were removed, frozen, sectioned and the medial preoptic, suprachiasmatic, and arcuate nuclei, median eminence and globus pallidus were microdissected. Serotonin was measured using high pressure liquid chromatographic methodology. We were unable to detect any feedback effect of hyperprolactinemia on 5-HT turnover in any brain area of ovariectomized or ovariectomized estradiol-treated rats at any time of day that we examined. Several potential reasons for the absence of an effect of hyperprolactinemia on serotonergic function are discussed.

Animals↗

PubMed1989

Increase in epithelial cell growth by hyperprolactinemia induces delay of castration-induced involution of mouse seminal vesicle.

Male (C57BL/6 x DBA)F1 hybrid mice were castrated on day 60 after birth; two pituitaries from 60-day-old female mice were immediately grafted under the capsule of the left kidney in half of the castrated mice to induce hyperprolactinemia. The seminal vesicles in the absence of androgen treatment were examined 15, 22, 30 and 60 days after castration with or without grafting. Significant increases in the weight (1.3-1.4-fold), DNA content (1.2-1.3-fold) and labeling index of epithelial cells (4-10-fold) of the seminal vesicles were found in mice with pituitary grafts compared to mice without grafts on days 15-30 after castration but not on day 60 after castration. Such stimulatory effects of hyperprolactinemia on mouse seminal vesicle cells were also observed on day 15 after castration plus adrenalectomy. Cell loss from the seminal vesicles was found to be similar in castrated mice with and without the grafts. The present findings demonstrate that hyperprolactinemia induces an increase in DNA synthesis of epithelial cells in the seminal vesicles until 30 days after castration and results in a significant delay of castration-induced involution of the weight and DNA content of the seminal vesicles for 1 month. However, the delay with increased epithelial cell growth by hyperprolactinemia disappeared 60 days after castration.

Adrenalectomy↗

PubMed1988

Effects of acute hyperprolactinemia on LH pulsatile secretion in hypogonadal and early follicular phase women.

To investigate the effects of acute hyperprolactinemia on the 24 h LH pulsatile pattern, 11 women in the early follicular phase (EF, days 3 and 4) and 8 postmenopausal women (PMW) were studied before and during administration of metoclopramide, a dopamine receptor antagonist. Sequential 24 h infusions of either metoclopramide (MCP, 30 micrograms/kg/h) or normal saline were conducted and pulsatile LH activity assessed for 48 hrs. In both EF women and PMW, a prompt (within 90 min, p less than 0.001) and sustained (greater than 45 micrograms/L, p less than 0.001) release of PRL was induced by MCP infusions. MCP-induced hyperprolactinemia failed to modify the LH pulsatile activity in both EF women and PMW. These observations suggest that acute hyperprolactinemia due to dopaminergic blockade has no discernible effect on LH pulsatility and that the reduced LH pulse frequency observed in association with endogenous hyperprolactinemia may result from different neuroendocrine mechanism(s) and/or is time dependent.

Adult↗

PubMed1991

Effects of nocturnal hyperprolactinemia on ovarian luteal function and galactorrhea.

To determine the effects of nocturnal hyperprolactinemia on luteal function and galactorrhea we studied six diurnal normoprolactinemic women with regular menstrual cycles. The diurnal serum levels of prolactin (PRL), luteinizing hormone (LH) and progesterone (Prog) and the nocturnal PRL levels at 1 h intervals were determined throughout the first menstrual cycle. Four of the women were nocturnally normoprolactinemic and two showed nocturnal hyperprolactinemia and low luteal progesterone values. In the second menstrual cycle, they were given metoclopramide (10 mg) at midnight before sleep every day, and their serum levels of PRL, LH and Prog were determined by the same protocol as in the first cycle. During treatment with metoclopramide, all the women showed nocturnal hyperprolactinemia, but their diurnal PRL levels remained within the normal range. Low luteal Prog values were observed in all of them and the peak LH levels decreased in all four nocturnally normoprolactinemic women. They had galactorrhea but neither of the nocturnally hyperprolactinemic women had galactorrhea. These results suggest that nocturnal hyperprolactinemia is a cause of luteal insufficiency and galactorrhea.

Adult↗

PubMed1992

Clinical history and outcome of 59 patients with idiopathic hyperprolactinemia.

OBJECTIVE: To investigate the clinical course of hyperprolactinemia without demonstrable cause. DESIGN: Prospective study of all patients with idiopathic hyperprolactinemia first seen between 1974 and 1985. SETTING: Outpatient Department of University Hospital. PATIENTS: Fifty-nine patients followed for 6 to 190 months (median 78 months). Medical treatment given only in case of anovulatory infertility or hypogonadism. OUTCOME MEASURES: Development of pituitary (micro)prolactinoma, prolactin (PRL) levels, and clinical signs of menstrual dysfunction. RESULTS: With exception of one woman in whom it probably had been missed by hypocycloidal tomography, no demonstrable prolactinoma developed. Prolactin levels rose in two patients, one using oral contraceptives and the other with prolactinoma. At the end of follow-up, 15 of 16 patients using a dopaminergic drug had a normal cycle; 13 had normal final PRL levels. From the 43 patients off medication, 28 (66%) had normal PRL levels and 23 (54%) had a normal cycle. There were no significant differences between women who had and had not been pregnant. Dopaminergic medication had no appreciable influence on the course of the disease. CONCLUSION: In idiopathic hyperprolactinemia, progression to pituitary prolactinoma seldom, if ever, occurs. There is a high tendency to spontaneous cure, and pregnancy or medication have no apparent effect. Frequent pituitary imaging was found to be not necessary in our patient population. It may best be reserved for situations in which the PRL level in symptomatic hyperprolactinemia is inconsistent with pituitary imaging results.

Adolescent↗

PubMed1985

Hyperprolactinemia in patients with renal insufficiency and chronic renal failure requiring hemodialysis or chronic ambulatory peritoneal dialysis.

Hyperprolactinemia is common in patients with renal failure. Because radiographic contrast material given during a computed tomographic (CT) scan of the sella as part of the evaluation for prolactinoma worsens renal insufficiency, we attempted to define the point at which hyperprolactinemia becomes an expected finding in patients with renal insufficiency in this study. Of 59 patients with serum creatinine levels of 1.5 to 12 mg/dL, 16 (27.1%) were hyperprolactinemic. Of these 16, nine were not taking medications known to raise prolactin levels and their prolactin levels were less than 100 ng/mL. In the eight patients taking medications prolactin levels were much higher. In one patient the prolactin level fell from 2,210 to 100 ng/mL when methyldopa was discontinued. In patients with chronic renal failure prolactin levels were similar regardless of the method of dialysis. We conclude that in the absence of medications known to affect prolactin secretion, hyperprolactinemia occurs infrequently (18.3%) and, when it occurs, is mild (less than 100 ng/mL). Marked hyperprolactinemia may occur in patients taking such medications. These should be stopped and the prolactin level rechecked before a CT scan is performed.

Creatinine↗

PubMed2004

Management of hyperprolactinemia in patients receiving antipsychotics.

Hyperprolactinemia is increasingly prevalent in patients with common psychiatric disorders due to increasing prescriptions of antipsychotics, particularly newer atypical neuroleptics, in these patients. However, measurement of prolactin levels is indicated only in symptomatic patients. When hyper-prolactinemia is diagnosed, work-up should include exclusion of other causes of hyperprolactinemia, particularly those that might require treatment. Once such causes have been ruled out, a minority of patients with antipsychotic medication-induced hyperprolactinemia, including those with clinically significant signs and symptoms, will require treatment. When treatment is indicated, specifically when hyperprolactinemia results in amenorrhea in women or testosterone deficiency in men, dopamine agonist therapy is generally not advisable. Hormone-replacement therapy, which involves estrogen/progestogen in women and testosterone in men, can often prevent modification and interruption of successful psychiatric medication regimens.

Antipsychotic Agents↗

PubMed1991

Alpha 2-adrenoceptor-mediated inhibition of prolactin release in suckling- or fenfluramine-induced hyperprolactinemia.

It has recently been shown that the specific and selective alpha 2-antagonist idazoxan (IDZ) displays prolactin-lowering activity on hyperprolactinemia induced in the rat either by suckling or serotonergic drugs. In an attempt better to understand the role of alpha 2-adrenoceptors under the above conditions, experiments were carried out to compare the effects of IDZ with that of the classic alpha 2-antagonist yohimbine (YOH), and also of the alpha 2-agonists clonidine (CLO) and B-HT 920, on prolactin (PRL) release during lactation and in hyperprolactinemia induced in male rats by the serotonergic drug fenfluramine (FEN). In lactating rats, both alpha 2-agonists decreased PRL release; this effect was enhanced by prior separation of the animals from their pups for several hours. A decrease of plasma PRL levels was also induced by IDZ but not by YOH, which tended further to increase hyperprolactinemia. In male rats treated with FEN, IDZ and CLO, a significant decrease of plasma PRL was produced, but YOH further enhanced PRL secretion. It is concluded that the alpha 2-agonists tested and also the alpha 2-antagonist IDZ display a unique inhibitory activity on PRL release during suckling or serotonergic-induced hyperprolactinemia.

Adrenergic alpha-Agonists↗