SEARCH · PubMed Health

Results for “hyperprolactinemia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources

PubMed1981

Influence of hyperprolactinemia induced by adenopituitary transplantation under the kidney capsule on the glutamic acid decarboxylase activity in various brain regions.

Glutamic acid decarboxylase activity was assayed in rat substantia nigra, corpus striatum, medial basal hypothalamus and cerebellum under conditions of hyperprolactinemia induced by transplantation of adenopituitary under the kidney capsule. The results indicate that hyperprolactinemia induces a slight increase in the glutamic acid decarboxylase activity of substantia nigra and medial basal hypothalamus and a more evident increase at striatal level. No change was observed in the cerebellum.

Animals↗

PubMed1980

Incidence of hyperprolactinemia during oral contraceptive therapy.

A study was undertaken to determine the incidence of increased serum levels of human prolactin (hPRL) in women during oral contraceptive therapy, and to correlate this with both the dose of oral contraceptive medication and the duration of its use. The 123 patients in this study were divided into 3 groups according to the dosage of estrogenic component of the combined oral contraceptives. Thirty percent of these women had hyperprolactinemia of varying degree. Neither the dosage of steroids within our range nor the duration of therapy correlated with the presence or degree of hyperprolactinemia. The actions of estrogen-progestin compounds on hPRL are discussed.

Adolescent↗

PubMed1976

Pituitary gonadotropin response in women with idiopathic hyperprolactinemia.

Inappropriate lactation and idiopathic hyperprolactinemia are frequently associated with amenorrhea. In these individuals, peripheral levels of follicle-stimulating hormone (hFSH) are usually normal, and luteinizing hormone (hLH) levels are often found in the low-normal range. The present study was undertaken to evaluate the functional capacity of the pituitary by the response of hFSH and hLH to synthetic gonadotropin-releasing hormone (Gn-RH). Six women with amenorrhea, inappropriate breast secretion, and idiopathic hyperprolactinemia (prolactin levels ranged from 45 to 355 ng/ml) were given 100 mug of Gn-RH intramuscularly. Serum hFSH and hLH levels were assessed in samples obtained at 15-minute intervals over the next 2-hour period. Initial hFSH levels were normal in all women, with a mean of 242 +/- 72 ng/ml. The absolute increase after Gn-RH administration averaged 486 +/- 193 ng/ml. Serum hLH was below normal in three of the six women, and normal in the remaining three women initially. The absolute increase averaged 1308 +/- 315 ng/ml. The greatest percentage increase in hLH was found in the women with the subnormal basal titers. In these women, hLH rose from a mean of 22 ng/ml to a mean of 1092 ng/ml. These data demonstate an exaggerated increase in hFSH and hLH levels after exogenous Gn-RH administration. This suggests that the amenorrhea associated with elevated serum prolactin levels is principally of hypothalamic origin.

Amenorrhea↗

PubMed1976

Amenorrhea, hyperprolactinemia and pituitary enlargement secondary to primary hypothyroidism. Successful treatment with thyroid replacement.

A 22-year-old nulliparous woman presented with primary amenorrhea, primary hypothyroidism, hyperprolactinemia, and radiologic evidence of pituitary enlargement. Investigation demonstrated limited reserves of ACTH and growth hormone. Circulating concentrations of TSH and prolactin were elevated; they increased in response to thyrotropin releasing hormone and decreased following L-dopa administration. After treatment with L-tri-iodothyronine, serum TSH and prolactin levels fell markedly, reserves of growth hormone and ACTH returned to normal, menstrual periods began, and the patient conceived. She experienced an uncomplicated prenatal, intrapartum, and postpartum course. It is thought that this patient represents a distinct clinical entity: a syndrome of amenorrhea, hyperprolactinemia, and pituitary enlargement, all secondary to primary thyroid failure. This syndrome should be distinguished from the Forbes-Albright syndrome, as it is reversible with thyroid replacement therapy. Recognition of this syndrome may thus spare the patient unnecessary, and potentially dangerous, pituitary surgery or irradiation.

Adult↗

PubMed1993

Transient hyperprolactinemia in gonadotropin-stimulated cycles for in vitro fertilization and its effect on conception.

The significance of transiently increased serum prolactin (PRL) levels on pregnancy rates in vitro fertilization (IVF) is unknown. The aim of this study was to evaluate PRL levels in IVF patients who conceived and in matched controls who did not. Ten IVF cycles resulting in pregnancy and forty nonpregnant cycles were compared. Prolactin was measured before ovarian stimulation with gonadotropins and estradiol (E2), progesterone (P) and PRL were measured 36 hours, 12 hours, 10 minutes before and 12 hours after human chorionic gonadotropin (hCG) administration at mid-cycle. Serum PRL levels at various time were not significantly higher in the nonpregnant women than in the pregnant women. Twelve hours before hCG, P levels were significantly higher in the nonpregnant women than in the pregnant women (1.5 +/- 0.2 ng/ml [mean +/- standard error] and 0.9 +/- 0.3 ng/ml, respectively; P < 0.05). All women had transient hyperprolactinemia for one to three times during ovarian hyperstimulation. There was no correlation between PRL and E2 in either group. These results do not support the treatment of transient hyperprolactinemia with dopamine agonists in IVF patients.

Chorionic Gonadotropin↗

PubMed2001

Effects of hyperprolactinemia on testosterone production in rat Leydig cells.

The pathogenesis of hyperprolactinemia (hyperPRL) induced hypogonadism has been suggested to be related with a dysfunction of hypothalamus-pituitary-testis axis. While the direct inhibitory effects of prolactin (PRL) on testosterone (T) release have been demonstrated, the mechanism is still unclear. Our previous study demonstrated a diminished T release in the testicular interstitial cells (TICs) from the anterior pituitary (AP)-grafted rats as compared with the control, and the pattern was in agreement with the in vivo model. However, TICs incubation cannot totally represent the response of the Leydig cells. Therefore, a Percoll gradient purified Leydig cell model was adopted to explore the response of T release under similar challenges in this study to investigate the effects of hyperPRL on the Leydig cells per se. HyperPRL in male rats was induced by grafting rat AP under the renal capsule. The control animals were grafted with rat brain cortex tissue (CX). Six weeks after grafting, the rats were sacrificed. Either TICs or Leydig cells were isolated, respectively, for in vitro incubation and challenge. Challenge drugs included human chorionic gonadotropin (hCG, 0.05 IU/ml), steroidogenic precursors (25-OH-cholesterol, 10(-6) M; pregnenolone, 10(-6) M), forskolin (an anenylyl cyclase activator, 10(-4) M) and 8-bromo-3':5' cyclic adenosine monophosphate (cAMP) (8-Br-cAMP 10(-4) M). T released by TICs or Leydig cells was determined by radioimmunoassay. The TICs from the AP-grafted rats showed lower levels of T release than the control group while the purified Leydig cells demonstrated a reverse pattern in response to challenges of hCG, steroidogenic precursors, forskolin and 8-Br-cAMP. In hyperPRL rats, a paradoxical pattern of T release between TICs and purified Leydig cells is observed. The purified Leydig cells from AP-grafted rats demonstrated a higher level amount of T release than the control after stimulation. The phenomenon can be attributed to the change of Leydig cell sensitivity to the stimulation after the effects of chronic hyperPRL. Moreover, another possibility is the role played by other interstitial cells to modulate steroidogenesis in Leydig cells.

Animals↗

PubMed1985

Reduction in prostatic concentration of endogenous dihydrotestosterone in rats by hyperprolactinemia.

Persistently high levels of circulating prolactin can be achieved in male rats when pituitaries from female donors are grafted under the renal capsule. Enhanced growth of the lateral prostate can be accomplished by an apparent synergistic effect of excess prolactin with subphysiologic doses of testosterone. To define this effect we measured the endogenous dihydrotestosterone (DHT) concentrations in rat prostate lobes. Twenty Sprague-Dawley male rats (250 g) were castrated and given subcutaneous implants of silastic tubing filled with 1 cm of crystalline testosterone. Ten of these rats simultaneously received two pituitary grafts under the renal capsule. The remaining ten rats received intrarenal skeletal muscle grafts as controls. Four weeks later, the weight (mg +/- SE) of the ventral and dorsal lobes were not significantly different between the two groups, while the lateral lobe was significantly (P less than 0.01) heavier in rats with pituitary grafts (121.4 +/- 7.5) than in controls (81.7 +/- 10.4). Endogenous DHT in the tissue extracts was determined by radioimmunoassay following KMnO4 treatment to eliminate testosterone. The concentration of DHT (ng/g tissue +/- SE) was significantly (P less than 0.01) lower in the lateral prostate of graft-bearing animals (4.40 +/- 0.29) than in the controls (5.98 +/- 0.34). These results indicate that, in the rat, hyperprolactinemia induced by pituitary grafts is associated with a heavier lateral prostate and a lower concentration of endogenous DHT in that tissue. These results also suggest that the action of prolactin in the rat prostate is not mediated through the action of androgen.

Animals↗

PubMed2001

Hyperprolactinemia complicating juvenile granulosa cell tumor of the ovary.

BACKGROUND: Granulosa cell tumors are known to be hormonally active. They usually produce estrogen and inhibin, and the serum inhibin level is often considered a useful tumor marker during the follow-up of this illness. CASE: We present a case of malignant juvenile granulosa cell tumor associated with hyperprolactinemia. In our patient, the serum prolactin concentration closely reflected the behavior of the disease. CONCLUSION: Our findings are consistent with the assumption that prolactin was a tumor marker in this patient.

Adult↗

PubMed1986

Mammosomatotroph adenoma of the pituitary associated with gigantism and hyperprolactinemia. A morphological study including immunoelectron microscopy.

A 29-year old giantess with growth hormone excess and hyperprolactinemia underwent transsphenoidal surgery to remove her pituitary tumor. Electron microscopy revealed a mammosomatotroph adenoma composed of one cell type. Immunoelectron microscopy, using the immunogold technique, demonstrated predominantly growth hormone or prolactin or a varying mixture of both growth hormone and prolactin in the adenoma cells. The presence of growth hormone and prolactin was found not only in the cytoplasm of the same adenoma cells but also in the same secretory granules. In the nontumorous adenohypophysis, somatotrophs and lactotrophs showed ultrastructural signs of hyperactivity. This finding is in contrast with the presence of suppressed somatotrophs and lactotrophs seen in nontumorous portions of adult pituitaries harboring growth hormone or prolactin-secreting adenomas. Our morphological study reinforces the view that growth hormone-producing pituitary tumors, originating in childhood, are different from those of the adult gland.

Adenoma↗

PubMed1987

Phenotypic and functional abnormalities of T lymphocytes in pathological hyperprolactinemia.

The phenotype and function of T cells circulating in patients with pathological hyperprolactinemia were analyzed and compared to those in sex- and age-matched control subjects. Two-color immunofluorescence study revealed an increased number of CD4+ TQ1+ cells and the presence of phenotypically immature CD1+ T cells, also exhibiting transferrin surface receptor, in peripheral blood of the hyperprolactinemic patients. After chronic treatment with the dopamine agonist bromocriptine, T-cell abnormalities disappeared. In addition, some untreated patients showed enhanced T-cell suppressor activity in an in vitro pokeweed mitogen-driven B-cell transformation assay. These immunological findings confirm a link between neuroendocrine and immune systems in humans.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1990

Transient hyperprolactinemia has no effect on endocrine response and outcome in in vitro fertilization (IVF).

Transient rises in plasma prolactin levels can be observed during the late follicular phases of both natural and stimulated cycles. It has been suggested that such a phenomenon might adversely affect the success of in vitro fertilization. This prospective study was designed to assess the effect of transient rises in prolactin levels on the endocrine response to ovarian stimulation and the outcome of in vitro fertilization treatment. A total of 90 treatment cycles in 87 couples was studied. Prolactin was measured in the mid and late follicular phases of the cycles. During the study period, 24 pregnancies occurred. There were no differences in those cycles in which pregnancy did or did not occur in either mid or late follicular prolactin levels. Neither the initial level nor the percentage rise in prolactin during the stimulation had any effect on the peak estradiol level achieved, the numbers of follicles seen, the number of eggs retrieved, or the incidence or outcome of pregnancy. It was concluded that transient hyperprolactinemia is of no significance in ovarian stimulation for in vitro fertilization.

Adult↗

PubMed1987

Chronic hyperprolactinemia and plasma lipids in women.

Plasma total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) were studied in 15 hyperprolactinemic women who had a prolactin (PRL) adenoma, in comparison to 15 age-matched control women. In the hyperprolactinemic group, plasma lipids were also correlated to age, excess body weight (EBW), plasma PRL, and estradiol-17 beta (E2). Plasma TC, TG, and LDL-C were similar in both hyperprolactinemic and control women, while plasma HDL-C was significantly lower (P less than 0.01) in the hyperprolactinemic group. The correlation study showed a significant negative correlation between HDL-C and EBW (r = -0.64; P less than 0.02) and a slightly significant positive correlation between TG and PRL (r = 0.54; P less than 0.05). The direct effect of PRL on plasma lipids is difficult to establish since many factors influencing lipid metabolism are altered during hyperprolactinemia.

Adolescent↗

PubMed1994

Acromegaly and hyperprolactinemia in a patient with polyostotic fibrous dysplasia: dynamic endocrine studies and treatment with the somatostatin analogue octreotide.

Acromegaly and hyperprolactinemia have been described in association with polyostotic fibrous dysplasia; the pathogenetic mechanisms involved in the development of the endocrinopathies is unknown. We report a 26-year-old man with polyostotic fibrous dysplasia and hypersecretion of GH and PRL. Plasma GH, PRL, and insulin-like growth factor-I (IGF-I) were elevated. Glucose-non-suppressible plasma GH concentrations, GH responsiveness to TRH and GHRH, and GH suppression after a test-dose of somatostatin, octreotide, and bromocriptine were found. Plasma GHRH levels were within the normal range (< 25 ng/l). Computed tomography of the sella turcica and visual fields were normal. [111In-DTPA-D-Phe1]-octreotide scintigraphy were used to localize a possible tumor; no radioactivity was visualized at the site of the hypothalamus, the pituitary or elsewhere in the body but a considerable accumulation of radioactivity was found in the os frontalis. Therapy with octreotide by continuous sc infusion partially suppressed GH and IGF-I (and normalized PRL). The results suggest that hypersecretion of GH in our patient is not due to a GH-secreting pituitary tumor, eutopic or ectopic hypersecretion of GHRH or autonomous somatotroph function. The origin of the disease in this patient might be an abnormal hypothalamic regulation of somatotrophs and/or an alteration in the transmembrane signalling systems.

Acromegaly↗

PubMed2003

Is hyperprolactinemia associated with insulin resistance in non-obese patients with polycystic ovary syndrome?

Insulin resistance is common in polycystic ovary syndrome (PCOS). Moderate elevations in serum PRL concentration may contribute to insulin resistance in PCOS. The aim of this study was to determine PRL on development of insulin resistance in non-obese hyperprolactinemic patients with PCOS. Ninety-eight non-obese subjects with PCOS and 100 non-obese healthy control were accepted in the study. Serum glucose, lipids, androgens, free androgen index (FAI), gonadotropins, fat mass and percentage, SHBG, and insulin levels were measured. Homeostasis model assessment (HOMA) was used as index of pancreatic beta-cell function and tissue insulin sensitivity. Independent t-test was used in comparison of results. In patients with PCOS, FAI and mean HOMA-(%B) level were higher than in the control group (p<0.0001), whereas mean HOMA-(%S) in subjects with PCOS was lower than in the control group (p<0.0001). Patients with PCOS were divided into subgroups according to their serum prolactin level (< 24 or > or = 24 ng/ml). Although FAI was not different, mean insulin and HOMA-(%B) levels in hyperprolactinemic patients were higher than in normoprolactinemic subjects (p<0.001). HOMA-(%S) in hyperprolactinemic patients with PCOS was lower than in normoprolactinemic patients (p<0.002). In conclusion, PCOS is associated with insulin resistance; non-obese hyperprolactinemic PCOS patients may be more insulin-resistant than normoprolactinemics and there may be an association between hyperprolactinemia and insulin resistance in PCOS.

Adult↗

PubMed1987

Effects of a new long-acting form of bromocriptine on tumorous hyperprolactinemia.

Recently, a new long-acting form of bromocriptine (Parlodel LA, Sandoz) has been developed and it has already been found to be effective in lowering plasma PRL levels in normal volunteers and postpartum women. This work reports the clinical, hormonal and radiological effects of a single 50 mg dose of long-acting bromocriptine in 10 patients with tumorous hyperprolactinemia (2 microprolactinomas, 6 macroprolactinomas, 1 acromegaly and 1 nonsecreting macroadenoma). A rapid and long-lasting (28 days) normalization of PRL levels was observed in patients with microprolactinoma, acromegaly and nonsecreting adenoma. None of the 6 patients with macroprolactinoma underwent normalization of plasma PRL, but the latter was markedly reduced (61-80% of basal levels). A second injection of the drug in 5 macroprolactinoma patients induced a further reduction of plasma PRL levels in 2 of them. No changes in the tumor size were observed either after the first or the second injection of long-acting bromocriptine in any of the patients. This injectable form of bromocriptine induced nausea and/or mild hypotension lasting a few h in 4 of the 10 patients and was better tolerated than the oral form as regards both the duration and intensity of the side effects. Thus, as this drug has proved to be efficacious and well tolerated by the patients, this long-acting form of bromocriptine may be a valid therapeutical approach for initiating medical treatment of patients with prolactinoma.

Acromegaly↗

PubMed1996

Langerhans cell histiocytosis, diabetes insipidus, hyperprolactinemia and empty sella: a four-fold association. Report of two cases.

Two cases of Langerhans cell histiocytosis (LCH) expressing as Hand-Schuller-Christian syndrome with diabetes insipidus, hyperprolactinemia and empty sella are here reported. Up-to-date this four-fold association is lacking in world literature and it is here discussed in the light if LCH is a cancer or the clinical expression of an immunologic disorder.

Adult↗

PubMedDate not supplied

Prolactin bioassay and hyperprolactinemia.

The Nb2 rat lymphoma bioassay (BA) for prolactin (PRL) was performed in 26 subjects with hyperprolactinemia, 17 of whom had radiologic evidence of a pituitary adenoma. All subjects were treated with the long acting dopamine agonist CV 205-502. The radioimmunoassay (RIA) PRL significantly decreased with treatment but the BA/RIA PRL remained essentially the same, indicating that the relative bioactivity was unaffected.

Adenoma↗

PubMedDate not supplied

Total body zinc depletion and its relationship to the development of hyperprolactinemia in chronic renal insufficiency.

Modulation of free plasma zinc levels has been implicated in the increase in plasma prolactin levels seen in patients with chronic renal insufficiency (CRI). The relative importance of this mechanism in comparison to others, however, has not been elucidated. Zinc equilibrium between plasma and red blood cells is partly dependent upon red blood cell carbonic anhydrase (CA). In the present paper, we have investigated the interrelationships among total plasma zinc, leukocyte zinc, prolactin, and erythrocyte CA in patients with CRI. Uremic patients were shown to have significantly increased levels of plasma prolactin and erythrocyte CA activity when compared to normal controls. Moreover, red blood cell CA total concentration and isoenzyme-I and-II levels, as well as plasma zinc were found to be significantly decreased in uremic patients in comparison to normal controls. In patients with CRI, a negative correlation was demonstrated between erythrocyte CA catalytic activity and plasma zinc, as well as between plasma zinc and plasma prolactin levels. Moreover, leukocyte zinc content, which is a reliable indicator of total body zinc stores, was found to be significantly decreased in uremic patients when compared to normal controls. A strong negative correlation between leukocyte zinc content and plasma prolactin levels was documented in CRI patients. Our results suggest that alterations in erythrocyte CA levels, enzymatic activity or isoenzyme profile are most probably mechanistically and etiologically unrelated to the high plasma prolactin levels in CRI patients. Contrariwise, depletion of total body zinc stores, rather than redistribution of this trace metal among extracellular compartments, may represent one of the major contributing mechanisms leading to uremic hyperprolactinemia.

Adult↗