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Results for “hyperprolactinemia”

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At least 253 records · Page 14Linked to original sources

PubMed1994

Longstanding hyperprolactinemia associated with systemic lupus erythematosus: possible hormonal stimulation of an autoimmune disease.

OBJECTIVE: To describe 4 women in whom hyperprolactinemia was associated with the development of systemic lupus erythematosus (SLE). METHODS: Clinical assessment and followup (2 cases). Chart review and interviews with the attending rheumatologist (2 cases). Detailed review and reassessment of multiple imaging studies of the pituitary. RESULTS: One patient had idiopathic hyperprolactinemia, and 3 had pituitary microadenomas. Serum 17 beta-estradiol concentrations were normal in all women, but serum testosterone was suppressed in 2. SLE flares occurred in 2 individuals, one and 6 months after bromocriptine therapy was discontinued, and reinstitution of bromocriptine therapy in a patient who refused corticosteroids resulted in resolution of her SLE disease activity. CONCLUSION: Hyperprolactinemia, which has the potential to exacerbate autoimmunity, may coexist with SLE. In these instances, bromocriptine may afford therapeutic benefit.

Adult↗

PubMed1994

[A study on bone metabolism in woman with hyperprolactinemia].

We studied bone metabolism in hyperprolactinemia in 21 hyperprolactinemic women, and compared it with 57 normal subjects. Second to fourth lumbar bone mineral density (BMD) was measured by dual energy X-ray absorptiometry (DXA). The mean BMD (g/cm2) in hyperprolactinemic women was 9% less than in normal subjects (0.940 +/- 0.115 (SD) vs. 1.030 +/- 0.106, p < 0.05). A negative correlation was found between BMD and the duration of hyperprolactinemia. The analysis of bone metabolic parameters, bone turnover, bone formation and bone absorption showed that they increase in the hyperprolactinemic state. The main mechanism of BMD loss in hyperprolactinemia is probably due to hypoestrogenemia, but a direct effect of prolactin cannot be excluded.

Absorptiometry, Photon↗

PubMedDate not supplied

[Hyperprolactinemia and autoimmunity].

Prolactin is a pituitary hormone with several functions, one of them, immunoregulatory. Patients with prolactinoma develop hyperprolactinemia. In the next two cases, patients with microprolactinoma, both autoimmune disease associated. First patient, male, with multiple sclerosis; the other one patient, female, with systemic lupus erythematosus. Treatment of hyperprolactinemia with bromocriptine was associated with satisfactory clinical evolution, and a reduction of dosage of immunosuppressor treatment. The patients with multiple sclerosis had neurological functions recovery and the patients with systemic lupus erythematosus had severe relapse of disease each time she dropped bromocriptine treatment. Pituitary function must be evaluated in autoimmune disease, to search alterations like hyperprolactinemia who influenced immune function.

Adult↗

PubMed1998

[Erectile dysfunction secondary to hyperprolactinemia. Apropos of 13 cases].

Hyperprolactinemia is the cause of erectile dysfunction in less than 1% of cases. From 1989 to 1996, 13 patients consulted for erectile disorders associated with hyperprolactinemia. The mean age was 47.5 years. 10 patients complained of decreased libido. 3 patients had gynecomastia. Plasma prolactin levels ranged from 31.3 ng/ml to 1,300 ng/ml. 7 patients had a plasma testosterone less than 4 ml/ng. 7 patients had a micro- or macroadenoma of the sella turcica visualized by MRI. After drug treatment, plasma prolactin levels returned to normal in all patients in whom assays were performed. 6 patients considered that their erectile function was restored. 5 of the 6 patients with no improvement of their sexual function had a concomitant disease able to explain the impotence. Hyperprolactinemia is a rare cause of erectile dysfunction, but it must be considered in any patient presenting with idiopathic erectile dysfunction associated with decreased libido, gynecomastia, and decreased plasma testosterone. Drug treatment is effective and MRI of the sella turcica should be performed looking for a pituitary adenoma.

Adult↗

PubMed1985

Hyperprolactinemia and estrogen-induced rhythms in LH and prolactin release in the ovariectomized rat.

Short-term (9 days) hyperprolactinemia induced by pituitary grafts reduced basal plasma LH levels in ovariectomized rats whereas long-term (31 days) grafts increased basal LH levels. Although long-term grafts inhibited estradiol-induced prolactin surges, hyperprolactinemia had no effect on the LH surge. It is concluded that the estrogen-treated ovariectomized rat is not suitable for studying the effects of hyperprolactinemia on LH release.

Animals↗

PubMed1983

Effects of sulpiride induced hyperprolactinemia on testosterone secretion and metabolism before and after HCG in normal men.

The purpose of the study was to investigate the effects of sulpiride-induced hyperprolactinemia on testicular functions, as assessed by evaluation of plasma testosterone (T), dihydrotestosterone (DHT) and 17 beta-estradiol (E2) levels. An HCG test (5000 IU on three consecutive days) was performed in basal conditions and after 12 and 26 days of sulpiride treatment (150 mg daily) in 7 male volunteers, 19 to 32 years of age, as well as in 6 sulpiride-free controls. The results show that after 12 days of induced hyperprolactinemia (mean increase 400%) the T response to HCG was similar to basal test; after 26 days however, the increase of T mean plasma levels was significantly greater. The increase in E2 significantly correlated to that of T during the first and second HCG tests, but no longer after 26 days of hyperprolactinemia, resulting in an imbalance of the E2/T ratio of plasma increments. The response of DHT to HCG was significant in basal conditions and after 26 days of sulpiride and always correlated with T behavior. Data obtained in our experimental conditions suggest that PRL might enhance T secretion. 5 alpha-reductase activity seemed to be partially affected after 12 days of treatment, while a significant inhibition seemed to be exerted on aromatase activity.

Adult↗

PubMed1984

Prolactin and calcium metabolism: influence of hyperprolactinemia on immunoreactive parathyroid hormone levels in man and in the rat.

Serum prolactin, parathyroid hormone, P and Ca serum levels were measured in 15 patients (12 women and 3 men) with hyperprolactinemia, and in 6 normal male volunteers who underwent a TRH test (100 micrograms by rapid iv injection) in order to obtain a short-term pharmacologically-induced hyperprolactinemia. A pituitary gland graft under the kidney capsule was carried out on 26 Sprague-Dawley male rats, which became hyperprolactinemic since the transplanted pituitary was stripped of the inhibitory hypothalamic control. Another group of 10 rats was injected with L-sulpiride (0.1 mg/kg). The serum PTH levels in patients and in subjects with induced hyperprolactinemia were within the normal range and there was no correlation between serum PRL and PTH levels. The same occurred both in transplanted and L-sulpiride injected rats. Our results suggest that prolactin does not modify PTH secretion in vivo and therefore, in contrast with previous data, it should not be considered a physiologically relevant secretagogue for parathyroid hormone.

Adolescent↗

PubMed1983

Hyperprolactinemia. Long-term effects of bromocriptine.

Patients with hyperprolactinemia may be managed by pituitary surgery or irradiation, bromocriptine treatment, or a combination of these methods, and some patients remain untreated. Little is known of the long-term consequences of some of these therapeutic regimens. Forty-six hyperprolactinemic patients (40 female and six male) managed solely with bromocriptine or no treatment over a period of 12 months to six years were therefore evaluated in this study. Nine patients with radiologically normal pituitary fossae were untreated and 10 received bromocriptine, 7.5 to 10 mg daily, while 20 patients with radiologic evidence of a pituitary tumor were treated with bromocriptine, generally 10 to 20 mg daily. Patients were assessed clinically, biochemically, and radiologically before treatment and at least six weeks after discontinuation of therapy. A further seven patients were similarly assessed before and after eight bromocriptine-induced pregnancies. Symptoms persisted in the untreated group of nine patients, although menstruation returned in four of the females with previous amenorrhea; serum prolactin levels remained elevated, other pituitary function did not change, and pituitary fossae remained normal radiologically. In all patients treated with bromocriptine, symptoms improved irrespective of radiologic findings on the pituitary, and were abolished in 67 percent during treatment associated with a decrease in serum prolactin levels in all, and a return of levels to within normal limits in 80 percent of patients. Persistent side effects were usually dose-related, but remained troublesome in 13 percent. Bromocriptine-induced tumor regression was evident radiologically in all patients with suprasellar tumor tissue and in some with purely intrasellar adenomas. This effect occurred rapidly and persisted or increased throughout follow-up. On discontinuation of treatment, prolactin levels remained significantly lower than before therapy (mean 2,934 versus 5,052 mU/liter, p less than 0.05) but were within the normal range in only two patients. Other pituitary function was unaltered, or improved in some patients with definite tumors. Bromocriptine-induced pregnancy produced no permanent change in clinical, biochemical, or radiologic status. Long-term bromocriptine treatment for hyperprolactinemia is thus highly effective in alleviating symptoms and suppressing prolactin secretion, and induces persistent tumor regression on treatment without deterioration of other pituitary function in patients with macroadenomas. On discontinuation of therapy, however, hyperprolactinemia usually recurs, and treatment may therefore need to be continued for years.

Adult↗

PubMed1983

Primary empty sella, hyperprolactinemia, and isolated ACTH deficiency after postpartum hemorrhage.

In a 20-year-old woman, a complicated full-term delivery was followed by a 14-month history of galactorrhea, amenorrhea, and symptoms of hypocortisolism. Evaluation revealed the presence of an empty sella, hyperprolactinemia, and an isolated pituitary deficiency of ACTH, resulting in secondary adrenal insufficiency. The defect in ACTH secretion was apparently due to intrinsic pituitary rather than hypothalamic disease, because administration of lysine vasopressin did not stimulate ACTH release. An empty sella with hyperprolactinemia has been described before. However, to the authors' knowledge, isolated ACTH deficiency as a complication of postpartum hypopituitarism (atypical Sheehan's syndrome) in association with an empty sella and hyperprolactinemia has not previously been reported.

Adrenocorticotropic Hormone↗

PubMed1981

Hyperprolactinemia--a significant factor in female infertility.

A prospective study was undertaken to determine the incidence of hyperprolactinemia in a group of referred infertile women, and to determine the association with (a) abnormal menstrual function and (b) presence or absence of galactorrhea. Of 113 referred infertile patients, 22 (19.5%) had elevated levels of serum prolactin. Five (4.4%) patients with hyperprolactinemia had neither abnormal menstrual function nor galactorrhea. This study demonstrates that hyperprolactinemia is a common finding in an infertile population, more so when galactorrhea and/or menstrual dysfunction is also present.

Adult↗

PubMed1982

Integrity of central dopaminergic system in women with postpartum hyperprolactinemia.

In order to elucidate the role of elevated prolactin (PRL) on the central dopaminergic systems, the suppressive effects on PRL were studied after the administration of L-dopa and L-dopa plus carbidopa on consecutive days to the following three groups: 10 normoprolactinemic subjects, six nonnursing normal puerperal women, and seven hyperprolactinemic women without any evidence of pituitary tumor. In the normoprolactinemic subjects (basal PRL 13 +/- 2 ng/nl mean +/- SE), the suppressive effects of L-dopa alone and L-dopa plus carbidopa were similar (48% +/- 4% and 58% +/- 6%, respectively). In puerperal hyperprolactinemic subjects, the basal PRL (116.8 +/- 16.4 ng/ml) was suppressed 77% +/- 2% after administration of L-dopa and 51% +/- 7% after L-dopa plus carbidopa, significantly different from that of L-dopa alone (p less than 0.005), but similar to that observed in normal subjects. In the patients with idiopathic hyperprolactinemia, the baseline PRL (131 +/- 38 ng/ml) decreased 56.3% after the administration of L-dopa. In the presence of peripheral dopa decarboxylase inhibition, the administration of L-dopa decreased plasma PRL values 30%, a drop significantly different from that of L-dopa alone (p less than 0.02). Women with idiopathic hyperprolactinemia exhibit reduced central dopaminergic inhibition of PRL secretion similar to that in patients with pituitary tumor; whereas the response to central dopaminergic inhibition in postpartum women with comparable baseline PRL levels is similar to that in normoprolactinemic subjects. This indicates that hyperprolactinemia per se is not associated with a state of reduced central dopaminergic inhibition. The increased pituitary sensitivity to L-dopa observed in puerperal women may be due to alterations in PRL receptors or vascularity.

Carbidopa↗

PubMed1983

Hyperprolactinemia and headaches.

We investigated the frequency of headaches in women with menstrual abnormalities and hyperprolactinemia. Twenty-seven of 46 (58%) women with hyperprolactinemia indicated that headache episodes occur once or more per week; patients with sellar abnormalities (macroadenoma) or previous cranial or pituitary operation were excluded from this group of hyperprolactinemic patients. The headache episodes occurred significantly more frequently than in the control group (N = 56), where 27% indicated one or more headaches per week (p less than 0.01). In the vast majority of the women with hyperprolactinemia, headaches had preceded the finding of elevated prolactin levels for years and had not developed after the patients had become concerned about the pituitary gland. The clinical impression was that the headaches of these patients typically lack features of prodromal signs and unilaterality and resemble, in general, tension headaches; they may last for hours and often require medication. We could not demonstrate a relationship between prolactin levels and frequency or severity of these headache episodes. The etiology of these headaches is unclear. The therapeutic effect of bromocriptine deserves further investigation. In conclusion, we present data to suggest that headaches are commonly an associated finding in hyperprolactinemic women who have no evidence of significant pituitary enlargement.

Adenoma↗

PubMed1978

Changes in catecholamine turnover in the anterior part of the mediobasal hypothalamus and the medial preoptic area in response to hyperprolactinemia in ovariectomized rats.

High serum prolactin levels in ovariectomized rats were induced by transplantation of additional pituitaries under the kidney capsule. Such high prolactin levels reduced serum LH but not FSH levels 3 days after pituitary transplantion. LH and FSH values were at a control levels at day 15 and above these levels at day 24, although prolactin values were still high. Dopamine (DA) and norepinephrine (NE) turnover in the anterior part of the mediobasal hypothalamus (AMBH) and in the medial preoptic area (MPO) was measured by following the decrease in NE or DA content after synthesis blockage with a-methyl-p-tyrosine. The content was measured using a radioenzymatic assay. DA turnover in the AMBH was significantly increased 3, 15 and 24 days after induction of hyperprolactinemia. Although NE concentration in the AMBH was also increased at these times an increased NE turnover was statistically significant only at day 24. DA as well as NE turnover rates in the MPO were reduced by day 3 after pituitary transplantation and at control values at day 15 and 24. It is concluded that the increased DA turnover in the AMBH depresses pituitary LH release probably by inhibiting hypothalamic LH-RH secretion. This inhibition is counteracted by the somewhat slower increase of NE turnover resulting in normalization of LH levels. The increased gonadotropin levels after long-lasting hyperprolactinemia may be due to desensitization of the DA receptor, which was reported earlier. The reduced NE turnover in the MPO 3 days after induction of hyperprolactinemia may be an additional factor in reducing pituitary LH release acting at the level of LH-RH-producing perikarya.

Animals↗

PubMed1983

Effects of estradiol benzoate and castration on LH in experimental hyperprolactinemia.

Female rats of the Wistar strain were rendered hyperprolactinemic by grafting one additional pituitary gland under the right kidney capsule at various ages (5 days group A; 30 days group B and 90 days group C). Age matched animals were sham operated to serve as controls. Plasma levels of PRL and LH were measured by specific double antibody RIA. Basal preoperative PRL levels were increased rapidly after grafting, reaching values over 100 ng/ml, in front of the 20 ng/ml showed by sham operated controls. Plasma LH levels were significantly decreased in all hyperprolactinemic groups as compared to controls. After Estradiol Benzoate (EB) administration all control rats showed an increase in PRL levels in a pulsatile manner with higher values found in the afternoon. PRL response in transplanted rats was less evident and with absence of pulsatility. LH responses to EB in control animals showed a biphasic pattern, with a negative feed-back in the first hours followed by a positive effect at 31 or 55 h after the injection. This pattern of response started in the control rats from group A at 19 days of age. Before that, only the negative feed-back effect was present. In grafted animals from the same group no positive feed-back effect could be detected at any time studied. In group B, a reduction in the positive feed-back effect, more evident after 90 days of hyperprolactinemia was detected. Animals of group C on the contrary showed an increased positive feed-back effect 40 days after grafting. Eight days after castration a reduction in PRL levels was detected in all groups, together with an increase in LH values. PRL values after ovariectomy were less reduced in grafted animals, and these rats also showed a less marked LH increase. This effect is more evident in group B. All these data seem to point out that hyperprolactinemia is capable of modifying the feed-back system between E2 and LH, and that the age at which hyperprolactinemia starts has a profound effect.

Animals↗

PubMed1981

Amenorrhea, galactorrhea, hyperprolactinemia syndrome and breast carcinoma in a young woman.

A young female patient with amenorrhea, galactorrhea and hyperprolactinemia developed a carcinoma of the breast a few years later. Examination of the amenorrhea--galactorrhea syndrome did not reveal any prolactinoma so that hyperprolactinemia remains unexplained. Treatment with bromoergocryptine 5 mg daily was successful. The carcinoma was treated in the classic way by amputation of the breast, axillary curettage and adjuvant chemotherapy. However, the association of amenorrhea, galactorrhea and breast carcinoma via hyperprolactinemia raises the question of whether there is any etiologic--pathogenetic relationship. Convincing evidence of such a relationship has not been found in the literature.

Adenocarcinoma↗

PubMed1991

Lack of an inhibitory effect of hyperprolactinemia on androgen-dependent marking.

An experiment was performed to determine if hyperprolactinemia (chronically elevated serum prolactin levels), which inhibits testosterone-activated male sexual activity, also affects other androgen-dependent behaviors. Thus defecation and urine marking in response to a novel environment were examined in sham-operated and pituitary-grafted (hyperprolactinemic) male rats that had been castrated or castrated and given subcutaneous testosterone implants. Both castration and pituitary grafting significantly inhibited defecation, with the inhibitory effects of hyperprolactinemia being most pronounced in the castrated non-testosterone-treated animals. In contrast, castration significantly reduced the amount of urine marking observed, but pituitary grafting was without effect on this behavior. Thus, although hyperprolactinemia may inhibit sexual activity through an antagonism of the activational effects of testosterone, these results suggest that this effect is specific to sexual behavior and does not involve a more generalized inhibition of the effects of testosterone on androgen-dependent behaviors.

Animals↗

PubMed1983

Hypothalamic catecholamine biosynthesis and pituitary gonadotropin secretion in vitro: effect of hyperprolactinemia.

The effect of hyperprolactinemia on central catecholamine biosynthesis and anterior pituitary hormone release was studied using an in vitro methodology. The incorporation of [3H]tyrosine into hypothalamic and neurohypophyseal catecholamines was determined using a new method which combines high performance liquid chromatography (HPLC) with amperometric detection (LCEC). Elevated plasma prolactin levels, induced by pituitary transplants, resulted in increased in vitro biosynthesis of medial basal hypothalamic (MBH) dopamine (DA), but not norepinephrine (NE). Neurohypophyseal DA biosynthesis (including the intermediate lobe) was not affected. Plasma LH levels were depressed by hyperprolactinemia although the content of hypothalamic luteinizing hormone-releasing hormone (LHRH) was not changed. In parallel studies, the anterior pituitaries from these animals were incubated in vitro using a paired-half technique and LH and PRL release measured. While the basal release of prolactin was not altered by hyperprolactinemia, LH release was significantly decreased. Gonadotroph responsiveness to LHRH was significantly increased, while the inhibition of prolactin by dopamine was not altered. There was a decrease in pituitary prolactin content with normal LH levels. These experiments confirm several in vivo reports which show that hypothalamic dopaminergic but not noradrenergic activity is increased by prolactin. This action is specifically localized in the tuberoinfundibular dopaminergic neurons. Furthermore, these experiments suggest that these central changes result in alterations in both gonadotroph and mammotroph function.

Animals↗

PubMed2006

Improvement in hyperprolactinemia and reproductive comorbidities in patients with schizophrenia switched from conventional antipsychotics or risperidone to olanzapine.

This open-label, prospective, 4-month study in hyperprolactinemic patients with schizophrenia explored whether prolactin levels decrease after switching antipsychotic therapy to olanzapine. A secondary objective was to determine if reproductive morbidities and sexual dysfunction occurring with hyperprolactinemia improved with prolactin normalization. Clinically stable patients with schizophrenia, who had hyperprolactinemia defined as >18.8 ng/ml for males and >24.2 ng/ml for females, were randomized to: remain on current therapy (n=27) or switch to olanzapine, 5-20 mg/day, (n=27). Baseline prolactin levels in female patients randomized to receive olanzapine (n=14) were 66.3+/-38.7 ng/ml and were 82.0+/-37.6 (p=.32) in those remaining on their pre-study antipsychotic medication (n=14). In male patients, baseline prolactin levels were 33.7+/-12.1 and 33.5+/-13.8 ng/ml (p=.97), respectively, for those randomized to olanzapine (n=13) or remaining on pre-study treatment (n=13). At study end, patients switched to olanzapine experienced significant reductions in mean serum prolactin levels of 19.8+/-18.1 ng/ml in males (p=.02), and 32.3+/-47.5 ng/ml in females (p=.01), but prolactin continued to be elevated in patients who remained on pre-study antipsychotic treatment. After switching to olanzapine treatment, male patients experienced significantly (p=.03) increased free testosterone levels but there were no significant improvements in total testosterone levels; some female patients experienced improved menstrual cycling, as well as resolution of galactorrhea and gynecomastia, and sexual functioning was significantly improved in both genders. Patients switched to olanzapine, as well as those remaining on their pre-study medication, maintained clinical stability, their symptoms continued to improve, although there were no significant between-treatment differences in improvement. Treatment-emergent adverse events did occur in both treatment groups; however, they were not significantly different between groups. Olanzapine-treated patients experienced significantly lower eosinophil counts and higher elevations in low-density lipoproteins and standing blood pressure than non-switched patients. Olanzapine treatment may offer sustained reduction in serum prolactin and improvement in sexual and reproductive comorbid symptoms in patients with schizophrenia who have treatment-emergent hyperprolactinemia.

Antipsychotic Agents↗