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PubMed1988

Hyperprolactinemia and impotence.

One hundred impotent men and 15 sexually active male volunteers served as the source for this study. Serum prolactin was estimated in all cases using radioimmunoassay technique. Cases with hyperprolactinemia were treated with bromocriptine for 3 months. Hyperprolactinemia was detected in three patients only (3%), with no findings of pituitary tumors. Treatment with bromocriptine markedly reduced the level of serum prolactin together with improvement of sexual libido and potency. The mere presence of 3 cases only with hyperprolactinemia among 100 impotent subjects suggested that hyperprolactinemia is not one of the main causes of impotence.

Adolescent↗

PubMed1998

Effects of chronic hyperprolactinemia on tuberoinfundibular dopaminergic neurons.

Prolactin (PRL) secretion is under the inhibitory regulation of the tuberoinfundibular dopaminergic (TIDA) system. Short-term elevation in PRL levels has been shown to increase the activity of TIDA neurons, however, the responsiveness of TIDA neurons to chronically elevated serum PRL levels is controversial. The purpose of this study was to investigate the effects of prolonged elevations of serum PRL on TIDA neuronal activity. Female Sprague-Dawley rats (2-3 months old) were ovariectomized and implanted (s.c.) with haloperidol (HAL), a dopamine receptor antagonist for 6 or 9 months to produce hyperprolactinemia. Ovariectomized, sham-implanted rats were used as controls. Other groups of intact rats were implanted with HAL or sham-implanted for 9 months and then were implanted with PRL-producing MMQ cells for 6 weeks to further increase circulating PRL levels. TIDA neuronal activity was measured in terms of tyrosine hydroxylase (TH) activity in the stalk-median eminence and was correlated with changes in serum PRL levels. After 6 months of treatment, TH activity in HAL-treated rats was 130% higher than that in the control rats. After 9 months of treatment, TH activity in HAL-treated rats was 81% higher than that in control rats. This increase was significantly less than the increase that occurred after 6 months of treatment. Nine months of HAL-induced hyperprolactinemia followed by implantation of PRL-producing MMQ cells, which resulted in very high levels of PRL, did not increase TH activity in the stalk-median eminence. These results demonstrate that hyperprolactinemia over a prolonged period reduces the responsiveness of TIDA neurons, and these effects vary depending on the duration and intensity of hyperprolactinemia.

Animals↗

PubMed2004

Cabergoline treatment of risperidone-induced hyperprolactinemia: a pilot study.

BACKGROUND: D(2) blockers, including the atypical antipsychotic risperidone, induce hyper-prolactinemia in a significant number of patients treated. The endocrine and sexual side effects related to hyperprolactinemia significantly impair tolerability and compliance in patients, including those with a good response to risperidone. This pilot study aimed to evaluate the efficacy and tolerability of a low dose of cabergoline, a D(2) agonist, in the treatment of risperidone-induced hyperprolactinemia. METHOD: Nineteen male and female DSM-IV-defined schizophrenic patients who were clinical responders to risperidone but were suffering from symptomatic hyperprolactinemia were treated with cabergoline, 0.125 to 0.250 mg/week for 8 weeks. Plasma prolactin level was assessed at baseline and at the end of the study. Data were collected from January 2002 to April 2003. RESULTS: After cabergoline treatment, the mean decrease in plasma prolactin levels was statistically significant (p <.05) for the total sample, and 11 patients showed remission of clinical signs with prolactin values within the normal range. No side effect was observed or reported, and the patients' psychopathology was unchanged. CONCLUSIONS: Results suggest that low-dose cabergoline treatment of risperidone-induced hyperprolactinemia may be safe and clinically effective in a relevant number of patients.

Adult↗

PubMedDate not supplied

Hyperprolactinemia.

Prolactinomas are the most common pituitary tumors. Hyperprolactinemia is characterized by increased production of prolactin, often leading to reproductive dysfunction and galactorrhea. Prolactinomas may also cause male-factor infertility by producing hypogonadism. In addition, if large, they can produce neurologic symptoms by mass effect in the sellar area. The diagnostic evaluation first requires exclusion of other causes of hyperprolactinemia, such as pregnancy, primary hypothyroidism, numerous medications, and miscellaneous causes. The second step in the diagnostic evaluation is to perform a head scan, preferably an MRI. This is essential in order to exclude a "pseudoprolactinoma" which would require surgery. Following diagnostic evaluation, the next step is to determine whether a patient with hyperprolactinemia has an indication for therapy, such as a macroprolactinoma (tumor >1 cm), hypogonadism (risk of osteoporosis), infertility, significant galactorrhea, acne, hirsutism, or headache. The treatment of choice for nearly all patients with hyperprolactinemic disorders is medical. In most cases, dopamine agonists (bromocriptine, pergolide, cabergoline) are extremely effective in lowering serum prolactin, restoring gonadal function, decreasing tumor size, and improving visual fields. The main limitation is side effects, particularly nausea or orthostatic dizziness. The newest dopamine agonist, cabergoline, can be given just once or twice a week, is more effective in normalizing prolactin and restoring menses than bromocriptine, and is significantly better tolerated. However, it is not yet recommended as first-line therapy for patients seeking fertility, because adequate safety data in pregnancy are not available. For the infrequent patient unable to tolerate, or resistant to, medical therapy, neurosurgical transsphenoidal resection may be necessary, particularly if the patient has a large lesion jeopardizing the optic chiasm. Hyperprolactinemia is a rewarding disorder to manage because patients typically respond well to medication, with restoration of menses and fertility.

Bromocriptine↗

PubMed1999

Management of hyperprolactinemia in infertility.

Hyperprolactinemia is a frequent cause of anovulatory sterility, although spontaneous pregnancy may occur occasionally. Dopaminergic treatment is highly effective for both idiopathic and tumoral hyperprolactinemia. If the only cause of infertility is chronic anovulation due to hyperprolactinemia, a 60-80% pregnancy rate can be achieved. These results mean that surgical treatment is still needed only rarely. Either spontaneous or drug-induced pregnancy is usually uneventful for the mother and is not associated with any increase in abortion, twins or malformations. Pregnancy-related tumor growth occurs rarely and can be treated successfully with dopaminergic drugs. Pregnancy frequently leads to some improvement in the biochemical and clinical disorders associated with hyperprolactinemia.

Anovulation↗

PubMed1999

[Hyperprolactinemia. II. Diagnosis and treatment].

Implementing various diagnostic methods in the past some decades has allowed to improve knowledge on hyperprolactinemia. In the diagnostics of hyperprolactinemia, besides measuring blood levels of PRL and other hormones, there may be also helpful: stimulative tests with metoclopramide and TRH, CT scans, MRI, ophthalmological examination, etc. There tumors such as prolactinoma or other reasons leading to hyperprolactinemia. Establishing cause of hyperprolactinemia is important because of various treatment modalities available.

Hormones↗

PubMedDate not supplied

[Heterogeneity of immunoreactive prolactin in hyperprolactinemia of various origin].

Study of molecular heterogeneity of immunoreactive prolactin in patients with macro- and microprolactinomas and idiopathic hyperprolactinemia has shown heterogeneity of the total blood immunoreactive prolactin pool in all the examined patients. This pool included three basic forms with molecular masses about 23, 50, and over 100 kD (23K-, 50K-, 100K-prolactin), whose ratios essentially differed in individual patients. Physiologically the most active monomeric 23K form of prolactin predominated in the blood of patients with hyperprolactinemia due to hypophyseal micro- and macroadenomas, parallelled by manifest signs of galactorrhea and hypogonadism; the content of this form may reach 95% of the total immunoreactive hormone. Patients with hyperprolactinemia of obscure origin present with quite the contrary ratio of prolactin immunoreactive forms with the predominance of high-molecular 100K form of the hormone, whose share may reach 80-90%. Such cases of hyperprolactinemia may be associated with the absence of clear-cut clinical manifestations, including such as galactorrhea and menstrual cycle disorders, and with inefficacy of traditional therapy. Such cases were tentatively classified as 'the high-molecular prolactin syndrome' and need further research.

Adenoma↗

PubMed1992

Management of psychotropic-induced hyperprolactinemia.

The effects of individual psychotropic medications on serum prolactin concentrations are described, and recommendations for dealing with adverse effects are provided. Hyperprolactinemia can result in galactorrhea, amenorrhea, irregular menses, and anovulation; in men, impotence and azoospermia, with or without lactation and gynecomastia, can occur. Antipsychotics may block dopamine receptors in the pituitary prolactin-secreting cells and prevent dopamine-induced reduction of prolactin release. The magnitude of the increase in prolactin concentration correlates with the amount of antipsychotic drug given. The treatment of choice is reduction of the antipsychotic dosage or discontinuation of therapy. If adjustments to the antipsychotic dosage fail to resolve symptoms, the dopamine agonists bromocriptine and amantadine may be tried. Antidepressants may produce elevated serum prolactin concentrations, especially with long-term administration. However, the frequency of antidepressant-induced hyperprolactinemia is much lower than that seen with antipsychotics, and serious adverse clinical effects are uncommon. Other psychotropic drugs such as lithium, valproic acid, buspirone, carbamazepine, and benzodiazepines either are only rarely associated with symptomatic hyperprolactinemia or do not produce clinically important changes in prolactin concentrations. Antipsychotic drugs are the psychotropic agents most likely to cause symptomatic hyperprolactinemia. Bromocriptine or amantadine may provide symptomatic relief if withdrawal or adjustment of the antipsychotic dosage does not eliminate the symptoms.

Antidepressive Agents↗

PubMed1992

[Primary hypothyroidism presenting with amenorrhea, galactorrhea, hyperprolactinemia and enlarged pituitary].

The combination of amenorrhea, galactorrhea, and hyperprolactinemia in a young woman usually suggests a prolactin-secreting adenoma of the anterior pituitary gland. Primary thyroid failure may also be associated with hyperprolactinemia, galactorrhea and suprasellar enlargement of the pituitary. 2 women, aged 23 and 28, respectively, presented with the latter syndrome. 1 was even a candidate for neurosurgery. However, because serum TSH and prolactin levels were elevated, thyroxin replacement therapy was started. It induced normal menses, galactorrhea stopped, and in follow-up CT scans the pituitary become normal in size. Hyperprolactinemia with secondary hypothyroidism, caused by a pituitary adenoma, must be distinguished from primary hypothyroidism, also a cause of hyperprolactinemia.

Adenoma↗

PubMed1991

Hyperprolactinemia induced by long-term domperidone treatment does not alter the sensitivity of striatal dopamine receptors.

We investigated the effect of hyperprolactinemia induced by long-term domperidone treatment (10.0 mg/kg, single daily dose, ip) on striatal dopamine (DA) receptor sensitivity in male Wistar rats weighing 250-300 g (N = 8). Domperidone treatment for 7 days continued to produce an increase in serum concentration of prolactin (PRL) from 17.3 +/- 2.2 to 33.1 +/- 7.3 and from 16.8 +/- 2.3 to 21.9 +/- 2.1, 2 and 72 h after domperidone withdrawal, respectively. Hyperprolactinemia induced by long-term domperidone treatment did not change binding sites (Bmax) and dissociation constant (Kd) of [3H]-spiroperidol binding when compared to controls. These results show that hyperprolactinemia induced by long-term domperidone treatment does not effect the sensitivity of striatal DA receptors presumably because the effect of neuroleptic drugs is due to their interaction with the receptors and not to the concomitant hyperprolactinemia.

Animals↗

PubMed1991

[A study on hyperprolactinemia in female patients with alcoholics].

The clinical signs and symptoms of sexual dysfunction with amenorrhoea, loss of libido and infertility, are frequently found in chronic alcoholic women. But few investigations have been made concerning hormonal changes in fertile aged women experiencing sexual dysfunction. In order to assess prolactin levels of fertile-aged women with alcoholism under 40 years of age-excluding those with liver cirrhosis were surveyed. We found that many of them (82.6%) had moderate elevations of plasma prolactin. Hyperprolactinemia is commonly associated with amenorrhoea and hypogonadism. An acute alcohol loading experiment was conducted on 6 healthy female volunteers in luteal phases of their menstrual cycles in order to evaluate the effects of alcohol on the hypothalamo-pituitary-ovarian axis. Evidence was obtained that alcohol intake caused transient hyperprolactinemia. The present results indicated that hyperprolactinemia can occur with high frequency among alcoholic women and this causes sexual dysfunction and ovarian dysfunction. The etiology of hyperprolactinemia could not be explained solely by the direct action of alcohol, rather, liver dysfunction must be implicated.

Adult↗

PubMedDate not supplied

[The causes of infertility in hyperprolactinemia].

A study was made of function of the hypothalamohypophyseal system in women with infertility combined with hyperprolactinemia. Changes in the levels of prolactin, LH, FSH and TSH in response to the administration of releasing hormones (gonado- and thyroliberin) and metoclopramide (dopamine antagonist) were determined in 28 women with hyperprolactinemic amenorrhea and in 5 women with a normal menstrual cycle. Resistance of lactotrophs to functional tests was revealed. It grew with an increase in a prolactin level. On the contrary, a response of gonado- and thyrotrophs to functional tests grew with an increase in a degree of hyperprolactinemia. The authors arrived at a conclusion that stable hyperprolactinemia resulted from disorder of the receptor apparatus of lactotrophs with the resultant nonsusceptibility of the latter to an inhibitory effect of dopamine to prolactin secretion. Proceeding from their own and literature data, the authors propose for discussion a scheme of fertility disturbance in stable hyperprolactinemia.

Adult↗

PubMed1988

Defective dopaminergic regulation of prolactin secretion in patients with hyperprolactinemia.

In order to evaluate the dopaminergic control of the lactotroph, we examined the plasma prolactin response to metoclopramide (a dopamine receptor blocker, 10 mg iv bolus) and to dopamine (1 microgram/Kg/min iv infusion for 120 min) in 52 hyperprolactinemic female patients and 19 healthy volunteer women. Three diagnostic categories were included: "idiopathic" hyperprolactinemia (21), microadenoma (24), and macroadenoma (7). Patients from all groups showed a marked blunting of the prolactin response to metoclopramide as compared to the prolactin rise in normal women (p less than 0.001). However, normal responses were observed in 8 patients with idiopathic hyperprolactinemia and in one patient with adenoma. The magnitude of the prolactin response to metoclopramide (percent of baseline level) correlated negatively with the level of basal prolactin in each group except for macroadenoma patients. Dopamine infusion significantly (p = 0.015) reduced the mean plasma prolactin levels in hyperprolactinemic patients and normal women. However, patients with idiopathic hyperprolactinemia were hyposensitive to dopamine (p less than 0.05). Furthermore, microadenoma patients were less responsive to dopamine suppression than were the patients with macroadenoma (p less than 0.05). The results indicate the presence of a relative resistance to dopamine in patients with idiopathic hyperprolactinemia and in patients with microadenoma. They also suggest that in these patients, the decrease in prolactin response to metoclopramide may be explained by the relative refractoriness to endogenous dopamine.

Adenoma↗

PubMed1995

[Role of absorptiometry in the evaluation of bone tissue status in women with primary hyperprolactinemia].

Mineral density of bone tissue was assessed in 22 patients with oligoamenorrhea caused by primary hyperprolactinemia. Primary hyperprolactinemia in the presence of pituitary adenoma was diagnosed in 8 patients, primary functional form of the disease in 14. Fifteen healthy women were controls. Blood serum concentrations of prolactin, estradiol, progesterone, testosterone, hydrocortisone, LH, and FSH were measured. Bone tissue mineral density was assessed by monophoton absorptiometry in the distal portion of the radial bone at sites 1/3 and 1/20 of its length two times with one-year interval. Abnormal loss of mineral density of bone tissue in 1/3 site was detected in 4 out of 14 patients with functional and in 3 out of 8 patients with tumorous hyperprolactinemia, in site 1/20 in 9 out of 14 and in 8, respectively. Reduction of mineral density of bone tissue was associated with pronounced hormonal imbalance in all the patients with accelerated loss of bone tissue, no matter what form of primary hyperprolactinemia they developed.

Absorptiometry, Photon↗

PubMed1995

Idiopathic hyperprolactinemia in a 15-year-old boy: a case report and literature review.

A 15-year-old boy with idiopathic hyperprolactinemia is described. He was markedly obese, in early puberty, and had gynecomastia and galactorrhea. Serum prolactin level was high, up to 220 pg/ml. Thyroid function test was normal. Idiopathic hyperprolactinemia was diagnosed on the basis of elevated prolactin level, and no demonstrable pituitary tumor was revealed by computerized tomography brain scan and magnetic resonance imaging. Bromocriptine was started initially at the dose 2.5 mg/day, then increased to 7.5 mg/day. Galactorrhea disappeared and prolactin level decreased to < 10 ng/ml. A review of the literature indicates that idiopathic hyperprolactinemia in adolescent males is extremely rare. To our knowledge, this patient is the youngest reported case of hyperprolactinemia in Thailand.

Adolescent↗

PubMedDate not supplied

[Prolactin and TSH response in functional tests in patients with primary hypothyroidism in a context of hyperprolactinemia].

It was previously proposed that hyperprolactinemia in primary hypothyroidism is caused by enhanced release of hypothalamic TRH leading to elevation of both TSH and prolactin levels. Since the dopaminergic system is involved in regulation of prolactin and TSH secretion, we attempted to evaluate the origin of hyperprolactinemia in patients with primary hypothyroidism using tests with metoclopramide, a dopaminergic blocker (10 mg, i.v.) and TRH. Two groups of patients were examined: 20 women with primary hypothyroidism and normal prolactin levels (group A) and 10 women with primary hypothyroidism and hyperprolactinemia (mean basal prolactin level 1514.8 +/- 300.8 mIU/ml). Prolactin reaction in metoclopramide test in group A was markedly increased vs. control group (1131 and 776%, respectively). In group B prolactin reaction in metoclopramide test was blurred (299%), similarly as in patients with microprolactinomas. We came to a conclusion that hyperprolactinemia in patients with primary hypothyroidism is unlikely to be caused by excessive TRH release, but possibly by the presence of subclinical microadenoma which manifests by the hypothyroid state or, possibly, by disturbed dopaminergic regulation of prolactin and TSH secretion in patients with primary hypothyroidism.

Adolescent↗

PubMed1994

[Detection and treatment of hyperprolactinemia in male infertility].

The role of prolactin in males has not been satisfactorily explained. It has been proved that hyperprolactinemia has a negative effect both on spermiogenesis and spermatogenesis. It is widely known that the secretion of the pituitary hormones is of a pulsating character and occurs in the diurnal rhythm. Therefore, in order to select a group of patients with hyperprolactinemia qualified for Bromocriptine treatment it was necessary to test them for prolactin. 3 morning tests were taken at 15 minute intervals. The selected male group was later treated with Bromocriptine, following the method of administration recommended by the producer. Next the level of prolactin in patients serum was again determined. It has been determined that a single prolactin test is sufficient to diagnose hyperprolactinemia. In most males 3 prolactin tests were always either pathologic or normal. Most of the selected hyperprolactinemia--affected males after Bromocriptine treatment displayed positive therapeutic effects. The level of prolactin has dropped considerably and the potency has increased. The improvement in the semen picture varied from patient to patient.

Adult↗

PubMed1997

Hyperprolactinemia in systemic lupus erythematosus.

BACKGROUND: Recent evidence demonstrates that hyperprolactinemia was found in active systemic lupus erythematosus (SLE). This indicates prolactin (PRL) is an important immunoregulator and may play a role in the pathogenesis of SLE. However, study of the prevalence and the clinical significance of hyperprolactinemia in SLE and other rheumatic disease has rarely been carried out. METHODS: From January 1995 to January 1996, 79 individuals were enrolled in this study. PRL levels of 30 cases of SLE were compared with those in 29 rheumatoid arthritis (RA) and 20 normal healthy volunteers. Moreover, a correlation between levels of PRL and SLE disease activity index (SLEDAI) in SLE patients was studied. RESULTS: The mean value of serum PRL level in SLE patients (19.35 +/- 11.33 ng/dl) was significantly higher than in RA patients (12.33 +/- 8.30 nd/dl, p < 0.05). The difference was more pronounced between SLE patients and healthy individuals (12.01 +/- 7.53 ng/dl, p < 0.01). However, patients with RA had no significant difference from the control group. Analysis made between SLEDAI and PRL levels in SLE patients revealed no significant correlation (r = 0.537, p = 0.07). Furthermore, no significant correlation was found between antinuclear antibody (ANA), C3, C4, anti-DNA and hyperprolactinemia. CONCLUSIONS: This study has shown that hyperprolactinemia is prevalent in random SLE patients, but not in RA patients. The elevated PRL levels seem not to be associated with disease activity and ANA positivity.

Adolescent↗