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PubMed1989

Medical therapy of hyperprolactinemia.

Although many causes of hyperprolactinemia exist, medications and prolactin-secreting pituitary tumors (prolactinomas) are the most common etiologies. The mainstay of medical management for pituitary tumors as well as for most causes of hyperprolactinemia is bromocriptine. The drug can be used alone or in conjunction with other therapeutic modalities, including surgical resection and pituitary irradiation, depending on the clinical scenario. Bromocriptine can lower serum prolactin, reduce tumor size, and restore fertility in those patients during pregnancy. As bromocriptine is not always well tolerated and requires frequent dosing, newer agents that may diminish side effects and improve compliance are under investigation.

Humans↗

PubMed1989

Effects of pregnancy, delivery and lactation in hyperprolactinemia with prolactin producing pituitary adenoma.

The effects of pregnancy, delivery and lactation on changes in serum prolactin (PRL) values were investigated in patients with hyperprolactinemia. Thirty-seven patients with hyperprolactinemia who wished to become pregnant were treated by transsphenoidal surgery, bromocriptine therapy, or a combination of the two. In 33 patients whose pre-pregnancy serum PRL concentration exceeded 30ng/ml, only in two did serum PRL return to the normal range below 30ng/ml after pregnancy, delivery and lactation. However, the serum PRL concentration was decreased in 28 patients. When classified according to the pre-pregnancy serum PRL concentrations, PRL less than or equal to 100 (Group A), 100 less than PRL less than or equal to 200 (Group B) and 200 less than PRL (Group C), patients with the greatest pre-pregnancy serum PRL concentration showed the greatest reduction. The ratios of post-pregnancy serum PRL to pre-pregnancy PRL in group A, B and C were 91.4 +/- 22.1%, 81.5 +/- 7.0% and 65.0 +/- 6.5% (Mean +/- SE), respectively. Group C with the highest pre-pregnancy serum PRL concentration consisted almost entirely of patients with macroadenoma. Thus, the reduction in serum PRL after pregnancy, delivery and lactation was considered to be the result of a decrease in the size of the adenoma due to adenoma enlargement over the sella turcica through the estrogen effects during pregnancy, and from impairment of pituitary circulation.

Adenoma↗

PubMed1988

[Disorder of hair growth in hyperprolactinemia].

Functional hyperprolactinemia was found in five female patients, 25-35 years old, seeking medical consultation for hair loss, together with hypertrichosis (4x), disturbances of cyclic bleeding periods (4x), secondary amenorrhea (2x), galactorrhea (2x), seborrhea (2x) and persisting acne (1x). Other hormonal parameters including testosterone levels and thyroid gland function tests were unchanged. Prolactinoma was excluded by x-ray diagrams, partly also by computer tomograms of the sella. In two patients increased telogen effluvium was found by trichogram examination with some dystrophic hairs; in one patient only dystrophic hairs were seen, whereas, in two cases, hair loss was not present at the time of our clinical examination. These observations indicate that cutaneous symptoms such as seborrhea, acne, hypertrichosis/hirsutism, alopecia(= SAHA syndrome) may evidently occur in hyperprolactinemia, representing or mimicking androgen-induced skin symptoms. In such cases, therefore, evaluation of prolactin levels together with androgen blood levels and thyroid gland function tests should be performed to exclude underlying endocrinopathy.

Acne Vulgaris↗

PubMedDate not supplied

Hyperprolactinemia: an unusual manifestation of suprasellar cystic lesions.

Two patients with suprasellar cysts and hyperprolactinemia are described. These lesions were diagnosed by CT metrizamide cisternography. Suprasellar cysts are a rare cause of pathologic hyperprolactinemia, which most commonly results from pituitary adenomas. Tissue diagnosis revealed suprasellar arachnoid cysts in the first patient and Rathke's cleft cyst in the second. The differential diagnosis of suprasellar cysts is presented, and distinguishing radiographic characteristics are discussed.

Adenoma↗

PubMed1987

Is idiopathic hyperprolactinemia a transitional stage toward prolactinoma?

The basal prolactin (PRL) levels on five different days, the PRL responses to thyrotropin-releasing hormone and to domperidone, and the thyroid-stimulating hormone (TSH) responses to domperidone were studied in 75 regularly menstruating women and 44 patients with moderate hyperprolactinemia. It was found that, for the entire sample, the responses to each of the stimuli could be described by a continuous function of the basal PRL levels. The present work provides evidence for the following conclusions: 1) The PRL responses to thyrotropin-releasing hormone and to domperidone merely bring additional diagnostic information relative to basal PRL levels in the occasional patients with macroprolactinemia; 2) there is a continuous spectrum of lactotroph activities in women, ranging from normal secretors through an intermediate group of hypersecretors (with progressively increased serum PRL levels and decreased responsiveness to stimuli) to full-blown prolactinomas; and 3) idiopathic hyperprolactinemia is a heterogeneous entity that includes the above intermediate group of patients, women with macroprolactinemia, and patients with undiagnosed prolactinomas.

Adult↗

PubMed1988

Hyperprolactinemia during cocaine withdrawal.

Plasma prolactin levels were determined for 8 patients (7 males and 1 female) who reported an average of 3.7 years of cocaine abuse. The mean prolactin level for these 8 patients 24 to 72 hours following admission to the hospital was 20.58 (S.E. +/- 3.2) ng/ml. Hyperprolactinemia (greater than 20 ng/ml) was detected in 4 patients and 3 others had high borderline prolactin levels. Only 1 patient had a normal prolactin value at the time of admission to the hospital. The mean prolactin level obtained prior to the patients' discharge from the hospital was 31.7 (S.E. +/- 5.3) ng/ml. Five of the 8 patients had an increase in prolactin levels between time of admission and discharge from the hospital. The mean increment in plasma prolactin levels for these 5 patients was 15.5 (S.E. +/- 4.2) ng/ml (P less than .02). Two patients who had significant hyperprolactinemia (greater than 50 ng/ml) at the time of discharge from the hospital reported self-administering the highest cocaine dose (6-8 gm per week) of the 8 patient cohort. Since cocaine blocks dopamine reuptake and prolactin secretion is regulated, in part, by dopaminergic inhibitory mechanisms, cocaine withdrawal may induce rebound supersensitivity of prolactin secretion. Findings obtained in this study suggest that cocaine-related derangements in prolactin secretion may be a biologic marker of a protracted cocaine abstinence syndrome.

Adult↗

PubMed1988

Marked hyperprolactinemia in subclinical hypothyroidism.

Hyperprolactinemia is common in primary hypothyroidism but, to our knowledge, marked elevation of serum prolactin in subclinical hypothyroidism has not been previously reported. A 45-year-old woman presenting with carpal tunnel syndrome was found to have a minimally elevated level of thyrotropin with a normal level of thyroxine. Thyrotropin releasing hormone stimulation testing revealed hyperresponsiveness consistent with primary hypothyroidism. An unstimulated prolactin level was 187 micrograms/L and returned to normal with levothyroxine therapy. Results of visual field testing were normal, and a computed tomographic scan of the pituitary gland revealed no evidence of a macroadenoma. This case demonstrates the occurrence of significant hyperprolactinemia in the absence of overt primary hypothyroidism.

Adult↗

PubMed1988

Selective effects of hyperprolactinemia on in vitro dopamine release from median eminence synaptosomes.

Prolactin is thought to exert an autoregulatory, negative feedback effect on its own secretion via stimulation of the tuberoinfundibular dopaminergic (TIDA) neurons. To investigate possible mechanisms involved in this feedback, the effects of experimentally induced hyperprolactinemia on the release of 3H-dopamine (3H-DA) were studied in nerve terminals (synaptosomes) isolated from rat median eminence (ME), the TIDA neuronal projection field. Synaptosomes were prepared from adult male rats treated with ovine prolactin (oPRL) or the vehicle for 48 hr. Synaptosomes were incubated in 0.1 microM 3H-DA at 30 degrees C until steady-state conditions were achieved, and then release of the preaccumulated transmitter was measured over 1-20 sec time intervals under basal and depolarizing conditions. Release of 3H-DA elicited by depolarization of the terminals was significantly greater in ME synaptosomes prepared from oPRL-treated animals as compared with preparations from controls. This effect of the hyperprolactinemia appeared to be specific to the TIDA neurons since oPRL treatment did not result in increased evoked release of 3H-DA from terminals prepared from the mesolimbic, tuberohypophyseal, or nigrostriatal dopaminergic neurons. Basal efflux in all preparations was not changed from controls. The increased evoked release in oPRL-treated ME occurred when depolarization was induced either with high external [KCl] or veratridine. The enhanced 3H-DA efflux was evident during depolarization over a wide range of external calcium concentrations (0.01-3.0 mM), in the presence of 20 nM Ni2+ to block Ca2+ influx through voltage-gated channels, or when all external Ca2+ had been chelated, indicating that this effect of oPRL involves DA released through a mechanism independent of external calcium.

Animals↗

PubMed1987

[Hyperprolactinemia in patients with non-functioning adenoma: analysis of 85 patients treated by transsphenoidal operation].

Today, many gynecologists consider that the first choice of the treatment of prolactinomas is bromocriptine therapy. Because bromocriptine not only decreases the levels of serum prolactin but also reduces the tumor size. On the other hand, the patients with non-functioning adenoma sometimes show hyperprolactinemia, probably because PIF (prolactin inhibiting factor) cannot reach the normal prolactin-producing cells of the adenohypophysis. Therefore non-functioning adenoma with elevated serum prolactin levels should be distinguished from prolactinoma. Eighty five patients with non-functioning adenoma were treated with transsphenoidal operation at Hiroshima University Hospital, and Kansai Rosai Hospital from May, 1978 to March, 1981 and at Osaka University Hospital, The Center for Adult Diseases, and Kansai Rosai Hospital from April, 1981 to May, 1986. Non-functioning adenomas were diagnosed by clinical feature, endocrinologic examination, and immunohistochemical study. There were 42 male and 43 female patients, whose age ranged from 17 to 76 years (mean: 49). The most frequent chief complaint was visual disturbance (86%). Amenorrhea-galactorrhea was complained by 9 female patients. However, 7 of them had visual disturbance at the same time. Hyperprolactinemia was seen in 21 patients (30%). The highest serum level of prolactin was 163.2 ng/ml. All of the patients had macroadenomas. There were 2 invasive adenomas and 83 expensive adenomas in them. After operation, cure or improvement of the visual disturbance was noted in almost all the patients. The serum levels of prolactin were normalized in 16 of 17 hyperprolactinemic patients. In conclusion, transsphenoidal operation is the best treatment of non-functioning adenomas. However, it is difficult to decide before operation whether the macroadenoma with serum prolactin level between 100 and 200 ng/ml is non-functioning adenoma or prolactinoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

PubMed1987

Prolactin as an inhibitor of granulosa cell luteinization: implications for hyperprolactinemia-associated luteal phase dysfunction.

Chronic and transient hyperprolactinemia have been associated with luteal phase dysfunction in both spontaneously cycling women and those subjected to ovarian hyperstimulation by exogenous gonadotropins. It is the objective of the in vitro and in vivo studies reported herein to examine the possibility that prolactin (PRL), a known constituent of ovarian follicular fluid, may account, at least in part, for the luteinization inhibitory (LI) activity exerted by follicular fluid (FF) under both physiologic and pathophysiologic circumstances. In vitro treatment with human PRL (100 ng/ml) reduced by 57% the specific binding of luteinizing hormone (LH) to follicle-stimulating hormone(FSH)-primed cultured rat granulosa cells, an effect associated with a 2.6-fold diminution of human chorionic gonadotropin (hCG; 10 ng/ml)-stimulated progesterone biosynthesis. Importantly, the ability of PRL to exert a direct inhibitory effect on FSH-supported LH binding was fully reproduced under in vivo conditions. Inasmuch as the acquisition of LH receptors and progesterone (P) biosynthetic capacity are acceptable as criteria of granulosa cell luteinization, the authors' findings indicate that PRL, acting at concentrations achievable in vivo within the ovarian FF, may account, if only in part, for physiologically encountered LI-like activity. Moreover, subject to limitations imposed by the rat model employed, consideration also must be given to the possibility that hyperprolactinemia-associated luteal phase dysfunction may not only reflect the suppressive effect(s) of PRL at the central level of the reproductive axis, but may also be due, at least in part, to the consequences of inappropriately elevated PRL at the level of the follicular microenvironment.

Animals↗

PubMed1985

Decreased apolipoprotein levels in women with hyperprolactinemia related to increased estradiol level: effect of hepatic lesion?

In 3 groups of women (1. with pathological hyperprolactinemia, but low estradiol level--19 patients; 2. with pathological hyperprolactinemia, but high estradiol level--17 patients; 3. 16 healthy control women) the level of prolactin, estradiol, cortisol, total cholesterol, triglycerides and apolipoproteins A-I, A-II and B in serum was estimated together with routine clinical examination. In both hyperprolactinemic groups a significant decrease of apolipoprotein A-I and A-II was found, while in the group with high estradiol also a significant decrease of apolipoprotein B was observed. It is suggested that the increased level of prolactin results in an impairment of apolipoprotein biosynthesis and, in addition, in a group with high estradiol level also a lesion of liver function might occur which results in its decreased degradation.

Apolipoprotein A-I↗

PubMedDate not supplied

Sleep-dependent hyperprolactinemia and Corpus luteum pathogenesis.

The results obtained in wake and sleep conditions by PRL determinations performed in 6 normoprolactinemic infertile women with luteal phase deficiency (LPD) are reported. Infertility was apparently due to LPD. PRL levels were determined by RIA in blood samples collected at 20-min intervals from 18(00) to 08(00). LPD has been previously demonstrated by endometrial biopsy, basal temperature and circulating progesterone determinations. PRL levels were also determined in 5 normal women used as control subjects under the same experimental conditions. The results obtained, expressed as means +/- SD of LPD vs. control group, were 15.9 +/- 4.6 vs. 11.6 +/- 3.3 ng/ml (p greater than 0.1) in wake conditions and 31.9 +/- 5.9 vs. 21.4 +/- 5.7 ng/ml (p less than 0.01) in sleep conditions. PRL values during the highest pulse (HP) in sleep and wake conditions were 20.9 +/- 5.2 vs. 17.0 +/- 3.3 ng/ml (p less than 0.1) and 51.1 +/- 17.1 vs. 34.3 +/- 2.4 ng/ml (p less than 0.01), respectively. In 2 out of the 6 patients mean PRL values were 22.0 and 26.5 ng/ml during sleep, and 26.0 and 33.0 ng/ml during HP. These values were not statistically significant when compared with those obtained in the control group. The results obtained show that 4 out of the 6 patients with LPD and normal PRL levels in wake conditions had sleep-dependent hyperprolactinemia due to the pulses with a more significant amplitude. These findings suggest that in some cases sleep-induced hyperprolactinemia might be involved in LPD pathogenesis.

Adult↗

PubMed1995

[What to do when faced with hyperprolactinemia?].

Hyperprolactinemia causes a certain number of clinical syndromes whose sequels vary much depending on the age group. It is a common affection as frequent in women as in males and it necessitates prolonged treatment. It may have several causes, the most frequent ones are: adverse drug reactions, prolactinomas, disturbed distribution of dopamine and hyperthyroidism. Evaluation includes repeated measurements of prolactin, T4, and TSH, a radiologic work-up including a CT-scan or magnetic resonance imaging. In the case of a prolactinoma the choice of treatment depends on size and evolution of the adenoma. Bromocriptine permits to correct hyperprolactinemia in the majority of cases. After adequate treatment of pituitary adenoma these are no contraindications for pregnancy, once fertility has returned.

Adult↗

PubMed1994

Hyperprolactinemia in Reiter's syndrome.

OBJECTIVE: Accumulated evidence suggests that certain immunoregulatory hormones including prolactin (PRL) may play a role in the pathogenesis and disease expression of certain autoimmune diseases. Our objective was to investigate the possible role of PRL in the pathogenesis and disease expression of the spondyloarthropathies, including Reiter's syndrome (RS). METHODS: Basal levels of PRL (serum) were determined by radioimmunoassay in patients with various types of spondyloarthropathies, patients with acute anterior uveitis (AAU), and healthy controls. Clinical manifestations at the time of serum collection were correlated with PRL levels. RESULTS: Hyperprolactinemia (PRL > 20 ng/ml) was found in 9 of 25 (36%) patients with RS. In contrast, only 1 of 34 (2.9%) (p < 0.001) patients with ankylosing spondylitis and none of the patients with psoriatic arthritis, AAU or healthy controls had hyperprolactinemia. The frequency of conjunctivitis, urethritis, dysentery, and uveitis was higher in hyper than in normoprolactinemic patients with RS. CONCLUSION: Our results suggest a possible role for this immunoregulatory hormone in the pathogenesis and disease expression of RS.

Acute Disease↗

PubMed1993

[Effect of hyperprolactinemia of varying origin on paracrine relationships in rat testes].

Light microscopy characteristics of mature rat testes were studied in control and hyperprolactinemia rats. The number of cells defined as granulocytes in interstitial regions adjacent to seminal ducts at stage VII and XII of spermatogenesis has been calculated. Normal deference difference between these parameters diminish in hyperprolactinemia. It is suggested that prolactin participates in intratesticular paracrine mechanisms regulation.

Animals↗

PubMed1993

Recent advances in the understanding of the pathophysiology and treatment of hyperprolactinemia.

Hyperprolactinemia is frequently diagnosed in patients with infertility and menstrual cycle irregularities. Control of prolactin secretion is complex and involves inhibition by dopamine and possibly endothelins, as well as stimulation by serotoninergic and opioidergic pathways, gonadotropin-releasing hormone, and possibly galanin. Some patients with hyperprolactinemia have underlying functional disorders, but by using magnetic resonance imaging, a microprolactinoma can be found in most. Prolactin circulates in a low-bioactivity glycosylated and a nonglycosylated form, and an antibody-bound form is found in a few hyperprolactinemic patients who are relatively asymptomatic. The majority of patients, particularly those with macroprolactinomas, will benefit from treatment with bromocriptine. Available alternatives for intolerant patients include vaginal administration of bromocriptine and pergolide mesylate. Other compounds, monthly injectable and slow-release forms of bromocriptine, quinagolide and carbegoline, are not yet available in the United States. Withdrawal of treatment during pregnancy is still recommended, with a low risk of tumor enlargement, and the need for life-long treatment is now being reconsidered.

Bromocriptine↗

PubMed1993

[Therapeutic efficacy of vaginal administration of bromocryptin in patients with hyperprolactinemia].

Oral bromoergocriptine (BEC) is currently the treatment of choice in women with hyperprolactinemia secondary to a prolactinoma. However, undesirable side effects (of variable type and intensity) are frequently present in these women due to both local irritation and to a direct effect upon the central nervous system. The present work was undertaken as a pilot study to assess the therapeutic effectiveness of vaginally administered BEC and to corroborate if the side effects are less frequent and of minor intensity when compared to oral BEC. Initially, 16 women were included, but two of them did not accept to continue in the study; thus, a total of 14 women with hyperprolactinemia (> or = 40 ng/ml) were divided in two groups: Group A encompassed five women, aged 27 to 36 years old, two with normal menstrual cycles and three with oligomenorrhea; all had primary or secondary sterility during 3 to 12 years and galactorrhea from 6 months to 3 years; in only one patient a brain computerized axial tomography (CAT) was performed which showed the existence of a macroprolactinoma. All received oral BEC (2.5-5 mg/day, except one patient with 10 mg/day). Group B included nine women, aged 26 to 36 years old, four had normal menstrual cycles and five had oligomenorrhea; all had primary or secondary sterility during the last 2 to 7 years and eight out of nine, also had galactorrhea during 1 to 8 years; in four of them a CAT was performed showing a pituitary microadenoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Hyperprolactinemia. Causes, consequences, and treatment options.

Hyperprolactinemia is one of the most common pituitary abnormalities. The cause can usually be determined by review of the patient's history, physical examination, selected laboratory tests and, when indicated, magnetic resonance imaging scans of the sella. Pituitary tumors and medications are the most common causes of hyperprolactinemia. Appropriate treatment is determined by the cause and by the patient's tolerance of the clinical consequences.

Humans↗