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PubMed2000

Experimental hyperprolactinemia in a rat model: alteration in centrally mediated neuroerectile mechanisms.

INTRODUCTION: The purpose of this study was to induce hyperprolactinemia in adult male rats and determine its effect on the central and peripheral mediated neurogenic as well as myogenic mechanisms of erectile function/dysfunction in a rat model. The use of penile reflexes in awake animals was used to test the effect of both central and peripheral mechanisms. Electrical stimulation of the cavernous nervous was used to test peripheral neural function and intracorporal injection of papaverine was used to test the intactness of the corporal smooth muscles. These mechanisms were further explored by administration of testosterone. METHODS: Eighteen Fisher-344 200-250 g rats aged 10 weeks were used in this study. Group 1 (n = 6) hyperprolactinemia was induced with subcutaneous (SQ) injection of 5 mg rat prolactin (NIDDK-r-PRL-B-7, biopotency 25 IU/mg) in two divided doses daily for 1 week. Testosterone propionate 100 mg/kg dissolved in sesame oil was given intramuscularly on day 1 (weekly dose). Group 2 (n = 6) control animals received SQ injection of vehicle twice daily and sesame oil I/M on day 1. Group 3 (n = 6) received testosterone propionate. Penile reflexes (erections, cups, flips and clusters) were assessed prior to induction (x 3) of and following one-week state of hyperprolactinemia (day 5, 6 and 7). All animals were trained three times before recording the penile reflexes. The penile reflexes being averaged to give a single composite score for each animal. All animals underwent dissections that isolated the cavernosal bodies and cavernosal nerves. Cavernous nerves were activated and intracorporal pressures were recorded at increasing current magnitude (range 0.5-10 mA). Following that corporal smooth muscle reactivity was determined by increasing injection of papaverine (100-3000 microg). Concentration response curves (CRCs) were then generated by plotting percent change (fractional change to make standardized comparison) to increasing neurostimulation or papaverine concentrations at half-log increments. Serum prolactin was determined by rPRL radioimmunoassay Kit-Amersham while serum testosterone was determined Testosterone ELISA Kit-Neogen. RESULTS: Penile reflexes were normal in all groups at the start of experiment but after 1 week of hyperprolactinemia, reflexes were totally abolished in hyperprolactinemia rats (Group 1) and unchanged in Groups 2 and 3. Response to cavernous nerve activation and resulting rise in intracorporal pressure to increasing current (range 0.5-10 mA) were statistically non-significant in any groups. Similarly the intracorporal pressure response to pharmacologic erection induced by papaverine (100-3000 microg) were also non-statistically significant in any groups. Serum prolactin level in all rats receiving prolactin were > 500 ng/ml and the rat group receiving testosterone, serum level were > 20 x higher than the control rat. CONCLUSIONS: This approach allowed more clear separation of central and peripheral mechanism of erection. This study shows a central neurological effect of hyperprolactinemia on erectile function. Hypogonadism does not seem to contribute to the impaired penile reflexes as documented by replacement of testosterone did not recover the centrally mediated penile reflexes. Lowered serum testosterone is secondary phenomenon. These observations may have important implications for the understanding, the mechanism and treatment of men with hyperprolactinemia as well as future research in this field.

Animals↗

PubMed1999

Cabergoline in the treatment of hyperprolactinemia: a study in 455 patients.

Cabergoline is a new long-acting dopamine agonist that is very effective and well tolerated in patients with pathological hyperprolactinemia. The aim of this study was to examine, in a very large number of hyperprolactinemic patients, the ability to normalize PRL levels with cabergoline, to determine the effective dose and tolerance, and to assess the effect on clinical symptoms, tumor shrinkage, and visual field abnormalities. We also evaluated the effects of cabergoline in a large subgroup of patients with bromocriptine intolerance or -resistance. We retrospectively reviewed the files of 455 patients (102 males and 353 females) with pathological hyperprolactinemia treated with cabergoline in 9 Belgian centers. Among these patients, 41% had a microadenoma; 42%, a macroadenoma; 16%, idiopathic hyperprolactinemia; and 1%, an empty sella. The median pretreatment serum PRL level was 124 microg/L (range, 16-26,250 microg/L). A subgroup of 292 patients had previously been treated with bromocriptine, of which 140 showed bromocriptine intolerance and 58 showed bromocriptine resistance. Treatment with cabergoline normalized serum PRL levels in 86% of all patients: in 92% of 244 patients with idiopathic hyperprolactinemia or a microprolactinoma and in 77% of 181 macroadenomas. Pretreatment visual field abnormalities normalized in 70% of patients, and tumor shrinkage was seen in 67% of cases. Side effects were noted in 13% of patients, but only 3.9% discontinued therapy because of side effects. The median dose of cabergoline at the start of therapy was 1.0 mg/week but could be reduced to 0.5 mg/week once control was achieved. Patients with a macroprolactinoma needed a higher median cabergoline dose, compared with those with idiopathic hyperprolactinemia or a microprolactinoma: 1.0 mg/week vs. 0.5 mg/week, although a large overlap existed between these groups. Twenty-seven women treated with cabergoline became pregnant, and 25 delivered a healthy child. One patient had an intended abortion and another a miscarriage. In the patients with bromocriptine intolerance, normalization of PRL was reached in 84% of cases, whereas in the bromocriptine-resistant patients, PRL could be normalized in 70%. We confirmed, in a large-scale retrospective study, the high efficacy and tolerability of cabergoline in the treatment of pathological hyperprolactinemia, leaving few patients with unacceptable side effects or inadequate clinical response. Patients with idiopathic hyperprolactinemia or a microprolactinoma, on average, needed only half the dose of cabergoline as those with macroprolactinomas and have a higher chance of obtaining PRL normalization. Cabergoline also normalized PRL in the majority of patients with known bromocriptine intolerance or -resistance. Once PRL secretion was adequately controlled, the dose of cabergoline could often be significantly decreased, which further reduced costs of therapy.

Adenoma↗

PubMed2003

Macroprolactinemia: a new cause of hyperprolactinemia.

Hyperprolactinemia is not only seen in pregnancy but also in several pathological conditions such as prolactin (PRL) secreting pituitary adenoma (prolactinoma), intracranial tumors compressing the pituitary stalk or hypothalamus, and PRL stimulative drugs. However, some patients with hyperprolactinemia are diagnosed as having idiopathic hyperprolactinemia because the causes are unknown. They are subjected to repeated radiological examinations to find a microadenoma, to a long-term treatment with bromocriptine, and even to a surgical intervention. There is accumulating evidence that macroprolactinemia, in which most circulating PRL forms large protein complexes (more than 150 kDa), is a major cause of idiopathic hyperprolactinemia. The patients with macroprolactinemia are clinically characterized by the lack of hyperprolactinemia-related symptoms such as amenorrhea and galactorrhea. We found that anti-PRL autoantibody is a leading cause of macroprolactinemia that might be heterogeneous in nature. Most patients with anti-PRL autoantibodies were symptom-free and pregnancy was possible despite a marked hyperprolactinemia. Identification of macroprolactinemia is clinically important to prevent unnecessary examinations and treatments in patients with idiopathic hyperprolactinemia.

Animals↗

PubMed1991

[The effects of pregnancy on prolactin secretion in occulted hyperprolactinemia].

The changes in the maternal prolactin level during pregnancy and puerperium were studied in 14 patients with occulted hyperprolactinemia, 5 patients with functional hyperprolactinemia, and 135 women with normoprolactinemia. All of those with occulted hyperprolactinemia and functional hyperprolactinemia became pregnant through bromocriptine treatment. Higher prolactin levels were noted in occulted hyperprolactinemic patients from the first to second trimester of pregnancy, but in the third trimester prolactin levels fell to the normal control levels. This change completely resembled the change in functional hyperprolactinemic patients. Prolactin secreting capacities after puerperium returned to normal in 4 of the 5 patients with occulted hyperprolactinemia. These 4 became pregnant for the second time without any treatment. However, the other patient, whose prolactin secreting capacity was aggravated after the first puerperium, became pregnant the second time through bromocriptine treatment. These results indicate the following: 1) most cases of occulted hyperprolctinemia which may be due to functional lesions return to normal after pregnancy, 2) in rare cases of occulted hyperprolactinemia, prolactin secretion capacity is aggravated after the pregnancy, 3) it is important to observe the natural history of the patient in the treatment of occulted hyperprolactinemia.

Bromocriptine↗

PubMed1989

Luteal phase hyperprolactinemia during ovulation induction with human menopausal gonadotropins: incidence, recurrence, and effect on pregnancy rates.

Hyperprolactinemia may develop during ovulation induction with human menopausal gonadotropins and hCG (hMG/hCG). Because elevated serum prolactin (PRL) has several adverse effects on female reproductive function, this event has been implicated as a factor to explain the difference between ovulation and pregnancy rates in hMG/hCG treatment cycles. The incidence and severity of hyperprolactinemia in the luteal phase of hMG/hCG-stimulated cycles was investigated in a large series of patients. We analyzed 240 consecutive, ovulatory hMG/hCG cycles in 96 women from July 1984 to January 1986. All women had failed to conceive with clomiphene citrate, and had normal luteal phase PRL levels during unstimulated cycles. Daily serum total estrogens were determined during hMG administration. Serum progesterone and PRL were determined in the mid-luteal phase (7 days post-hCG administration). In 7.5% of the cycles, luteal phase PRL elevations were greater than 25 ng/mL. Only 2.5% of cycles had levels of PRL greater than 35 ng/mL. Hyperprolactinemia infrequently recurred in different cycles of the same patient (two of 16 patients, 12.5%). Cycles with hyperprolactinemia were found to have significantly higher preovulatory estrogen levels. Serum progesterone levels were not significantly decreased in cycles with elevated PRL. Pregnancy rates in cycles with and without hyperprolactinemia were similar (7.7 versus 11.1%, respectively; P greater than .05). We conclude that the development of luteal phase hyperprolactinemia during ovulation induction with hMG/hCG is an isolated event. High preovulatory estrogen levels may predispose to its development. Because hyperprolactinemia is uncommon and is usually mild, other factors must be responsible for the difference between ovulation and pregnancy rates using hMG/hCG.

Chorionic Gonadotropin↗

PubMed1989

Hyperprolactinemia and nonpuerperal mastitis (duct ectasia).

In 108 patients with nonpuerperal mastitis (inflammatory symptoms of duct ectasia), serum prolactin levels were determined before, during, and after treatment. Twenty-nine patients (26.8%) exhibited transiently elevated prolactin levels during the period of inflammation (mean +/- SD level, 42 +/- 22 micrograms/L) that returned to normal within 4 weeks. Twenty-two patients (20.4%) presented with more severe hyperprolactinemia (78 +/- 56 micrograms/L), and 15 were found to have pituitary microadenomas. In 11 cases, mastitis was the first symptom of hyperprolactinemia. A second group of 83 patients with known hyperprolactinemia and 83 normoprolactinemic controls were interviewed with regard to recent symptoms or past treatment of nonpuerperal mastitis. Sixteen hyperprolactinemic women (19.3%) and none of the controls reported that they had experienced mastitis. We conclude that duct ectasia is due in part to increased prolactin secretion. Thus, nonpuerperal mastitis may be a symptom of hyperprolactinemia. On the other hand, nonpuerperal mastitis may induce transient hyperprolactinemia (neurogenic hyperprolactinemia) of about 3 weeks' duration that is less pronounced than central hyperprolactinemia.

Adenoma↗

PubMed1982

Unremitting suppression of the postovariectomy rise in plasma LH by tumor-induced hyperprolactinemia.

The plasma LH response to ovariectomy was studied at different periods in the development of hyperprolactinemia in rats bearing the transplantable prolactin-secreting pituitary tumors 7315a or MtTW15. Rats were subcutaneously inoculated with tumor cells and ovariectomy was performed at 3 times during the subsequent growth of the solid tumor: (1) coincident with tumor cell implantation; (2) when solid tumors first became palpable, and (3) when solid tumors were large. The values for circulating prolactin and LH were serially determined following ovariectomy for 63, 35 and 28 days, respectively. In other studies, tumor cells were implanted into animals which had undergone ovariectomy 3 months earlier. In the presence of hyperprolactinemia caused by the prolactin secreting tumors, the plasma LH following ovariectomy was either reduced following an initial increase, prevented from increasing, or reduced from chronically elevated levels. Hyperprolactinemia of approximately 7-50 micrograms/ml caused marked suppression of LH secretion, while hyperprolactinemia in the range of 0.2-6 micrograms/ml resulted in significant but slower and lesser suppression of LH which did not reach noncastrate levels. The inhibitory effect of hyperprolactinemia on plasma LH after ovariectomy was persistent and unremitting for the duration of each experiment, and there was no tendency for suppressed LH to return to levels expected for the ovariectomized state. The model of hyperprolactinemia induced with transplantable prolactin-secreting tumors in the ovariectomized rat may prove to be valuable in understanding the mechanism of depression of gonadal function by hyperprolactinemia.

Animals↗

PubMed2000

Efficacy of bromocriptine in the treatment of metastatic breast cancer- and prostate cancer-related hyperprolactinemia.

OBJECTIVE: Hyperprolactinemia is a frequent evidence occurring in both metastatic breast cancer and prostate cancer, and it has been proven to be associated with poor prognosis and reduced efficacy of the anticancer therapies. Therefore, the pharmacological control of cancer-related hyperprolactinemia could improve the prognosis of advanced breast and prostate carcinomas. Unfortunately, at present it is still controversial which may be the treatment of cancer-related hyperprolactinemia, which could depend at least in part on a direct autocrine production by cancer cells themselves. The present study was performed to evaluate the acute effects of the long-acting dopaminergic agonist bromocriptine on cancer-related hyperprolactinemia. METHODS: The study included 10 women affected by metastatic breast cancer and 10 men with metastatic prostate cancer, showing persistent hyperprolactinemia. Venous blood samples were collected before bromocriptine, and 2, 4, 10 and 24 hours after bromocriptine administration (2.5 mg orally) serum levels of PRL were measured with the double antibody RIA method. RESULTS: Bromocriptine induced a normalization of PRL levels in both groups of patients with breast and prostate cancers. Moreover, mean levels of PRL persisted significantly lower than those found before therapy during the whole 24-hour circadian period. DISCUSSION: This preliminary study shows that low-dose bromocriptine is sufficient to acutely normalize PRL secretion in both metastatic breast cancer and prostate carcinoma patients, irrespectively of the mechanisms involved in inducing cancer-related hyperprolactinemia. Therefore, low-dose bromocriptine could be recommended in association with the classical antitumor therapies in the treatment of metastatic breast cancer and prostate carcinoma patients showing cancer-related hyperprolactinemia, in an attempt to improve the efficacy of anticancer therapies themselves.

Journal Article↗

PubMed1980

Prevalence of hyperprolactinemia in anovulatory women.

To determine the prevalence of hyperprolactinemia in an ovulatory patients presenting to a general gynecology clinic, a 1-year prospective study (1978) was instituted. A total of 119 patients with at least 3 months of anovulation were screened with serum prolactin determinations. Those patients demonstrating hyperprolactinemia were further evaluated with a serum TSH level and hypocycloidal polytomography of the pituitary sella. In patients with anovulation with or without galactorrhea, a hyperprolactinemia prevalence rate of 15% was established. Anovulatory patients with galactorrhea had a hyperprolactinemia prevalence rate of 43%. This was compared to the 9% prevalence of hyperprolactinemia in patients with nongalactorrheic anovulation (P less than .001). Twenty-two percent of the patients with nongalactorrheic anovulation (2 of 9) were found to have a prolactin-secreting pituitary adenoma. In patients with hyperprolactinemia, galactorrhea, and anovulation, 67% (6 of 9) of patients had a prolactin-secreting pituitary adenoma. The authors therefore conclude that the 15% prevalence rate of hyperprolactinemia in all anovulatory women is sufficiently high to warrant continued screening of serum prolactin determinations in all anovulatory women.

Adenoma↗

PubMed2000

Use of the dopamine agonists bromocriptine and cabergoline in the management of risperidone-induced hyperprolactinemia in patients with psychotic disorders.

Risperidone is a novel antipsychotic agent that blocks both dopaminergic and serotonergic receptors. In several reports, clinically significant hyperprolactinemia has been reported in patients on this agent. However, the optimal management of risperidone-induced hyperprolactinemia has not been clarified. We reviewed the records of 5 patients with psychotic disorders who were evaluated for risperidone-induced hyperprolactinemia. There were 4 females and 1 male patient, aged 30-45 yr. All patients had significant hyperprolactinemia, with prolactin (PRL) levels ranging from 65.5 to 209 microg/l. All but 1 of these patients had manifestations of hypogonadism. In these 4 patients, risperidone therapy was continued and the dopamine agonists bromocriptine or cabergoline were added. In 3 out of 4 patients, such additional therapy reduced the PRL level and alleviated hypogonadism. None of the patients treated with these agents had a worsening of psychosis. We conclude that risperidone can cause clinically significant hyperprolactinemia in patients treated with this drug. If risperidone therapy must be continued in such patients, addition of the dopamine agonists bromocriptine or cabergoline may successfully alleviate hyperprolactinemia and the associated manifestations without worsening psychotic symptoms.

Adult↗

PubMed1993

Role of melatonin in nocturnal prolactin secretion in women with normoprolactinemia and mild hyperprolactinemia.

OBJECTIVE: Our objective was to clarify the relationship between the nocturnal melatonin surge and the nocturnal prolactin release in women with normoprolactinemia and mild hyperprolactinemia. STUDY DESIGN: Nocturnal serum melatonin and prolactin levels were determined for a various awake/sleep and light/dark conditions in a total of 23 healthy normoprolactinemia and 9 mild hyperprolactinemia. Patterns of prolactin and melatonin levels were subject to analysis of variance. RESULTS: During sleep deprivation under continuous illumination in normoprolactinemia, neither melatonin nor prolactin increased in concentration. In contrast, during sleep deprivation in a dark environment, both hormones were increased. The maximal prolactin levels in mild hyperprolactinemia under physiologic sleep/dark were significantly higher (p < 0.01) and were reached 2 hours earlier than in normoprolactinemia. However, each woman with mild hyperprolactinemia had similar melatonin surges. Oral administration (1 mg) of melatonin to normoprolactinemia and mild hyperprolactinemia in the daytime resulted in release of prolactin in a fashion similar to that observed during the night. CONCLUSION: Melatonin can regulate nocturnal prolactin secretion independent of sleep-related factors. Furthermore, the nature of the response to exogenous melatonin administration suggests that mild hyperprolactinemia may be unusually sensitive to melatonin.

Adult↗

PubMed2003

Hyperprolactinemia in response to antipsychotic drugs: characterization across comparative clinical trials.

BACKGROUND: Atypical antipsychotic drugs for the treatment of schizophrenia provide effective treatment of psychotic symptoms with a safety profile superior to conventional antipsychotic medications. Neuroendocrine abnormalities in patients with schizophrenia, such as chronic hyperprolactinemia, may now potentially be minimized by the use of newer prolactin-sparing antipsychotic drugs. A discrimination of prolactin-sparing versus prolactin-elevating antipsychotic drugs may provide the clinician with treatment choices in order to avoid or mitigate hyperprolactinemia-associated morbidity. METHODS: Results from five clinical trials were used to characterize factors that may influence antipsychotic drug effects on levels of serum prolactin. Factors investigated included drug treatment, gender, time course, potential for reduction or reversibility, and age. RESULTS: Factors that influenced the risk of hyperprolactinemia included gender, with females appearing to be more sensitive than males, and drug treatment, with risperidone and conventional antipsychotic agents increasing prolactin more than olanzapine. Patients of all ages demonstrated sensitivity to increased prolactin. Furthermore, patients with hyperprolactinemia sustained the effect over time. Hyperprolactinemia reversed when patients were switched to a prolactin-sparing antipsychotic medication. CONCLUSION: Effects of antipsychotic medications on serum prolactin are multi-factorial. Evidence for sexual, reproductive, and general medical consequences of antipsychotic-induced hyperprolactinemia is developing, and identifying antipsychotic drugs with a favorable prolactin profile would be important in mitigating these consequences. Most notably for women, atypical or novel antipsychotic drugs with a prolactin-sparing profile may offer effective clinical treatment with preservation of physiological hormonal function.

Adult↗

PubMed2005

Switching female schizophrenic patients to quetiapine from conventional antipsychotic drugs: effects on hyperprolactinemia.

INTRODUCTION: Conventional antipsychotic medications are associated with elevated prolactin levels, resulting in hyperprolactinemia and a number of unwanted side effects. Several atypical antipsychotics, on the other hand, are less likely to evoke hyperprolactinemia. The aim of this study was to investigate the prevalence of hyperprolactinemia induced by conventional antipsychotic drugs, examine changes in serum prolactin levels and psychiatric symptoms after switching to quetiapine, and identify the relevant characteristics of patients who may be suitable to switch to quetiapine. METHOD: Sixty-nine of 74 consecutive female patients who had received conventional antipsychotic drugs were initially included in the study. Of these, 49 (71 %) patients suffered from hyperprolactinemia, of which a further 25 were subsequently switched to quetiapine. Psychiatric symptoms were assessed by the Positive and Negative Syndrome Scale (PANSS), and serum prolactin levels were measured just before and at 4 and 8 weeks after switching. RESULTS: Eight of the 25 (32 %) "switch" patients dropped out due to psychotic exacerbation during the 8 weeks. In the remaining 17 (68 %) patients, serum prolactin levels were significantly decreased without any significant change in PANSS scores after switching. The 17 patients who completed the switch had previously demonstrated significantly lower positive symptom scores compared to the 8 dropout patients. CONCLUSION: The present findings suggest that 71 % of female patients receiving conventional antipsychotic drugs may suffer from hyperprolactinemia and that approximately two-thirds of patients can be switched to quetiapine, resulting in an improvement in hyperprolactinemia. The main characteristic of the switched patients may be fewer positive symptoms.

Antipsychotic Agents↗

PubMed2003

Daily changes of GABA and taurine concentrations in various hypothalamic areas are affected by chronic hyperprolactinemia.

This study was designed to characterize, in anterior, mediobasal, and posterior hypothalamic and median eminence, the 24h changes of gamma aminobutyric acid (GABA) and taurine (TAU) contents in adult male rats and to analyze whether chronic hyperprolactinemia may affect these patterns. Rats were turned hyperprolactinemic by a pituitary graft. Plasma prolactin (PRL) levels increased after pituitary grafting at all time points examined. A disruption of the circadian rhythm was observed in pituitary-grafted rats, whereas GABA and TAU content followed daily rhythms in all areas studied in controls. In the mediobasal hypothalamus, two peaks for each amino acid were found at midnight and midday. In the anterior hypothalamus, GABA and TAU showed only one peak of concentration at midnight. In the posterior hypothalamus, the values of both GABA and TAU were higher during the light as compared to the dark phase of the photoperiod. In the median eminence GABA content peaked at 20:00h, the time when TAU exhibited the lowest values. Hyperprolactinemia abolished the 24h changes of GABA in the mediobasal hypothalamus and reduced its content as compared to controls. Hyperprolactinemia advanced the diurnal peak of TAU to 12:00h in the mediobasal hypothalamus and did not modify the 24:00h peak. In the anterior hypothalamus, hyperprolactinemia increased GABA and TAU contents during the light phase while it decreased them during the dark phase of the photoperiod. In the posterior hypothalamus hyperprolactinemia did not modify GABA or TAU patterns as compared to controls. In the median eminence hyperprolactinemia increased the 20:00h peak of GABA and shift advanced the decrease in TAU content at 20:00h and its maximum at 24:00h as compared to controls. These data show that GABA and TAU content exhibit specific daily patterns in each hypothalamic region studied. PRL differentially affects the daily pattern of these amino acids in each hypothalamic region analyzed.

Animals↗

PubMed2005

Sexual dysfunction in women with hyperprolactinemia: a pilot study report.

PURPOSE: Hyperprolactinemia is a common hormonal disorder in women that may affect the phases of female sexual function (FSD). We investigated sexual function in patients with hyperprolactinemia. MATERIAL AND METHODS: A total of 25 women with primary hyperprolactinemia and 16 age matched voluntary healthy women who served as the as control group were evaluated with a detailed medical and sexual history, including a female sexual function index (FSFI) questionnaire and the Beck Depression Inventory. Serum prolactin, dehydroepiandrosterone sulfate, free testosterone, androstenedione, 17alpha-hydroxyprogesterone, estradiol, free thyroxin and thyrotropin were measured. These variables were compared statistically between the 2 groups. RESULTS: Except for prolactin serum hormone levels in women with hyperprolactinemia were not different from those in the control group. The median total FSFI score was 23.40 (IQR 17.70 to 27.30) in the hyperprolactinemic group, whereas healthy women had a median total FSFI score of 31.10 (IQR 27.55 to 32.88, p < 0.0001). FSD was diagnosed in 22 of 25 patients (88%), while 4 of 16 healthy women (25%) had FSD (p = 0.03). Desire (p = 0.001), arousal (p < 0.0001), lubrication (p = 0.001), orgasm (p = 0.001), satisfaction (p = 0.07) and pain (p = 0.003) domain scores were also significantly lower in women with hyperprolactinemia. Total FSFI (p = 0.009, r = -0.405), desire (p = 0.001, r = -0.512), arousal (p = 0.002, r = -0.466), orgasm (p = 0.026, r = 0.348) and satisfaction (p = 0.041, r = -0.320) scores negatively correlated with mean prolactin but not with the other hormones measured. CONCLUSIONS: A significant percent of women with hyperprolactinemia whom we evaluated had sexual dysfunction. No hormonal changes other than prolactin and no depression was found as a cause of FSD.

Adult↗

PubMedDate not supplied

The favorable prognostic significance of surgery-induced hyperprolactinemia in node-positive breast cancer patients: ten-year disease-free survival results.

It has been shown that each manipulation of the mammary region, including breast surgery, may stimulate prolactin secretion. However, it has also been observed that in more than 50% of breast cancer patients surgical removal of the tumor is not followed by enhanced prolactin secretion. This might be indicative of an altered psychoneuroendocrine control of the mammary gland, which could lead to the onset of more biologically aggressive breast cancer. In fact, surgery-induced hyperprolactinemia has been proven to be associated with a better prognosis in terms of survival in node-negative breast cancer patients. The present study was performed to investigate the impact of postoperative hyperprolactinemia on the disease-free survival (DFS) of breast cancer patients with axillary node involvement. The study included 100 consecutive node-positive breast cancer patients who were followed for at least 10 years. Surgery-induced hyperprolactinemia occurred in 45/100 (45%) patients without any significant correlation with the main prognostic variables including number of involved nodes and ER status. The two groups of patients received the same adjuvant therapies. After a median follow-up of 151 months, the recurrence rate in patients with surgery-induced hyperprolactinemia was significantly lower than in patients with no postoperative hyperprolactinemia (23/45 vs 43/55, p<0.01). Moreover, DFS was significantly longer in hyperprolactinemic patients than in patients who had no enhanced secretion of prolactin postoperatively. In agreement with the results described previously in node-negative breast cancer, our study demonstrates the favorable prognostic significance of surgery-induced hyperprolactinemia in terms of DFS duration also in breast cancer patients with axillary node involvement, independent of the other well-known prognostic variables, thereby confirming that the psychoneuroendocrine status of cancer patients may influence the prognosis of their disease.

Adult↗

PubMed2002

Antipsychotic-induced hyperprolactinemia and sexual dysfunction.

This overview of antipsychotic-induced hyperprolactinemia provides a summary of the current literature in relation to conventional antipsychotic agents and the five atypical antipsychotics currently available in the United States--clozapine, risperidone, olanzapine, quetiapine, and ziprasidone. Dopaminergic antagonism within the tuberoinfundibular system causes elevation in plasma prolactin levels. Conventional antipsychotic medications and the atypical agent risperidone cause significant elevations in prolactin. Clozapine, olanzapine, quetiapine, and ziprasidone cause minimal effects on prolactin levels in adults, which may be due to a higher 5-HT2A:D2 binding ratio and differential effects on dopamine neurotransmission, with less interference in the tuberoinfundibular pathway. Antipsychotic-induced hyperprolactinemia presumably causes clinical side effects similar to those caused by other forms of hyperprolactinemia. Clinical and endocrinologic changes of hypogonadism also likely occur during chronic antipsychotic-induced hyperprolactinemia. Because hyperprolactinemia may cause clinically significant side effects in patients treated with antipsychotic medications, clinicians should be familiar with the evaluation and treatment of antipsychotic-induced hyperprolactinemia.

Animals↗

PubMed1992

Effects of hyperprolactinemia on prolactin and LH pulsatile pattern in female rats.

Prolactin (PRL) and luteinizing hormone (LH) secretions are very closely-related. To further understand these mechanisms, the pulsatile secretion pattern of both hormones in experimentally-induced hyperprolactinemia has been studied in adult female rats. Hyperprolactinemia was induced by the transplanting of two pituitary glands. Nine days after the transplant operation, rats were bled (75 or 100 microliters/7 min for 3 h). Serum samples were analyzed for prolactin and LH values by RIA. Hyperprolactinemia modifies pulsatile PRL secretion by increasing the absolute amplitude and duration of the peaks together with a decrease in their frequency. Also, the mean values of the hormone during the whole studied period were increased. Hyperprolactinemia was followed by an increase in the mean values of LH and in the absolute amplitude of the peaks. All these results suggest that hyperprolactinemia induced by pituitary grafting in adult female rats, is followed by a significant change in prolactin and LH pulsatility, which may explain, to some extent, the effects of hyperprolactinemia on reproduction.

Animals↗