Basal Serum Prolactin Levels Research Articles

The association between serum prolactin levels and live birth rates in non-PCOS patients: A retrospective cohort study.

This paper aimed to analyze the relationship between baseline prolactin (PRL) levels and live birth rates (LBRs) in patients undergoing embryo transfer who did not have polycystic ovarian syndrome (PCOS) using a retrospective design. Patient(s): A total of 20,877 patients who had undergone IVF/intracytoplasmic sperm injection (ICSI) between December 2014 and December 2019. We examined the association between PRL concentrations and LBRs using multivariate regression analysis. In addition, a model for nonlinear relationships based on a two-part linear regression was developed. Following adjustment for confounding factors, multivariate regression analysis confirmed a statistically significant correlation between serum PRL and LBR. Particularly, when blood PRL content was less than 14.8 ng/mL, there exists a positive relation between serum PRL and LBRs. In contrast, once PRL concentrations surpassed the inflection point at 14.8 ng/mL, a meaningful relationship could no longer be inferred between serum PRL and LBR. Basal serum PRL levels were segmentally connected with LBRs.

Lower serum PRL is associated with the development of non-alcoholic fatty liver disease: a retrospective cohort study

BackgroundNon-alcoholic fatty liver disease (NAFLD) has become an epidemic worldwide and has been linked to a series of metabolic co-morbidities. Prolactin (PRL) has recently been found to have a negative effect on NAFLD, but a causal relationship is not well-understood. Here we investigated the causative relationship between PRL and NAFLD occurrence.MethodsIn this retrospective cohort study, we enrolled patients without NAFLD who were diagnosed by abdominal ultrasonography undergone serum PRL testing at 8.00 a.m. at baseline, and followed up for a median of 32 (19, 46) months.ResultsThis study enrolled 355 persons [215 men and 140 women; media age 56 (49, 64) years], in which 72 (20.28%) patients who eventually developed NAFLD. Compared with those in the non-NAFLD group, basal serum PRL levels of patients were lower in the NAFLD group [male: 7.35 (5.48, 10.60) vs. 9.13 (6.92, 12.50) ug/L, P = 0.002; female: 5.66 (4.67, 9.03) vs. 9.01 (6.31, 11.60) ug/L, P = 0.009]. The prevalence of NAFLD was significantly decreased along with the increased quartile of basal serum PRL levels in both genders (P < 0.05). Serum PRL concentration was independently associated with NAFLD development [male: OR, 0.881 (0.777, 0.998), P = 0.047; female: OR, 0.725 (0.554, 0.949), P = 0.019].ConclusionOur study is the first to find that basal serum PRL level can predict the occurrence of NAFLD and it may be a potential biomarker to prevent and treat NAFLD.

Role of Estradiol in the Regulation of Prolactin Secretion During Late Pregnancy.

Estrogen action is necessary for evidencing the stimulatory action of mifepristone and naloxone on prolactin (PRL) secretion during late pregnancy. Our aim is to determine the mechanism mediating this facilitator action of estrogens. To investigate the hypothalamic mechanisms involved in estrogen actions in PRL secretion at the end of pregnancy, we measured the effect of pretreatment with the estrogen antagonist tamoxifen on the expression of tyrosine hydroxylase (TH), hormone receptors (ERα and β, PRs, PRLR(long)), and μ- and κ- opioid receptors (ORs) at mRNA (by semiquantitative RT-PCR) and protein (by western blot for TH, PRLR(long), ERα, PRs, μ- and ORs) levels in extracts of medial basal hypothalamus (MBH) and serum PRL, E2 and P4 levels (by RIA) in mifepristone- and naloxone-treated rats. Tamoxifen administration partially prevented PRL release induced by the combined treatment. TH expression diminished and ERα expression increased in mifepristone-treated rats at mRNA and protein levels and tamoxifen partially prevented these changes with no effect on PRs expression. Mifepristone increased PRLR(long) mRNA levels; this increase was blocked by tamoxifen. Combined tamoxifen and mifepristone treatment decreased μ- and k-ORs mRNA but not protein levels. In conclusion, E2 induces neuroadaptive mechanisms necessary to facilitate PRL release preceding delivery. Acting through ERα, E2 modulates hypothalamic dopaminergic neurons activity, regulating TH, μ- and κ-ORs and PRLR(long) expression, and is necessary for evidencing the effects of P4 withdrawal. Its presence on days 14 and 15 of pregnancy is crucial to facilitate the opioid system modulation of PRL secretion at the end of pregnancy in the rat.

Thalamic neuropeptide mediating the effects of nursing on lactation and maternal motivation

Nursing has important physiological and psychological consequences on mothers during the postpartum period. Tuberoinfundibular peptide of 39 residues (TIP39) may contribute to its effects on prolactin release and maternal motivation. Since TIP39-containing fibers and the receptor for TIP39, the parathyroid hormone 2 receptor (PTH2 receptor) are abundant in the arcuate nucleus and the medial preoptic area, we antagonized TIP39 action locally to reveal its actions. Mediobasal hypothalamic injection of a virus encoding an antagonist of the PTH2 receptor markedly decreased basal serum prolactin levels and the suckling-induced prolactin release. In contrast, injecting this virus into the preoptic area had no effect on prolactin levels, but did dampen maternal motivation, judged by reduced time in a pup-associated cage during a place preference test. In support of an effect of TIP39 on maternal motivation, we observed that TIP39 containing fibers and terminals had the same distribution within the preoptic area as neurons expressing Fos in response to suckling. Furthermore, TIP39 terminals closely apposed the plasma membrane of 82% of Fos-ir neurons. Retrograde tracer injected into the arcuate nucleus and the medial preoptic area labeled TIP39 neurons in the posterior intralaminar complex of the thalamus (PIL), indicating that these cells but not other groups of TIP39 neurons project to these hypothalamic regions. We also found that TIP39 mRNA levels in the PIL markedly increased around parturition and remained elevated throughout the lactation period, demonstrating the availability of the peptide in postpartum mothers. Furthermore, suckling, but not pup exposure without physical contact, increased Fos expression by PIL TIP39 neurons. These results indicate that suckling activates TIP39 neurons in the PIL that affect prolactin release and maternal motivation via projections to the arcuate nucleus and the preoptic area, respectively.

Serum Prolactrin and Blood Glucose Levels Before and After an Oral Glucse-load in Patients with Diabetes Mellitus and Liver Cirrhosis

Serum prolactin and blood glucose levels were measured in 13 patients with type II diabetes mellitus and nine patients with liver cirrhosis (Bilharzial or post-hepatic or mixed) in addition to 13 normal controls. Basal serum prolactin levels in diabetic patients did not differ significantly from levels reported for control, while those of liver cirrhosis patients were significantly higher than those of both diabetic patients and controls. After oral glucose load, all the patients showed decreased glucose tolerance accompanied with hyperprolactinemia that was more apparent and persistent in liver-cirrhosis patients. Serum insulin levels that were feasible to be measured in six liver-cirrhosis patients, showed concomitant delayed insulin rise following the glucose load that was maintained longer than in control. These findings of glucose intolerance and hyperprolactinemia were discussed and interpreted on a suggestion to be secondary to various mechanisms including peripheral insulin resistance, gluconeogenesis and/or altered response of pancreatic B-cells to glucose loading.

Basal Serum Prolactin Levels in Obesity—Unrelated to Parameters of the Metabolic Syndrome and Unchanged After Massive Weight Loss

Prolactin (PRL) has been proposed to play an important role in the pathophysiology of obesity. To further elucidate the relationship between PRL and obesity-related metabolic disturbances, we performed a large cross-sectional study and also reassessed serum PRL levels in a subsample approximately 1 year after gastric bypass surgery. In the cross-sectional part of the study, we assessed basal serum PRL levels in 344 obese subjects (68% women; BMI mean+/-SD, 44.3+/-6.6 kg/m2; range 27.0-67.0 kg/m2) along with measurements of glucose, insulin, C-peptide, triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol, high sensitive (hs) C-reactive protein, and fat mass assessed by bioelectrical impedance analysis. In 38 patients, we reassessed PRL levels approximately 1 year after they have undergone a gastric bypass operation. Women displayed higher basal PRL levels than men (9.0+/-4.8 vs. 7.9+/-3.6 microg/l, P=0.03). Basal PRL levels were neither significantly correlated with the BMI of the subjects (r=-0.05, P=0.77) nor with any other of the assessed variables (all r<0.16, P>0.06) even after adjusting for the influence of sex. After massive surgically induced weight loss that on average almost approached 50 kg, basal serum PRL levels remained completely unchanged (before vs. after, 9.1+/-6.0 vs. 9.2+/-4.6 microg/l, P=0.86). However, preoperative PRL levels significantly correlated with that assessed after the operation (r=0.47; P=0.005). In contrast to our expectation, we could detect neither any significant association between basal PRL levels and the degree of obesity or related metabolic disturbances nor any systematic changes in basal concentrations of the hormone after massive weight loss. In sum, our data do not support the notion of a major role of PRL in the pathophysiology of obesity.

Increased prolactin secretion and thyrotrophin response to thyrotrophin releasing hormone in Klinefelter's syndrome

The reports published thus far on prolactin and thyrotrophin secretion in patients with Klinefelter's syndrome are controversial. The aim of the present study was to investigate the interrelation between prolactin on one hand, and hormones of the hypothalamic-pituitary-gonadal axis and thyrotrophin, on the other, in males with Klinefelter's syndrome. Fifteen patients with Klinefelter's syndrome, aged between 17 and 43 years, and 15 healthy males, aged 22-35 years, were studied. Mean +/- SD basal serum prolactin levels were 529.6 +/- 174.6 mU l-1 in the patients, and 270.1 +/- 113.0 mU l-1 in the control group (P < 0.001). Following 200 micrograms thyrotrophin releasing hormone, an enhanced prolactin response was seen in the males with Klinefelter's syndrome. There was no evidence of any of the well-known causes of hyperprolactinaemia. The response of thyrotrophin to thyrotrophin releasing hormone was more pronounced in Klinefelter patients in comparison with controls. Presumably, in Klinefelter's syndrome both alterations--of prolactin and thyrotrophin secretion--may be caused by decrease of testosterone levels or they could reflect a disturbance in neuroendocrine regulation with some neurotransmitter imbalance.

Serum Prolactin Levels in Hla-B27-Associated Uveitis

To evaluate basal serum prolactin levels in patients with HLA-B27-associated uveitis. Prospective, nonrandomized comparative trial. Thirty-three patients with HLAB27- associated uveitis and 30 age- and sex-matched healthy control subjects were included. Age, systemic disease, treatment, and uveitis activity were recorded for comparative analysis between groups. Fourteen out of 23 patients with arthritic disease had ankylosing spondylitis. Basal serum prolactin levels were determined by electrochemiluminescence immunoassay on a Modular Analytics E170 analyzer. Prolactinemia was significantly higher (mean=15.84 ng/mL) in patients vs controls (mean=11.50 ng/mL) (p=0.026). Subgroup analysis revealed prolactinemia in arthritic disease patients (mean=17.21 ng/mL) significantly higher than controls (mean=11.50 ng/mL) (p=0.009) and in ankylosing spondylitis (mean=17.65 ng/mL) vs controls (mean=11.50 ng/mL) (p=0.006). No correlation was found between prolactinemia and systemic treatment. Prolactinemia did not correlate with disease activity. Autoimmunity features also correlated with higher prolactinemia (mean=17.26 ng/mL) vs controls (mean=11.50 ng/mL) (p=0.015). These results suggest the role of serum prolactin levels in HLA-B27-associated uveitis pathogenesis and its subgroups. There was no correlation with disease activity.

Neuroendocrine regulation of sexually dimorphic brain structure and associated sexual behavior in male rats is genetically controlled.

Steroid hormones, particularly 17beta-estradiol (E2), regulate the development and expression of neural structures and sexual behavior. Recently, we demonstrated that E2-regulated responses are controlled by quantitative trait loci. In this study, we quantified 1) volume of the sexually dimorphic nucleus (SDN) of the preoptic area (POA); 2) medial basal hypothalamic (MBH)-POA aromatase and 5alpha-reductase enzyme activities during prenatal development and in adults; 3) serum LH, testosterone, FSH, E2, prolactin (PRL), and corticosterone levels; 4) reproductive organ (i.e., testis and ventral prostate) weights; and 5) male mating behavior in Noble (NB/Cr) and Wistar-Furth (WF/NCr) rat strains to determine the genetic influence on the measured parameters. Maximal phenotypic divergence in male SDN-POA volumes was seen between NB/Cr versus WF/NCr and BDIX/Cr rats (among nine rat strains initially examined), with the average SDN-POA volume of NB/Cr male rats being significantly greater ( approximately 30%) than that of either WF/NCr or BDIX/Cr males. Subsequent experiments investigated WF/NCr versus NB/Cr male rats in further detail. Significantly higher MBH-POA aromatase activity was seen in adult WF/NCr versus NB/Cr males, while MBH-POA 5alpha-reductase rates were not significantly different (within or between sex) for the two rat strains assayed. Serum LH levels were significantly higher (by greater than sixfold) in WF/NCr versus NB/Cr males, whereas testis organ:body weight and ventral prostate:body weight ratios in WF/NCr versus NB/Cr males were significantly smaller (by approximately 6-fold for testis and approximately 1.5-fold for prostate values). Serum FSH levels were significantly higher (by twofold) in WF/NCr versus NB/Cr males. However, serum testosterone levels were not significantly different, whereas E2 levels were approximately twofold higher (but not significantly different) in WF/NCr versus NB/Cr animals. No significant differences were found in basal (i.e., nonstress) serum PRL or corticosterone levels between the WF/NCr and NB/Cr males. In male copulatory tests, NB/Cr males exhibited significantly more aggressive sexual behavior (e.g., in mounting, intromission, and ejaculation parameters) compared with WF/NCr males. Taken together, these findings indicate that WF/NCr males are, in general, low responders, whereas NB/Cr males are high responders to hormonal signals. The obtained data suggest that the correlative, phenotypic variation in SDN-POA volume (i.e., structure) and reproductive hormone patterns and mating behavior (i.e., function) of WF/NCr versus NB/Cr males is regulated by potentially E2-mediated mechanisms that are genetically controlled.

Depot Medroxyprogesterone Acetate and Basal Serum Prolactin Levels in Lactating Women

In Brief Objective To study the effect of depot medroxyprogesterone acetate on basal serum prolactin levels in lactating women. Methods We compared basal serum prolactin levels in 25 lactating women after depot medroxyprogesterone acetate injection and in 25 lactating women of similar age who were using a copper T380A intrauterine device (control group). This sample size was required in order to have 95% power to detect a significant difference. Basal prolactin levels were evaluated by time-resolved fluoroimmunoassay three times (6 weeks postpartum and 3 and 6 weeks after beginning either contraceptive method). Results At 6 weeks postpartum, before beginning either contraceptive method, the mean prolactin levels in the study and control groups were 991.31 and 948.75 mU/L, respectively (P = .850, 95% confidence interval [CI] −407.57, 492.70). Three weeks later, the mean prolactin levels in the study and control groups were 1156.12 and 860.10 mU/L, respectively (P = .116, 95% CI −76.20, 668.26). At the last follow-up, the mean prolactin levels in the study and control groups were 1127.83 and 710.97 mU/L, respectively (P = .026, 95% CI 51.97, 781.73). There were no significant within-group differences at 6 weeks postpartum before contraception and at 6 weeks after beginning contraception in the study and control groups (P > .05, 95% CI −327.99, 243.02 and −46.76, 522.33, respectively). Conclusion Contraception with depot medroxyprogesterone acetate in lactating women produced higher basal prolactin levels than contraception with copper T380A intrauterine device. Contraception with depot medroxyprogesterone acetate in postpartum lactating women produced higher basal prolactin levels than contraception with a copper T380A intrauterine device.

Depot medroxyprogesterone acetate and basal serum prolactin levels in lactating women

Objective: To study the effect of depot medroxyprogesterone acetate on basal serum prolactin levels in lactating women. Methods: We compared basal serum prolactin levels in 25 lactating women after depot medroxyprogesterone acetate injection and in 25 lactating women of similar age who were using a copper T380A intrauterine device (control group). This sample size was required in order to have 95% power to detect a significant difference. Basal prolactin levels were evaluated by time-resolved fluoroimmunoassay three times (6 weeks postpartum and 3 and 6 weeks after beginning either contraceptive method). Results: At 6 weeks postpartum, before beginning either contraceptive method, the mean prolactin levels in the study and control groups were 991.31 and 948.75 mU/L, respectively ( P = .850, 95% confidence interval [CI] −407.57, 492.70). Three weeks later, the mean prolactin levels in the study and control groups were 1156.12 and 860.10 mU/L, respectively ( P = .116, 95% CI −76.20, 668.26). At the last follow-up, the mean prolactin levels in the study and control groups were 1127.83 and 710.97 mU/L, respectively ( P = .026, 95% CI 51.97, 781.73). There were no significant within-group differences at 6 weeks postpartum before contraception and at 6 weeks after beginning contraception in the study and control groups ( P > .05, 95% CI −327.99, 243.02 and −46.76, 522.33, respectively). Conclusion: Contraception with depot medroxyprogesterone acetate in lactating women produced higher basal prolactin levels than contraception with copper T380A intrauterine device.

Evaluation of Serum ProlactinLevels in Patients with Endometriosisand Infertility

The aim of this study was to clarify the significance of serum prolactin concentrations in patients with infertility and endometriosis. Forty patients with infertility and laparoscopically proven endometriosis were recruited into the study. Basal serum prolactin levels and prolactin levels after TRH administration were measured. The mean basal serum prolactin concentrations were 12.5, 16.5, 19.5, and 26.5 ng/ml and those after thyrotropin-releasing hormone (TRH) administration were 88.3, 114.2, 125.3 and 138.8 ng/ml in patients with stages I, II, III and IV endometriosis, respectively. A statistically significant relationship was found between the basal serum prolactin levels as well as those after TRH injection and the stage of the endometriosis. The patients were divided in two groups. Group I consisted of 20 patients who did not receive any treatment, while group II consisted of 20 patients who were initially treated with GnRH analogues for 24 week and subsequently with several therapeutic schemes in order to improve their fecundity. The pregnancy rate was not different between the two groups. The patients, however, who did not become pregnant had higher serum prolactin concentrations after TRH administration as compared to those who conceived. We conclude that occult hyperprolactinemia may be a cause of infertility in patients with endometriosis.

NMDA receptor antagonists block stress-induced prolactin release in female rats at estrus

In order to evaluate the role of glutamate in prolactin secretion, we examined the effects of N-methyl- d, l-aspartic acid (NMDA) receptor antagonists on serum prolactin levels at both resting and restraint-stress conditions in female rats at estrus. NMDA increased basal serum prolactin levels. Administration of the selective NMDA receptor antagonist, cis-4-phosphonomethyl-2-piperidine carboxylic acid (CGS 19755) (5 and 10 mg/kg i.p.), to rats under resting conditions enhanced basal prolactin levels. A low dose of CGS 19755 (3 mg/kg) was unable to modify the hormone serum level. Under stress conditions the pretreatment with CGS 19755 (3 and 5 mg/kg) prevented the increase in serum prolactin levels. This effect was reversed by NMDA (60 mg/kg s.c.). The NMDA receptor antagonist (5 mg/kg) decreased the median eminence concentration of the dopamine metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), without modifying dopamine content. To examine the probable link between serotonin (5-HT) and glutamate in prolactin release, the 5-HT 2A/5-HT 2C receptor antagonist, ritanserin, was used. Under resting conditions, a dose of 5 mg/kg s.c. blocked the NMDA-induced prolactin release. In rats submitted to restraint, ritanserin decreased the prolactin response and NMDA was unable to correct the stress serum prolactin levels. The 5-HT 1A receptor agonist, 8-hidroxypropyl-amino tetralin (8-OH-DPAT) (3 mg/kg s.c.), increased basal serum prolactin levels and restored serum prolactin in stressed animals pretreated with CGS 19755 (5 mg/kg). The present data strongly suggest that the glutamatergic system participates in the regulation of prolactin secretion. A stimulation tone seems to be exerted via the tuberoinfundibular dopaminergic system, and the prolactin release evoked by restraint apparently involves glutamate/NMDA receptors linked to a serotoninergic pathway.

Is there any change in the prolactin levels of nurses in the morning after night shift?

Our purpose was to determine if blood samplings in the mornings after night shifts should be avoided for measuring the basal serum prolactin levels in women working at night and with regular menses; 20 nurses with regular menses, all working only at night shifts, were enrolled in this study. Serum prolactin levels of the subjects were determined twice, first in the morning after a typical night's sleep, with no intercourse within the previous 24 hours, second, in the morning after a typical night shift. All measurements of serum prolactin levels were performed in the follicular phase of the menstrual cycle. Prolactin levels in the mornings after typical night's sleeps and in the mornings after typical night shifts were not significantly different. Prolactin level in the morning after a night shift of a woman with regular menses may represent basal prolactin level of that woman.

Effect of chronic l-DOPA administration on serum luteinizing hormone levels in male rats

We examined whether the repeated oral administration with a high dose of l-3-(3,4-dihydroxyphenyl)-alanine ( l-DOPA) in 0.5% carboxymethyl cellulose increases serum luteinizing hormone (LH) levels in male rats. Serum LH levels were increased 4 h after a single administration of 1000 mg/kg l-DOPA to male rats, and returned to control levels within 8 h after administration. Four hours after a single administration, serum LH levels were significantly increased by l-DOPA at 1000 mg/kg, but not at 20, 100 or 200 mg/kg. Decreases in body weight and relative weight of the prostate were observed after 7 and 14 days of administration of 1000 mg/kg per day l-DOPA, but no changes were observed in weight of the testis, epididymis or seminal vesicle. The administration of l-DOPA at 500 or 1000 mg/kg per day for 7 or 14 days resulted in increased basal serum LH levels and decreased basal serum prolactin levels 24 h after the last administration. Serum testosterone levels tended to be higher in treated than in control rats. The levels of two metabolites of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in rats treated with 500 mg/kg per day tended to be slightly higher than those in control rats after 7 days of administration. Levels of DA, DOPAC and HVA were significantly increased after 7 and 14 days of administration of 1000 mg/kg per day and after 14 days of administration of 500 mg/kg per day. The level of norepinephrine, but not its metabolite 3-methoxy-4-hydroxyphenylglycol, was significantly increased after only 7 days of administration of 1000 mg/kg per day. No significant changes were observed in levels of 5-hydroxytryptamine or its metabolite 5-hydroxyindole-3-acetic acid with administration of 500 or 1000 mg/kg per day. These findings suggest that a prolonged treatment with a high dose of l-DOPA in male rats induces release of LH from the pituitary, resulting in sustained elevation of LH levels in peripheral circulation.

Effects of advancing age on cerebrospinal fluid concentrations of prolactin in the female rat

Studies were conducted to determine the effects of advancing age on serum and cerebrospinal fluid (CSF) prolactin (PRL) concentrations in the female rat. In young rats with basal serum PRL levels, CSF PRL was maintained at 1.1–2.1% of serum PRL levels. In middle-aged rats, CSF PRL levels and the ratio of CSF to serum PRL was low in rats which maintained estrous cycles, but was increased 4- to 10-fold in rats which were in constant estrus. In aged constant estrous rats, CSF PRL concentrations were increased markedly and the CSF to serum PRL ratio increased to 31%. Collectively, these data indicate that (i) in young female rats, only a fraction of serum PRL reaches the CSF; (ii) that CSF PRL concentrations are low in middle-aged rats which exhibit estrous cycles and (iii) that aging and the constant estrous state are associated with elevated CSF PRL concentrations. As such, the age-related elevation in serum PRL levels and the fraction of PRL which accumulates in the CSF may contribute to the age-related dysfunction in brain PRL-responsive neurons.

Effects of haloperidol and prolactin secreting tumors on cerebrospinal fluid concentrations of prolactin in the female rat

Studies were conducted to determine the effects of acute and chronic elevations in prolactin (PRL) secretion on serum and cerebrospinal fluid (CSF) PRL concentrations in the female rat. Young female rats showed a dose-dependent increase in serum and CSF PRL in response to haloperidol. A time-course evaluation of serum and CSF PRL levels after haloperidol indicated that serum PRL concentrations increased markedly by 30 min and declined thereafter; while CSF PRL increased more slowly, peaking at 2 to 8 h. In young rats with basal serum PRL levels, CSF PRL was maintained at 0.8 to 2.1% of serum PRL levels. During acute hyperprolactinemia, the CSF to serum PRL ratio increased to about 4%. During chronic severe hyperprolactinemia, induced by the growth of a MtT·W15 tumor, CSF PRL concentrations increased to 75 ng/ml, but this represented only 1.5% of serum PRL concentrations. Collectively, thse data indicate that the blood-brain barrier effectively limits access to the brain of circulating PRL.

Basal and metoclopramide-stimulated prolactin (PRL) serum levels in users and non-users of a copper intrauterine device (TCu-380 IUD)

The study was undertaken to analyze the basal and metoclopramide-stimulated serum PRL levels in healthy parous women users (group 1, n=12) and non-users (group 2, n=12) of a TCu-380 IUD. All women had regular menses and were studied between days 18 to 22 of their cycle; none had lactated nor regularly ingested any type of medication during the last six months. After a 10–12 hour overnight fast, peripheral venous blood samples were obtained through an indwelling catheter at -30, -15 and 0 minutes and at 60, 90 and 120 minutes after oral metoclopramide (10 mg). There were no significant differences in serum PRL between both groups, in basal levels nor throughout the test, whether analyzing the mean values at each sampling time, the sum of PRL levels from 60–120 minutes, or the peak levels. No correlation was observed between PRL levels and any of the clinical or obstetric characteristics of the women in both groups. Serum progesterone was ≥ 4.0 ng/ml in all women. Thus, the use of a TCu-380 IUD did not induce any significant changes in basal nor in stimulated serum PRL levels.

A Giant Prolactinoma and the Effect of Chronic Bromocriptine Therapy on Basal and TRH-Stimulated Serum Prolactin Levels

The role of bromocriptine as primary therapy for prolactin-producing tumors is currently well accepted in the literature. Bromocriptine decreases the concentration of serum prolactin and this decrease precludes tumor shrinkage, despite the lack of correlation between amount of decrease in tumor size and baseline serum prolactin. We submit the case of a patient on chronic bromocriptine therapy followed by measuring baseline and thyrotropin-releasing hormone (TRH)-stimulated serum prolactins. Bromocriptine affects both release and storage of prolactin. The literature has suggested that the effects of bromocriptine on storage and synthesis may be responsible for its effects on tumor size. It was felt that TRH stimulation would more accurately reflect storage and synthesis, and thus correlate better with tumor size. The pituitary was initially debulked via a right frontal approach; then the patient was placed on bromocriptine therapy and postoperatively followed with baseline and TRH-stimulated serum prolactins. The size of the pituitary was measured by computed tomography. Baseline serum prolactin levels rapidly decreased, but despite the slow decrease in TRH-stimulated prolactins no change was noted in tumor size. Because of the time difference between the baseline and TRH-stimulated prolactin levels, we conclude that clinically bromocriptine affects primarily secretion of prolactin and secondarily storage and synthesis. We also show that TRH-stimulated prolactin does not correlate with size of prolactin-secreting pituitary tumors and therefore tumor size should be independently measured. The literature has shown that prolactinomas do not respond well to TRH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Neonatal chronic stress induces subsensitivity to chronic stress in adult rats. I. Effects on forced swim behavior and endocrine responses

An influence of early stimulation on sensitivity to acute stress in adulthood has been reported. The purpose of the present work was to determine the effect of exposure of male and female rats to three models of chronic stress (unpredictable stress, cold stress and handling) from day 2 to day 15 of life on behavioral and endocrine sensitivity to chronic stresses in adulthood. The chronic stresses applied in adulthood were a model of intermittent cold stress (daily 30-min sessions at −20°C for 15 days) and the Katz's model of unpredictable chronic stress (15 days). Forced swim behavior and serum concentration of the stress-sensitive hormones, corticosterone and prolactin, were chosen to investigate stress sensitivity. It was found that all neonatal treatments stimulated body weight gain, did not cause infant mortality and did not affect forced swim behavior as adult. The repetitive exposure to cold stress in adulthood did not cause major impairment of forced swim behavior and did not affect basal levels of serum corticosterone and prolactin in either control or experimental rats. These findings support the view that repeated stressors can induce behavioral and endocrine adaptation in rats. The neonatal treatments did not affect this characteristic. The exposure of control rats to the unpredictable stress model severely impaired forced swim behavior and increased basal levels of serum corticosterone and prolactin. This observation conforms to the view that standard laboratory rats cannot adapt to unpredictable chronic stress. This has been reported to cause a behavioral depression syndrome comprising forced swim deficit and endocrine alterations. The exposure of rats to the neonatal stress models provided protection to these behavioral and endocrine effects of the unpredictable chronic stress in adulthood. Though minor between-sex and between-treatment differences were apparent, all neonatal treatments were effective. The results suggest that mild neonatal stresses might increase resistance of rats to some behavioral and endocrine effects of chronic aleatory stress in adulthood.