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PubMed2001

Determination of endometrial prolactin in vivo as a marker for endometrial development in spontaneous ovulatory cycles and in vitro fertilization cycles.

Decidual prolactin was directly determined in endometrial tissue in order to assess its potential role in improving the accuracy of the diagnosis of luteal-phase defect (LPD). Endometrial biopsies of 124 women with regular cycles (group 1) and 13 women with controlled ovarian hyperstimulation and progesterone-supported cycles (group 2) were evaluated in the secretory phase. In addition, decidual prolactin was measured in the luteal phase of the in vitro fertilization (IVF) cycles. The biopsies dated on or after day 25 showed a significant increase in the slope of the regression line of the cycle day versus decidual prolactin content (p < 0.05). Delayed endometrium was not characterized by a lower amount of decidual prolactin compared with biopsies with the same histological dating. On day 27 of the cycle, less prolactin was measured in the out-of-phase biopsies (p < 0.05). A large inter-individual variation in endometrial prolactin tissue content was noticed. In group 2 all biopsies but one were in phase. Compared to the in-phase biopsies of group 1, a significantly higher amount of prolactin was found in group 2. Production of endometrial prolactin in vivo is associated with decidualization of the stromal cells. However, because of the large inter-individual variation, determination of prolactin is not of adjuvant diagnostic value for clinical assessment of LPD. Three factors might explain the higher amount of decidual prolactin in group 2 compared to group 1: (1) a higher serum progesterone concentration owing to an increased production by multiple corpora lutea, or because of the administered progesterone; (2) increased estradiol levels and thus progesterone receptors; and (3) direct stimulation of decidualization by gonadotropins.

Adolescent↗
PubMed2001

Secretion of prolactin and growth hormone in relation to ovarian activity in the dog.

In pregnant bitches an apparent increase in plasma prolactin concentrations is observed during the second half of pregnancy, mean plasma prolactin concentrations peak on the day of parturition, fall for the next 24-48 h and then rise again. During lactation, high plasma prolactin concentrations are observed. Plasma prolactin levels in non-pregnant bitches appear to be lower than in pregnant animals, particularly in the last part of the luteal phase. Pulsatile secretion of prolactin has been observed during the luteal phase and mid-anoestrus. Progression of the luteal phase is found to be associated with an increase in prolactin release. The association of a strong increase of prolactin release and a decrease of plasma progesterone concentrations has also been demonstrated in overtly pseudopregnant bitches. Elevated prolactin secretion during progression of the luteal phase in the bitch may play a role in mammogenesis and is important because of the luteotrophic action of prolactin. Acromegaly is a syndrome of tissue overgrowth and insulin resistance due to excessive growth hormone (GH) production. In the bitch, acromegaly can be induced either by endogenous progesterone or by exogenous progestagens. Progestagen-induced GH production in this species originates from foci of hyperplastic ductular epithelium of the mammary gland. Pulsatile secretion of GH has been observed in normal cyclic bitches. In contrast with the pulsatile GH secretion seen in healthy dogs, the progestagen-induced plasma GH levels in bitches with acromegaly do not have a pulsatile secretion pattern. Just as with prolactin, the plasma progesterone levels influence the secretion pattern of GH in the bitch. The pulsatile secretion pattern of GH changes during the progression of the luteal phase in healthy cyclic bitches, with higher basal GH secretion and less GH being secreted in pulses during the first part of the luteal phase. The progesterone-induced GH production may promote the proliferation and differentiation of mammary gland tissue during the luteal phase of the bitch by local autocrine/paracrine effects and may exert endocrine effects.

Acromegaly↗
PubMed1976

Prolactin receptors and androgen-induced regression of 7,12-dimethylbenz(a)anthracene-induced mammary carcinoma.

Prolactin reverses the inhibitory effects of pharmacological doses of androgen on 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth (Quadri, S.K., Kledzik, G.S., and Meites, J.J. Natl. Cancer Inst., 52: 875-878,1974). To determine whether this effect is due to an alteration in the ability of the tumor cell to bind prolactin, we have quantitated prolactin receptors in androgen-responsive and nonresponsive tumors. Prolactin receptors were measured with 125I-labeled ovine prolactin in a subcellular fraction which reproducibly contained 60 to 80% of the total receptor present in tumor homogenates. Prolactin binding was reversible, reached a steady state in 9 hr, and was completed by excess unlabeled prolactin. Prolactin bound to its receptor with a Kd of approximately 1 X 10(-10) M. Growing tumors were biopsied, and rats bearing regrown tumors were given injections of 4 mg testosterone propionate twice a week. Prolactin receptors were reduced in most of the tumors, which regressed after testosterone treatment by an average of 63% compared to the pretreatment biopsy specimens. Nonresponsive tumors and vehicle-injected controls showed no signifcant alterations in receptor content. This reduction of prolactin receptors is probably insufficient to account for androgen-induced mammary tumor regression.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Size heterogeneity of immunoreactive prolactin in hyperprolactinaemic serum following stimulation with TRH and insulin hypoglycaemia, and suckling in postpartum period.

Three immunoreactive prolactin molecules have been separated according to size by chromatography and typified by radioimmunoassay. In the circulation immunoreactive prolactin exists in three forms designated as "extra-big", "big" and "small" after gel filtration on Ultrogel AcA 54. Most immunoassayable prolactin occurs in the small form, which corresponds to monomeric prolactin and presents totally 73.8 +/- 8% in normal subjects. This pattern is not significantly different from that obtained from the serum of normal subjects stimulated by thyroid releasing hormone (TRH) or insulin hypoglycaemia and from pregnant women. The response of big and small prolactin was in proportion to the rise in total prolactin and decrease in the proportion of big-big prolactin in normal women. In no instance was a big prolactin response seen in the absence of a total prolactin response in normal or hyperprolactinaemic patients. Essentially different stimuli have the increase in concentration of big prolactin toward the end of the tests.

Blood Glucose↗
PubMed1990

Prolactin and breast cancer risk.

A study of 424 women was undertaken to determine whether there was an association between serum prolactin levels and breast cancer; whether prolactin levels would reflect degrees of risk of developing breast cancer; and whether associations between known risk factors for breast cancer and serum prolactin concentrations could be demonstrated. Prolactin levels higher than the median value in control subjects were found to be associated with a more than two-fold increase in the risk of breast cancer (relative risk, 2.1; confidence interval [CI], 1.0-4.5). Moreover, a relative risk of 1.7 (CI, 0.9-3.3) for a group of women with benign epithelial hyperplasia (high risk of developing breast cancer), and a relative risk of 1.0 (CI, 0.6-1.8) for a group with benign fibrocystic disease (low risk of developing breast cancer), provided supportive evidence that prolactin plays a role in the development of breast cancer. A considerable fall in the concentration of prolactin at menopause was noted, so those women who have an early menopause have a reduced period of exposure to high concentrations of prolactin. Similarly, there was a considerable reduction in prolactin concentration after the first pregnancy. Finally, our results showed that, in premenopausal women, a high intake of saturated fats was associated with a high prolactin concentration. Our study supports the concept that parity, menstrual status, and saturated fat consumption influence a woman's exposure to prolactin and therefore the risk of developing breast cancer.

Adult↗
PubMed1979

Prolactin receptors in human breast cancer cells in long-term tissue culture.

Prolactin receptors have been identified for the first time in a number of human breast cancer cell lines and a normal human breast cell line maintained in long-term tissue culture. Optimal conditions for determining the binding of 125I-labeled human prolactin to these cells were established. Five different tumor cell lines have different content of prolactin receptors ranging from 2,300 to 26,000 sites/cell. All tumor cell lines contained more prolactin receptors than does one normal breast cell line (1700 sites/cell). The prolactin receptors in these human mammary tumor cells not only bind human prolactin but also recognize other lactogenic hormones such as human growth hormone, human placental lactogen, and sheep prolactin, but not animal growth hormone, which are not lactogenic. The affinity (Ka) of binding of human prolactin to these cells is 4 x 10(9) M-1 (Kd = 2.5 x 10(-10)M). The hormone specificity and affinity for hormone of these human mammary tumor cells are very similar to that found for the rabbit mammary gland. These human mammary tumor cell lines in long-term culture should prove very useful to study the biology of prolactin receptors in living human cells and the role of prolactin in the tumorigenesis of the human breast.

Breast↗
PubMed1990

Acute effects of nicotine on prolactin release in the rat: agonist and antagonist effects of a single injection of nicotine.

The effects of nicotine on prolactin release were studied in conscious, unrestrained rats in which an indwelling jugular cannula allowed multiple samplings of blood after i.v. administration of nicotine. Intravenous administration of nicotine bitartrate dihydrate increases plasma prolactin concentrations in a dose-dependent manner with an ED50 of approximately 100 micrograms/kg (200 nmol/kg) and this effect is blocked completely by pretreatment with mecamylamine, indicating that it is mediated by a nicotinic cholinergic receptor. Intracerebral ventricular injection of 1 microgram of nicotine also increases plasma prolactin levels, but i.v. injection of this same amount of nicotine has no effect, indicating that nicotine acts within the brain to release prolactin. A single i.v. injection of nicotine resulted in desensitization of the prolactin response to a subsequent injection of nicotine given 1 to 2 hr later, thus confirming a previous report by Sharp and Beyer (J. Pharmacol. Exp. Ther. 238: 486-491, 1986). The prolactin response to nicotine was restored within 24 hr after a single injection. The acute desensitization after a single injection of nicotine appears to be specific to release of prolactin by nicotine because the prolactin response to morphine was unaffected 1 hr after injection of nicotine. A single injection of nicotine appears to desensitize the prolactin response to a subsequent injection of nicotine with an ED50 of approximately 20 micrograms/kg (40 nmol/kg), indicating that nicotine is even more potent in stimulating desensitization of nicotinic cholinergic receptors than in stimulating prolactin release. These results support the concept that nicotine acts as a time-averaged antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Prolactin in animal experimentation. Report on the workshop conference of the German Society for Clinical Chemistry held on November 8 to 9, 1984 in Rödermark, FRG.

Work in recent years has revealed that prolactin can no longer be considered exclusively as a lactation hormone, and must be seen in a much wider physiological perspective. Biochemical and pharmacological studies in animals have made a special contribution, and prolactin is becoming increasingly important in toxicological investigations. The general custom of using rats for such studies has its own inherent problems, involving both the analytical methodology and the special requirements that must be observed in the housing and handling of these experimental animals. The aim of workshop conference was to review these special problems, together with our present knowledge of the mechanisms of prolactin secretion, and to present examples of pharmacological and toxicological studies on prolactin. Döhler (Hannover) spoke on the effect of experimental and pre-experimental conditions on the results of prolactin determination in rats. He described in detail the influence of sex, age and animal strain, and of biological rhythms. Alongside these physiological factors, however, a very great influence is exerted by the conditions of housing, and any external interference leads to often dramatic alterations in prolactin secretion. Wuttke (Göttingen) discussed the mechanisms of prolactin secretion in the rat. Here, dopamine holds a key position. This is also pharmacologically important, because prolactin secretion is stimulated by all dopamine antagonists and inhibited by all dopamine agonists. Vasointestinal polypeptide (VIP) and thyroliberin (TRH) stimulate prolactin secretion directly. The contribution by Nagy (Budapest) dealt with prolactin secretion in lactating rats and its modification by various transmitters.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1980

CSF prolactin determination in patients following operation for pituitary tumor.

Serial cerebrospinal fluid (CSF) and plasma prolactin concentrations were determined from patients during prolactin stimulatory testing with thyrotropin-releasing hormone or during pneumoencephalographic stress. Six patients had been operated on for suprasellar extension of pituitary tumor and one had been irradiated for suprasellar extension of a pituitary tumor. Prior to testing, four patients had had no clinical evidence of tumor recurrence and 3 patients had had tumor recurrence. One of the recurrent tumors had again extended into a suprasellar location. Basal CSF prolactin was undetectable in all patients who had had no recurrence. In 3 of the 4 patients without recurrence, however, prolactin became detectable in CSF during stimulatory testing. CSF prolactin values also increased during stimulatory testing in the patient with suprasellar recurrence of the tumor. A basal CSF-to-plasma prolactin ratio was 0.1 or less in all patients without recurrence. In the 2 patients with recurrence but without suprasellar extension, the CSF-to-plasma prolactin ratio was 0.18 or less. The patient with suprasellar recurrence had a strikingly elevated CSF-to-plasma prolactin ratio of 1.1. Thus, an increase of CSF prolactin during stimulatory testing does not necessarily indicate suprasellar recurrence of a pituitary tumor. However, an elevated CSF-to-plasma prolactin ratio appears to remain a valid indicator of suprasellar extension despite prior pituitary surgery.

Adenoma, Acidophil↗
PubMed1983

Prolactin-like activity of antiprolactin receptor antibodies in rat mammary tumor explants.

The effects of prolactin and a serum containing antiprolactin receptor antibodies on some lactogenic and mammogenic responses were investigated in nitrosomethylurea-induced mammary tumors in organ cultures. Prolactin was able to induce an increase in lactose synthetase activity, DNA synthesis, and prolactin-binding sites at moderate (i.e., physiological) concentrations of prolactin; at higher concentrations, desensitization of the tissues was observed for DNA synthesis and lactose synthetase activity, whereas the "down-regulation" of prolactin receptors occurred. Prolactin had no effect on casein synthesis. Antiprolactin receptor serum was capable of inducing an increase in lactose synthetase activity, DNA synthesis, and prolactin-binding sites, however, lower than that observed with prolactin, thus mimicking prolactin action. The antiserum did not induce any change in casein synthesis. These findings suggest that, in rat mammary tumors, as it has been observed in the normal mammary gland, the prolactin molecule is not required beyond the initial binding to its receptor for its action to be attained. It appears also that a differentiated function has lost its hormonal dependence in these tumors, although their hormonal dependence for other functions and growth is maintained.

Animals↗
PubMed1984

Decidual, amniotic fluid, maternal and fetal prolactin in normal and abnormal pregnancies.

In the present studies, the content and the in vitro production of prolactin by decidua as well as the concentrations of prolactin in amniotic fluid, maternal and fetal serum in normal term pregnancies, induced abortions at various gestational ages, and in pregnancies complicated by diabetes mellitus, preeclampsia, chronic hypertension, and polyhydramnios were measured. Maternal and fetal prolactin levels varied considerably throughout gestation, but at term did not differ significantly between normal and abnormal pregnancies. Prolactin levels in amniotic fluid as well as decidual prolactin content and production were significantly lower only in pregnancies complicated by either hypertension or polyhydramnios. In both normal and abnormal pregnancies, decidual prolactin production correlated strongly with amniotic fluid concentrations. The present data suggest that 1) maternal and fetal prolactin levels do not differ significantly between normal and abnormal pregnancies, 2) the decidua is the principal source of amniotic fluid prolactin, and 3) the significantly lower levels of prolactin in amniotic fluid of pregnancies complicated by hypertension or polyhydramnios are probably due to adverse effects of these conditions on the synthesis and release of prolactin by decidua.

Amniotic Fluid↗
PubMed1983

Epidermal growth factor and thyrotropin-releasing hormone interact synergistically with calcium to regulate prolactin mRNA levels.

The regulation of prolactin RNA sequences by Ca2+, epidermal growth factor (EGF), and thyrotropin-releasing hormone (TRH), singly and in combination, was studied in GH3 cells incubated in a chemically defined medium. Ca2+ increased all large prolactin RNA sequences in the nucleus, thus suggesting a transcriptional site of action. A recently developed cytoplasmic dot hybridization procedure was employed to study regulation of cytoplasmic prolactin mRNA. Ca2+ alone stimulated prolactin mRNA with a lag of between 3 and 9 h and yielded a sizable final increase (14- to 18-fold) of prolactin mRNA. With EGTA present to chelate any residual Ca2+, prolactin mRNA was not detectably increased by TRH, showing that TRH requires Ca2+ to stimulate prolactin mRNA. Under these conditions, prolactin mRNA was only slightly (4-fold) increased by EGF. Either peptide plus an optimal concentration of Ca2+ yielded a 60- to 70-fold increase in prolactin mRNA, showing that both EGF and TRH regulate prolactin mRNA synergistically with Ca2+.

Animals↗
PubMed1982

Estradiol regulates the transcription of the prolactin gene.

The effect of estradiol on prolactin gene transcription in pituitaries from ovariectomized, female rats has been investigated. Analysis of the multiple prolactin mRNA species present in pituitary cells demonstrated that estradiol increases the concentration of all the large, potential nuclear precursors of prolactin mRNA. To further examine possible estradiol effects on prolactin mRNA synthesis, nuclei were isolated from rat pituitaries and allowed to continue RNA synthesis in vitro in the presence of [alpha-32P]UTP. Newly synthesized prolactin mRNA sequences were quantitated by hybridization of [32P]RNA to immobilized plasmid DNA containing prolactin cDNA sequences. After 24 h of estradiol treatment, prolactin mRNA synthesis was increased 4-fold. Estradiol effects on prolactin gene transcription were detected as early as 20 min after injection of the steroid. These findings suggest that estradiol increases prolactin mRNA levels by increasing the transcription of the prolactin gene.

Animals↗
PubMed1994

Reciprocal changes in prolactin and growth hormone secretion in vitro after in vivo estrogen treatment.

Female rats were treated in vivo with estrogen for three weeks. The pituitaries were then removed and their responses to somatostatin, dopamine, TRH, hGHRH(1-44)NH2, or their combination were examined in a superfused pituitary cell system. Somatostatin did not decrease basal prolactin secretion in the control cells, but it caused a dose-dependent decrease in prolactin release from the estrogen pretreated cells. Estrogen pretreatment did not alter the sensitivity of pituitary cells to dopamine; dopamine was equally effective in the control and estrogen pretreated pituitaries in decreasing the basal prolactin secretion and TRH induced prolactin release. Prolactin release from the estrogen pretreated cells, stimulated by 25 nM TRH was inhibited by 1 nM somatostatin and nearly totally abolished by 25 nM somatostatin, whereas in the control cells only the higher dose of somatostatin caused some decrease in the prolactin release. Estrogen pretreated cells showed a reduced response to GHRH. Somatostatin did not decrease the basal secretion of GH in either group, but at 1 nM dose it completely abolished the GH release induced by equimolar concentration of GHRH. However, after somatostatin was eliminated from the system, a delayed GH release could be observed that was greater in the control pituitaries than in the estrogen pretreated pituitaries. It is concluded that in vivo treatment with estrogen reduces GH secretion in response to GHRH and increases prolactin secretion after TRH stimulation. After estrogen treatment, the basal and TRH stimulated prolactin release can be effectively reduced by somatostatin. These effects could be observed in vitro using estrogen free tissue culture medium for up to 36 hours after the removal of the pituitaries. The reciprocal changes in GH and prolactin secretion support the concept of the transdifferentiation of GH and prolactin secreting cells.

Animals↗
PubMedDate not supplied

[Dosage of prolactin in normal and pathological subjects (author's transl)].

Homologous radioimmunoassay of human prolactin was performed and used to investigate the secretion of this pituitary hormone under normal and pathological conditions. The following data were developed in this paper: --During the menstrual cycle, prolactin levels are more elevated during ovulatory and luteal phases than during follicular phase; --During pregnancy, prolactin levels progressively increase to reach their maximum at the end of gestation; --During lactation, prolactin levels increase for the two days following delivery, then progressively decrease; --Bromocryptine oral administration drastically reduces prolactin levels within the 24 hours as it inhibits the prolactin release normally induced by suckling. Assays of prolactin is useful to define the role of this hormone in the genesis of the galactorrhea. Bromocryptine as L Dopa reduce the hyperprolactinemia either functional or tumoral in origin. TRH provokes prolactin release which is more pronounced in females than in males. Pituitary prolactin reserve may be appreciated in several pathological conditions. It appears to be of first interest to assess the residual function of the pituitary gland after surgical removal of adenoma. Depuis 1971, la prolactine humaine peut être dosée dans les milieux biologiques par méthode radio-immunologique (G. BRYANT et coll., 1971; M. L'HERMITTE et coll., 1972; H. FRIESEN et coll., 1972; SINHA et coll., 1973). En 1974 nous avons proposé une méthode de dosage radio-immunologique homologue (A. REUTER et coll., 1976). Grâce à celle-ci nous avons exploré la sécrétion de cette hormone hypophysaire dans certaines conditions normales et pathologiques.

Amenorrhea↗
PubMed1997

[Predictive value of cervical-vaginal prolactin in the evaluation of premature labor risk].

OBJECTIVES: To determine whether the presence of cervico-vaginal prolactin during pregnancy is significantly associated with preterm delivery. STUDY DESIGN: A cohort of 64 pregnant women between 21 and 34 weeks of amenorrhea underwent a washing of the exocervix and vaginal fornices with a normal saline solution. The fluid was then aspirated and centrifuged. Samples were stored at -70 degrees C and later prolactin level was determined by radioimmunoassay. Test was considered as positive for a prolactin concentration higher than 2 ng/ml. Statistical analysis were realized by Student's t test, Fisher's exact test and chi 2 test. RESULTS: In patients with preterm labor, positive cervico-vaginal prolactin had a positive predictive value of 36% and a negative predictive value of 94% for a preterm delivery before 34 weeks of gestation (respectively 45% and 79% before 37 weeks). The sensitivity of a positive test was 31% for preterm delivery before 37 weeks of gestation and specificity was 87% (respectively 57% and 88% before 34 weeks). Patients with a positive prolactin test had a significantly shorter latency between testing and delivery (33.7 days vs 52.4 days; p < 10(-9)). No delivery occurred during the following weeks for patients with a negative prolactin test and, among those, only one delivery occurred during the second week following the test. Positive prolactin tests correlated with a mean cervical dilatation of 1 centimetre at the time of testing, while it was of 0.6 centimetre for patients with a negative prolactin test. CONCLUSIONS: Cervico-vaginal prolactin seems to be a non convincing marker for preterm delivery but indicative of a shorter latency from testing to delivery in symptomatic patients. Further investigations are necessary to evaluate accuracy of cervico-vaginal prolactin as a biochemical marker for imminent delivery in patients with preterm labor.

Adult↗
PubMed1976

A synergistic effect of oestradiol and prolactin influencing the incidence of 3-methylcholanthrene induced cerivical carcinomas in mice.

Castrated NMRI mice were laparotomized and a thread impregnated with beeswax-methylcholanthrene was inserted into the uterine cervix. Beginning on the day of operation and for a further 5 days the animals were injected with oestradiol, prolactin, oestradiol-prolactin, oestradiol-prolactin-progesterone, or the solvents for the hormones only. One group of animals were injected with oestradiol-prolactin for 6 days and later with progesterone every third day until death. The animals were killed one or 4 weeks after the operation. Among the one-week animals the number of cervices presenting epithelial downgrowths ("buds") into the stroma was higher after treatment with a combination of oestradiol and prolactin than after treatment with each hormone separately or among the controls. Four weeks after operation, the incidence of squamous cervical carcinomas was seen to be significantly higher among animals injected with both oestradiol and prolactin than in controls or in those injected with oestradiol or prolactin alone. Progesterone had no definite effect on the oestradiol-prolactin induced incidence. The mechanism behind the synergistic effect of prolactin and oestradiol is discussed.

Animals↗
PubMed1997

The acute and long-term effect of olanzapine compared with placebo and haloperidol on serum prolactin concentrations.

Prolactin elevation is both a common and a persistent event with the currently marketed antipsychotics, excluding clozapine. Elevations have been associated with both acute (galactorrhea, amenorrhea) and chronic (predisposition to osteoporosis) treatment-emergent adverse events. One of the defining criteria for an atypical antipsychotic is the relative lack of persistent prolactinemia. A double-blind, placebo- (N = 68) and haloperidol- (Hal: 15 +/- 5 mg/day, N = 69) controlled trial of three dose ranges of olanzapine (Olz-L: 5 +/- 2.5 mg/day, N = 65; Olz-M: 10 +/- 2.5 mg/day, N = 64; Olz-H: 15 +/- 2.5 mg/day, N = 69) in the treatment of schizophrenia afforded the opportunity to assess the temporal course of the influence of olanzapine and haloperidol on serum prolactin concentration. Consistent with its potent D2 antagonism, haloperidol was associated with a statistically significantly higher incidence of treatment-emergent prolactin elevation (72%) than seen with placebo (8%; p < 0.001) at week 2 of therapy. Expectedly, this elevation was also persistent at weeks 4 and 6. In contrast, olanzapine-associated treatment-emergent prolactin elevations were both lower in magnitude and transient. At week 2, 38% of the Olz-H, 24% of the Olz-M, and 13% of the Olz-L treatment groups exhibited a treatment-emergent prolactin elevation, with a mean increase of 0.35, 0.52, and 0.61 nmol/l, respectively; for haloperidol the mean increase was 1.23 nmol/l. For only the Olz-M and the Olz-H treatment groups did the week 2 incidence of treatment-emergent prolactin elevations differ statistically significantly from placebo. Both the incidence of elevations and the mean increase, in prolactin concentration were less than that seen with haloperidol. Furthermore, by treatment week 6, all three olanzapine groups exhibited incidences of treatment-emergent prolactin elevation that were comparable to placebo and were statistically significantly less than observed with haloperidol. Rapid adaptation was observed in the temporal course of prolactin elevations associated with olanzapine based on both the categorical analysis of treatment-emergent high values and the analyses of temporal change in mean concentrations. In contrast to haloperidol, the magnitudes of the treatment-emergent elevations associated with olanzapine were minimal. The rates of elevation were approximately one-half to one-third those observed with haloperidol and were significantly more transient. Olanzapine, even at the highest doses (15 +/- 2.5 mg/day) used, was not associated with persistent elevations of prolactin, consistent with an 'atypical' pharmacologic profile.

Adult↗