Mean Prolactin Concentrations Research Articles

Prolactin in impotent men

Serum prolactin and testosterone were measured in 57 subjects aged 19 – 65 yr (mean age 37.4 ± 12 S.D.), who presented solely with impotence and/or disturbance of libido, in order to investigate the role of prolactin in the pathophysiology of this sexual dysfunction. Fifty-one subjects who complained only of impotence were found absolutely healthy on physical, biochemical and radiological examination. The remaining six, who along with impotence had a diminution or loss of libido, were found to harbour a non-functioning pituitary adenoma. Mean serum prolactin concentration was not different in the 51 otherwise healthy individuals with impotence (6.5 ng/ml) when compared to that of 30 normal adults (5.7 ng/ml) who served as controls. Prolactin levels were normal (1.5–7.5 ng/ml) in five of the six men with pituitary adenoma and were slightly elevated in one (30 ng/ml). Mean serum testosterone (±S.E.M.) was lower in the 51 impotent men (5.56±0.35 ng/ml) than in 90 young normal males aged 17–23 yr (7.68±0.34 ng/ml), but when the group with impotence was subdivided according to their age, the age group of 19–29 yr, comprising 18 subjects, had a mean testosterone of 6.81±0.56 ng/ml, which was not statistically different from that of the controls. The six patients with pituitary adenoma had testosterone concentrations in the hypogonadal range (0.95–1.80 ng/ml). From the above results it is concluded that: (1) Among the subjects presenting uniquely with impotence and/or disturbance of libido a percentage (10.5% in the present series) have pituitary damage that may be inadvertently overlooked. (2) Prolactin levels are normal in otherwise healthy impotent men. (3) Sexual dysfunction in patients with pituitary adenoma is not necessarily associated with abnormal basal prolactin secretion. (4) Testosterone concentration does not seem to be reduced in otherwise healthy impotent men. (5) A notable difference in the manifestation of sexual inadequacy exists between healthy individuals and those having pituitary damage. The former complain of impotence only, while the latter also present disturbances of libido. This can be attributed to the low testosterone concentration in the patients with pituitary gonadotropic deficiency.

Periovulatory enhancement of spontaneous prolactin secretion in normal women

The role of endogenous estrogen in the regulation of prolactin secretion in man is controversial. To study this question further, spontaneous prolactin patterns were determined over 5 hr in 10 normal women during the early follicular and again during the periovulatory phases of the menstrual cycle. Steroid determinations revealed significant elevations in mean ±1 SE E 1 (113 ± 20 versus 55 ± 5 pg/ml), E 2 (144 ± 47 versus 48 ± 9 pg/ml), and 17-OHP (1,301 ± 266 versus 639 ± 46 pg/ml) during the periovulatory compared to the early follicular phase period. Each subject demonstrated increased mean plasma prolactin concentration during the higher estrogen state. Mean prolactin concentration (calculated from the individual mean values of samples obtained at 15 min intervals for 5 hr) during the midcycle study period was 10.7 ± 1.0 ng/ml compared to the early follicular phase period of 8.1 ± 1.0 ng/ml ( p < 0.0005). The mean percent increment in plasma prolactin during the periovulatory period was 39% with a range of 9 to 117%. There was no correlation between mean prolactin and serum E 1, E 2, P, or 17-OHP levels during either study period. However, the incremental change in prolactin showed a positive correlation with the incremental increase in E 2 (correlation coefficient, r = 0.66, p < 0.05). In contrast, no significant correlation was present between mean incremental change in prolactin and E 1, P, or 17-OHP. These data suggest that enhanced cyclic estrogen secretion during the periovulatory phase of the menstrual cycle is associated with significantly increased serum prolactin concentrations.

Pinealectomy mildly disturbs the secretory patterns of prolactin and growth hormone in the unstressed rat.

Secretory profiles of prolactin and growth hormone (rGH) over a period of 6 h were obtained from unrestrained pinealectomized or sham-operated control male rats, both groups having been chronically implanted with right atrial cannulae and acclimatized to isolation in special blood sampling cages with a strict cycle of 12 h light: 12 h darkness (L: D). Hormone profiles were obtained from 2 h before to 4 h after the commencement of the light period. In intact animals, secretion of prolactin was episodic without a clear ultradian rhythm except that secretory bursts tended to be larger during the dark period. Furthermore, a peak of prolactin occurred regularly at the commencement of the light period, even though subsequent peaks were diminished in amplitude. Mean concentrations of prolactin during the dark period were significantly higher than later daytime values, supporting the view that there is a diurnal prolactin rhythm. Pinealectomy altered the secretory patterns in prolactin so that peaks became more prominent early in the light period but mean concentrations of prolactin eventually fell as they did in control animals and there was no difference in concentrations of prolactin over a period of 6 h between the two groups. Pinealectomy, therefore, slightly delayed the fall in mean prolactin concentrations which normally occurs in the light period. Secretion of rGH was rhythmic with interpeak intervals and mean concentrations in which there were no differences between control and pinealectomized groups. Inhibition of secretory episodes of rGH by the interface between darkness and light was impaired in pinealectomized animals with a delay in the appearance of the first diurnal trough. It was concluded that pinealectomy attenuates L: D cycle regulation of secretory rhythms of prolactin and rGH to a minor degree.

Immunocytochemical analysis of prolactin production by monolayer cultures of GH3 rat anterior pituitary tumor cells: II. Variation in prolactin content of individual cell colonies, and dynamics of stimulation with thyrotropin-releasing hormone (TRH).

The preceeding report (Hoyt and Tashjian, '80) correlates immunocytochemical localizations and mean prolactin concentrations in GH3 monolayers maximally stimulated with TRH; the present does so over the duration of TRH treatment. Low density seeding produced numerous discrete GH3 cell colonies. Cultures were harvested 1/2, 4, 12, 24, 72, and 144 hr after administration of TRH (50 ng/ml) or saline (control). All cells (42,658 total) in at least 10 microscopic fields/monolayer, 1 cell colony/field, were classed as unstained, heavily (H), moderately (M), or weakly (W) stained for prolactin. In controls, colonies contained 51-91 prolactin-positive cells/100 of population. Colonies with few positive cells had many more W than M cells, and the reverse was true in those with many positive cells. In all colonies, the effect of TRH was biphasic, Initial (0-4 hr) release of prolactin was overlapped, beginning at 3-4 hr, by a progressive increase of intracellular hormone. After 144 hr, the prolactin content of treated cultures had increased to 190% of control, and prolactin-positive cells were more numerous (114% of control). These increases were lower than those reported in the preceeding paper after 48 hr of TRH treatment, when intracellular prolactin equalled 450% of control and positive cells equalled 129% of control. These inconsistencies reflect differences in the control level of prolactin production rather than in the absolute effects of TRH, which were virtually identical in the successive experiments. We conclude that: 1) TRH acts to alter hormone production in cells already making prolactin; 2) TRH increases somewhat the number of prolactin-containing cells; 3) the relative contribution of such "new" cells to increased hormone output depends on the basal level of prolactin production, which differs among individual GH3 cell colonies and varies over time in culture. This diversity does not diminish the usefulness of GH3 cells as biochemical models of hormone biosynthesis. It does hinder their valid morphological evaluation, which apparently must be controlled as carefully as biochemical experiments and should include immunocytochemical localizations, at least for the hormone at issue.

Effects of season, lactation and plane of nutrition on prolactin concentrations in ovine plasma and the role of prolactin in the control of ewe fertility.

Plasma prolactin concentrations during the first 2 months after lambing, at oestrus, and during early pregnancy were investigated in 2 experiments in which Finn x Dorset Horn ewes were mated at an induced oestrus approximately 9 weeks after lambing. Mean prolactin concentrations between lambing and mating were dependent on seasons, being greater than 260 ng/ml plasma in lactating ewes mated in July and less than 150 ng/ml in those mated in October. Within 8 days of weaning of the lambs at 50 days post partum values declined to 122 and 30 ng/ml respectively. Plane of nutrition had little effect on prolactin levels. Higher prolactin values were recorded during oestrus in ewes mated in March or July, the normal period of anoestrus, than in December, the normal breeding season, mean values being approximately 200 ng/ml and 35 ng/ml respectively. The mean increases in the concentrations of prolactin during oestrus were smaller in lactating than non-lactating ewes. It is suggested that these differences in prolactin levels may be responsible for the effects of season and lactation on ewe fertility.

Reduction of androstenedione by skin in vitro and serum levels of gonadotrophins and androgens in men with hypospadias.

The reduction of 4-[1,2-3H]androstene-3,17-dione (androstenedione) in vitro by scrotal skin was measured in samples from nine men (16--34 years old) with hypospadias and from ten male control subjects. The reduction of androstenedione was also studied in axillary and upper arm skin of seven control subjects. Androstenedione was reduced to material with chromatographic characteristics of 5 alpha-androstane-3,17-dione and to 3 alpha- and 3 beta-hydroxy-5 alpha-androstan-17-one. No difference in 5 alpha-reductase activity (defined as the sum of these three metabolites formed) was found in scrotal skin from hypospadic and control men. The mean concentration of 5 alpha-dihydrotestosterone in serum from men with hypospadias was lower than that in serum from control subjects (P less than 0.01). The mean ratio of the serum concentrations of testosterone and 5 alpha-dihydrotestosterone was higher in hypospadic men than in control subjects (P less than 0.05). No differences between the two groups were found in the mean serum concentrations of LH, FSH, prolactin, dehydroepiandrosterone, androstenedione, testosterone or testosterone-binding globulin.

OESTROGEN MODULATION OF GONADOTROPHIN AND PROLACTIN RELEASE IN WOMEN WITH ANOVULATION AND THEIR RESPONSES TO CLOMIPHENE

An LHRH test was performed before and at both 44 and 92 h after the administration of 2.5 mg oestradiol benzoate in eleven patients with hyperprolactinaemia, eight with idiopathic secondary amenorrhoea and seven with oligomenorrhoea. The basal serum hormone concentrations and the responses to LHRH were compared with the same tests performed on ten normal subjects during the early follicular phase of their menstrual cycles (days 4--6). Mean basal concentrations of oestradiol in each group of patients and oestrone in those with hyperprolactinaemia were significantly lower than in the normal subjects. The mean concentration of prolactin in women with secondary amenorrhoea remained lower than in the normal women throught the tests (P less than 0.05). The LH and FSH responses to LHRH before oestrogen in patients with hyperprolactinaemia and of FSH in those with secondary amenorrhoea, were greater than in the normal subjects (P less than 0.001). After oestrogen treatment the responses were similar in all groups except in those with oligomenorrhoea where LH and FSH responses at 44 h (P less than 0.05 and P less than 0.01 respectively) and LH responses at 92 h (P less than 0.01) were lower than in normal controls. The responses at 92 h in all groups were greater than at 44 h (amplification) but the amplification at 92 h and at 44 h compared to the pre-treatment responses, tended to be lower in each group of patients compared to the normal controls. In the hyperprolactinaemic group of patients there was a negative correlation between the basal prolactin concentration and the gonadotrophin amplifications at 92 h (P less than 0.01), and a positive correlation between the basal oestrone levels and the amplifications at 92 h (P less than 0.01). The results of the oestrogen amplification test in eleven of the non-hyperprolactinaemic anovular patients were compared with the ovulatory response to 100 mg clomiphene given for 5 days. Six showed a normal oestrogen amplification and they all ovulated. Two patients failed to show greater amplification at 92 than at 44 h and required human chorionic gonadotrophin (HCG) as well as clomiphene to ovulate. The other three showed a diminished LH amplification at 92 h; they required 200 mg clomiphene and showed a prolonged follicular phase. The responses of the hyperprolactinaemic patients to clomiphene were poor and there was a negative correlation between prolactin concentration and oestrogen production (P less than 0.01). All ten hyperprolactinaemic patients treated with bromocriptine ovulated and eight conceived. The oestrogen amplification test appears to have some value in predicting the subsequent response to clomiphene in non-hyperprolactinaemic anovular women.

Ineffectiveness of pyridoxine in evalution and treatment of the hyperprolactinemic amenorrhea-galactorrhea syndrome

Pyridoxine hydrochloride (vitamin B6) has been proposed as a diagnostic and therapeutic agent for patients with amenorrhea and galactorrhea associated with elevated serum prolactin levels. Therefore five normal premenopausal women and nine consecutive patients with amenorrhea, but with no other evidence of pituitary tumor, were given 200 to 300 mg of pyridoxine IV. Mean serum prolactin and growth hormone concentrations did not change significantly from baseline following the infusion in either group. Eight of the nine amenorrhea patients had elevated serum prolactin levels and were treated with oral PDX for 91.0 ± 10.1 (S.E.) days, including 42.0 ± 8.2 days at a maximum dosage of 600 mg. per day in divided doses. Mean serum prolactin concentrations of the eight patients at completion of therapy (82.6 ± 19.1 ng. per milliliter) did not differ significantly from the pretreatment value (69.1 ± 18.4 ng. per milliliter). No subject acquired normal prolactin levels, and in two patients the serum prolactin levels increased during treatment. Galactorrhea diminished very slightly in three of the seven lactating patients but was unchanged in the remainder. Amenorrhea persisted throughout pyridoxine treatment in all eight patients. While receiving 600 mg. per day, three patients complained of headaches, lethargy, and lightheadedness which subsequently resolved when the PDX was discontinued. Thus, pryidoxine does not appear to be a useful agent for evaluation or treatment of the galactorrhea-amenorrhea syndrome.

Effect of chronic metoclopramide therapy on serum pituitary hormone concentrations.

The effect of chronic (3--9 months) therapy with metoclopramide on serum levels of pituitary and thyroid hormones was studied in 4 males and 1 female. The mean serum prolactin concentration during metoclopramide therapy was significantly higher than after discontinuation of metoclopramide. Serum prolactin concentrations increased acutely after each dose of metoclopramide. Serum prolactin concentrations increased acutely after each dose of metoclopramide, and gradually returned to normal by 6--12 h. There was no sifgnificant differences in the serum TSH, T3, T4, GH, and gonadotrophin levels during and after metoclopramide administration. In the male subjects the mean serum testosterone was normal, but significantly lower during metoclopramide therapy.

Inhibition of prolactin release by serotonin antagonists in hyperprolactinemic subjects

Metergoline (4 mg) and methysergide (3 mg), two serotonin antagonists known to inhibit prolactin secretion in normal subjects, and the dopaminergic agonist, bromocriptine (2.5 mg) were orally administered in hyperprolactinemic patients. Mean serum prolactin concentration was significantly decreased between 120 and 240 min following the ingestion of all three drugs in comparison with a placebo; a consistent reduction to below 50% of basal values occurred in 10 of 14 patients after metergoline, in 5 of 10 after methysergide, and in 11 of 14 after bromocriptine administration. These data indicate that serotonin antagonists may acutely lower serum prolactin levels in hyperprolactinemic patients similarly to bromocriptine, though their mechanism of action is most likely different.

Response of amenorrheic patients with normal serum prolactin to chlorpromazine during administration of human menopausal gonadotropin

To study the effects of graded amounts of estrogens on prolactin (PRL) secretion, PRL response to chlorpromazine (CPZ) during administration of human menopausal gonadotropin (hMG) was determined. A control CPZ test was done prior to initiation of hMG therapy and the test was repeated when endogenous estrogen secretion reached the physiologic range (350 to 400 pg. per milliliter) which stimulates luteinizing hormone surge in the normal ovulatory menstrual cycle. Six euprolactinemic women with secondary amenorrhea were studied. Studies showed that there was no significant change in the mean serum prolactin concentrations during control and repeat CPZ testing procedure (5.8 ± 2 and 10.8 ± 2 ng. per milliliter, p < 0.1). The maximal response of PRL to CPZ was significantly higher during hMG-induced high estrogenic state than during control testing (69.9 and 32.3 ng. per milliliter, p < 0.01). This finding suggests that endogenous estrogen may play a role in the regulation of serum prolactin concentration during the menstrual cycle.

Seasonal variation in plasma LH, FSH, prolactin, and testosterone concentrations in adult male white-tailed deer.

Blood samples were collected monthly from captive and wild adult (12 months old or older) male white-tailed deer (Odocoileus virginianus) over 1 year in southwest Virginia. Plasma was assayed for luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), and testosterone (T) using radioimmunoassays. LH and T levels for the captive and wild deer were essentially similar and followed a distinct annual cycle. LH concentrations (nanograms per millilitre) peaked earlier (October, captive, 4.5 ± 1.8 (mean ± standard error); September, wild, 3.3 ± 0.9) than T concentrations (nanograms per millilitre) (November, captive, 13.3 ± 2.7; November, wild, 23.7 ± 7.8) and dropped off sharply prior to, or concomitant with, T concentrations. LH and T levels were lowest during the late winter and spring. T concentrations were closely correlated with androgen levels (Mirarchi, R. E., P. F. Scanlon, R. L. Kirkpatrick, and C. B. Schreck. J. Wildl. Manage. 41: 178–183 (1977)) determined by competitive protein binding assay. Mean PRL and FSH concentrations in wild and captive deer also displayed seasonal variations. Prolactin concentrations (nanograms per millilitre) were highest in May (147.5 ± 0.0) and lowest in November while FSH levels (nanograms per millilitre) peaked in September (180.2 ± 22.4) and were lowest in March. Differences in hormone concentrations between deer and sheep, and the relationship between PRL and antler growth and FSH and spermatozoan production, are discussed.

Primary empty sella, galactorrhea, hyperprolactinemia and renal tubular acidosis

Discussed here is a 41 year old woman with galactorrhea associated with the empty sella syndrome and mild renal tubular acidosis. Basal serum prolactin (PRL) levels were normal, but a 24 hour serum PRL secretory profile demonstrated an increased mean PRL concentration. Serum PRL was appropriately suppressed by the administration of L-dopa; however, chlorpromazine stimulation resulted in a blunted serum PRL response. Pituitary luteinizing hormone, follicle stimulating hormone, ACTH and thyroid stimulating hormone levels were normal. Thus, galactorrhea associated with an enlarged sella does not establish the diagnosis of a pituitary tumor, and pneumoencephalography must be performed to exclude the empty sella syndrome.

Neuroendocrine dysfunction in galactorrhea-amenorrhea after oral contraceptive use.

Nonpuerperal alactorrhea and amenorrhea have been reported following the use of oral contraceptives. Treatment of this condition with ergot alkaloids has proved to be of great therapeutic value. Pretreatment plasma hLH and hFSH concentrations in 13 women with postqill galactorrhea-amenorrhea (PPGA) were 6.6 plus or minus 0.6 (SE.) and 5.0 plus or minus 0.8 mlU/ml, respectively. The mean prolactin concentration was 80.7 plus or minus 13.2 ng/ml. After complete evaluation in which diagnostic evidence of pituitary tumor was absent, the patients were treated with ergocryptine (CB-154). The mean hPRL concentration at 14 days of therapy was 7.8 p;us or minus 1.9 ng/ml. Cyclic gonadotropin secretion resumed in all but one instance; ovulation was confirmed on the basis of a biphasic temperature chart and in 5 cases, endometrial biopsy. Measurement of serum dopamine-beta-hydroxylase (DBH) activity indicated a significant decline at the end of 8 weeks of CB-154 therapy. The fall in hPRL was not necessarily associated with a fall in DBH. The majority of women in this study exhibited a consistent personality suggesting varying degrees of anxiety unrelated to the PPGA and usually antedating the use of oral contraceptives. PPGA was found in women without hyperprolactinemia, but altered hPRL secretion was evident in all instances. The data suggest that the disorder of cyclic gonadotropin secretion is related to altered hPRL secretion, but the mechanism is possibly related to a catecholamine abnormality. The data support the presence of an inherent cyclic mechanism for the secretion of gonadotropins. CB-154 therapy does not affect conception, and no teratogenic effects were observed in 2 infants born to women who had received CB-154 during the first 40 days of gestation.

Nonpuerperal lactation and normal prolactin regulation.

Prolactin secretion was evaluated in 11 consecutive patients referred with nonpuerperal lactation who did not have clinical evidence of pituitary tumors. Six patients had normal fasting prolactin (PRL) levels, 13.8 plus or minus 1.8 ng per ml (Group I), and the other 5 women had elevated basal serum PRL concentrations, 182 plus or minus 72 ng per ml (Group II). All Group II patients had amenorrhea; however, 5 of 6 Group I patients had menstrual periods. The 24-h mean serum PRL concentrations were 12.8 plus or minus 1.2 (SEM), 13.3 plus or minus 0.7, and 165 plus or minus 62 ng per ml for the controls and Group I and II, respectively. A pattern of intermittent PRL discharge during the day characterized each group; however, a normal sleep related increase in serum PRL concentration was absent in the Group II patients. Chlorpromazine produced greater than two-fold increases in serum PRL concentrations in the controls and Group I patients; however, this response was absent in Group II. L-Dopa produced appropriate suppression of serum PRL concentrations in the normals and both patient groups. Normal serum growth hormone, thyroxine, and plasma cortisol characterized each group. Serum estrogen and/or LH and FSH were decreased in 3 of 5 Group II patients; however, the serum concentrations of these hormones were normal in 5 of 6 Group I patients. Short term L-dopa therapy was effective in suppressing lactation in 3 of 5 Group II patients, and it also decreased lactation in the 4 treated Group I patients without significantly altering 24-h mean serum PRL concentrations in the latter group. hypothalamic-pituitary dysfunction was present in certain patients with nonpuerperal lactation who had elevated 24-h mean PRL concentrations and no PRL release following chlorpromazine and sleep. Frequently, however, nonpuerperal lactation is associated with normal prolactin secretion.

Serum prolactin levels in unmedicated schizophrenic patients.

Excessive dopaminergic activity in some dopaminergic tracts may be involved in the cause of some types of schizophrenia. We studied serum prolactin levels in newly admitted, unmedicated, psychiatric patients to determine if the prolactin levels in schizophrenic patients might be diminished to reflect increased dopaminergic activity in the tuberoinfundibular tract or the increases associated with psychological stress. Mean serum prolactin concentration was found to be within the normal range in 22 unmedicated, acutely disturbed, newly admitted schizophrenic patients but tended to be elevated in two manic patients and one patient with a severe anxiety state. It may be possible to use these findings to assess the degree of dopaminergic activity of the tuberoinfundibular tract. It appears that the mechanism that causes stress to increase serum prolactin may be abnormal in some schizophrenic patients.

Hypothalamic-pituitary function in diverse hyperprolactinemic states.

Prolactin secretion in normal adults is characterized by periods of episodic secretion which increase in magnitude during sleep. In this study, we report the 24-h mean prolactin concentrations, prolactin secretory patterns, and associated pituitary hormone function in nine patients (seven women and two men) with hyperprolactinemia of diverse etiologies. Four of the women and one of the men had clinically demonstrable pituitary tumors, one boy had a hypothalamic tumor, and the three other women had "functional" hyperprolactinemia. The 24-h mean prolactin concentrations derived from averaging the 20-min interval samples for 24 h ranged from 28.6 to 1,220 ng/ml. The plasma prolactin patterns in these patients showed persistence of episodic secretion in all and loss of the normal sleep-wake difference in plasma prolactin in seven of nine. Three of the patients with galactorrhea and comparable 24-h mean prolactin concentrations (58.3, 59.7, and 64.3 ng/ml) showed similar prolactin secretory patterns despite different etiologic mechanisms. Evaluation of the secretory patterns of luteinizing hormone (LH) in these patients showed loss of normal pulsatile LH release and a low 24-h mean LH concentration in the patient with the pituitary tumor, while the two patients without clinically demonstrable pituitary tumors ("post-pill" galactorrhea and "idiopathic" galactorrhea) showed normal LH secretory patterns and 24-h mean LH concentrations. The 24-h mean cortisol concentrations and secretory patterns were normal in five of the seven patients who had these parameters measured. The patient with the hypothalamic tumor had a low 24-h mean cortisol concentration and production rate and absent response to metyrapone. The patient with "idiopathic" galactorrhea had an elevated 24-h mean cortisol concentration but normal cortisol production rate and urinary 17-hydroxycorticoid excretion. Growth hormone secretion was abnormal in four of the patients (one with the hypothalamic tumor and three with pituitary tumors). Thyrotropin-releasing hormone (TRH) administration in four patients resulted in normal TSH release in two patients (one of whom developed galactorrhea after the test), an absent response in the patient with the hypothalamic tumor, and a blunted response in one of the women with a pituitary tumor. The two men had low 24-h mean plasma testosterone concentrations (69 and 30 ng/100 ml) and symptoms of impotence and loss of libido. Five of the women (four with pituitary tumors and one with Chiari-Frommel syndrome) had either low 24-h mean LH concentrations, abnormal LH secretory patterns, or both. These data indicate that patients with hyperprolactinemia encompassing a varied etiological range frequently show loss of the normal sleep-associated increase in prolactin secretion as well as abnormalities in the regulation of the other hypothalamic pituitary-regulated hormones. The finding that the abnormalities in LH, growth hormone, thyrotropin, and cortisol (adrenocorticotrophic) secretion were almost uniformly confined to the patients with the clinically demonstrable hypothalamic or pituitary tumors suggests that the size of the lesion is the critical factor.

Prolactin secretion in sixty-five patients with galactorrhea

Pituitary prolactin (PRL) secretion was evaluated in 65 galactorrheic individuals with nonfunctioning hypothalamic-pituitary tumors, acromegaly, prolactin-secreting tumors, Chiari-Frommel syndrome, Argonz-del Castillo syndrome, history of phenothiazine or α-methyldopa intake, primary hypothyroidism, use of contraceptive medications, and in patients with idiopathic galactorrhea. Mean serum prolactin concentrations in patients with prolactin-secreting pituitary tumors were significantly higher than those in other groups but over all there was no correlation between the serum prolactin levels and the grade of galactorrhea. Neither a single elevated serum prolactin level nor the degree of suppressibility after L-dopa administration was diagnostic of a pituitary tumor. However, a history of consistently high serum prolactin concentrations was highly indicative of a prolactin-secreting tumor.

Circulating prolactin levels during the menstrual cycle: Episodic release and diurnal variation

Assessment of temporal relationship between levels of prolactin (PRL), gonadotropins, and ovarian steroids in 14 ovulatory cycles was made. Serum PRL concentrations were determined by a homologous radioimmunoassay. Our data showed that, although the highest mean PRL concentration was found on the day of LH-surge and the day after estrogen peak, a consistent pattern of circulating PRL in daily morning samples was not present in ovulatory cycles; variations in random fluctuation with erratic spikes were observed within cycles and between subjects. In two cycles studied, despite markedly elevated PRL levels (eightfold) induced by amphetamine, optimal ovulatory events occurred in terms of both hormonal patterns and luteal function. These findings implicate a lack of apparent physiologic role of PRL in the regulation of ovarian function in human subjects. The random daily fluctuation of PRL was further characterized in samples obtained at 10 to 30 minute intervals during different days of five ovulatory cycles and continuous sampling during day and night was made in three of five studies; a clear episodic nature of PRL release was disclosed. A circadian rhythm with marked elevation during sleep which was composed of multiple peaks with larger excursions than those found during waking periods was revealed. The event of sleep-induced PRL rise was initiated shortly (30 to 90 minutes) after the onset of sleep and ceased upon wakening. In one subject a quantitatively greater nocturnal PRL release around midcycle (eightfold) than during the follicular and the luteal phases (threefold) was found. These data would facilitate future elucidation of the inapparent role as well as the neuroendocrine regulation of PRL secretion during the human menstrual cycle.

Utility of L-dopa and water loading in evaluation of hyperprolactinemia.

Basal serum prolactin concentration was determined by radioimmunoassay in normal male and female subjects and patients with functional galactorrhea and pituitary tumors. Mean serum prolactin concentration was 34 ± 25.5 (1 sd) ng/ml for normal males, 45 ± 31.5 ng/ml for normal females, 96 ± 73.5 ng/ml for functional galactorrhea patients, and 12,444 ng/ml for pituitary tumor patients. There was considerable overlap in the serum prolactin levels of functional galactorrhea patients with levels found in normal females. Likewise, basal serum prolactin concentration in 2 of 8 patients with pituitary tumors was not clearly higher than some patients in the functional galactorrhea group. In order clinically to separate patients with pituitary tumors from patients with other causes of hyperprolactinemia, we administered l-dopa and a water load to individuals in each group. l-dopa resulted in greater than 50% suppression of serum prolactin concentration in all normal subjects and all patients with functional galacto...