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Macroprolactinomas have been well documented in men over the past several years. By contrast, to the best of our knowledge, there have been no reports of microprolactinomas in men. We describe here 14 cases of microprolactinomas occurring in male patients (14 to 53 years old) and discovered on the basis of endocrine symptoms. Nine patients complained of impotence and/or decreased libido, 8 had gynecomastia with or without galactorrhea, 1 had undergone incomplete puberty. All patients had hyperprolactinemia (225 +/- 65 micrograms/l, mean +/- SEM, N less than 13 micrograms/l); plasma testosterone levels were low in 9 (162 +/- 33 ng/dl, mean +/- SEM; N = 308 - 876 ng/dl), while plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels and their responses to LH-releasing hormone (LHRH) were normal in all cases. Among the 14 patients, 12 had no hypopituitarism and 2 had only partial corticotrope insufficiency; none had visual disturbances and only one complained of headaches. The sella turcica was normal in size and shape in 2 cases but a double floor and/or a thinner part of the floor was observed in 12. CT scan of MRI demonstrated in all cases an intrasellar microadenoma with a mean size of 7 mm (range, 3 to 10 mm) and no preferential localization. One patient was treated with bromocriptine, while the others underwent surgery via the transsphenoidal route. Immunocytochemistry demonstrated immunoreactive-prolactin (IR-PRL) cells in all the adenomas. Surgery resulted in normalization of plasma PRL in 11 of the 13 patients and in lowering PRL levels in the others 2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prolactin microadenoma in men. Study of 14 cases]. 153 Feb 27

Dopamine is known to be the prolactin-release inhibiting factor, but the effects of dopamine itself on regulation of prolactin messenger RNA have been little studied because of the instability of dopamine. We have compared the effects of dopamine and bromocriptine on the levels of prolactin mRNA and on the rates of synthesis, storage, and release of prolactin in primary cultured rat pituitary cells. The cells were incubated for 72 h with no secretagogue (control group) or in the presence of either dopamine (10 mumol/L) plus ascorbic acid (100 mumol/L) or bromocriptine (0.1 mumol/L). Prolactin mRNA was measured in cell extracts by means of slot blots, and newly synthesized prolactin was measured in similar incubations by the addition of [3H]leucine, followed by gel electrophoresis. The levels of total prolactin were measured by radioimmunoassay. Prolactin mRNA was reduced to 78 +/- 9% (mean +/- SEM) of control levels in bromocriptine-treated cells and to 59 +/- 7% in dopamine-treated cells, demonstrating that dopamine stabilized by ascorbic acid was able to reduce the levels of prolactin mRNA in rat pituitary cells in culture. Dopamine may act at sites in addition to the dopaminergic D2 receptor, since the level of prolactin mRNA was reduced more by a supramaximal dose of dopamine than by a supramaximal dose of bromocriptine. The results of the [3H]prolactin and prolactin measurements suggested that availability of mRNA was not a major factor in controlling the rate of prolactin synthesis.
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PMID:The effects of dopamine on prolactin mRNA levels in rat pituitary cells in culture. 160 Apr 72

From preclimacteric women (n = 10, 45-50 years of age) with gross cystic breast disease, levels of beta-endorphin, estradiol, progesterone, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, cortisol and prolactin were assayed radiochemically in the breast cyst fluid and in plasma. The beta-endorphin concentration (fmol/ml) was increased more than fourfold in the breast cyst fluid (17.6 +/- 4.6 SEM) than in plasma (4.2 +/- 0.5 SEM). In the breast cyst fluid, estradiol was increased 41-fold (1738.2 +/- 350.5 SEM pg/ml), and progesterone 47-fold (65.47 +/- 8.25 SEM ng/ml) more than in plasma. The significantly increased values of beta-endorphin, estradiol and progesterone in the breast cyst fluid and the identification of beta-endorphin in cyst-lining epithelia demonstrate the local synthesis. Growth factor-like properties of beta-endorphin and estradiol are accountable for the propagation of cystic changes. The autonomic formation and function of beta-endorphin, estradiol and progesterone in cyst compartments can not be related with the levels of luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone and cortisol, which were significantly higher in plasma than in the breast cyst fluid. In the breast cyst fluid, prolactin could not detected to be significantly higher than in plasma. In addition the plasma-concentration of testosterone, androstenedione, thyroxin, triiodothyronine, thyroid-binding globulin, sexual-hormone-binding-globulin could be detected within the normal range. In this study we could demonstrate the synergism of beta-endorphin, steroid hormones and peptide hormones which advance the growth of gross cystic disease of preclimacteric women. Beta-endorphin was also examined by immunocytochemical assays (fluorescence, alkaline phosphatase and horseradish peroxidase method), in 11 women with pure fibrocystic disease, in 7 women with fibrocystic disease combined with a carcinoma in situ and in 15 women with fibrocystic disease combined with invasive carcinoma of the breast. Sections of frozen and paraffin embedded tissue of the same patient were reacted with anti-beta-endorphin antiserum. The immunoreactivity of beta-endorphin was intense in normal, proliferative altered and cyst-lining epithelia of fibrocystic disease and decreased in atypical epithelia and carcinoma cells of the breast. The degree of beta-endorphin staining is related to the degree of cell differentiation. In addition, nuclear receptors for estrogen and progesterone were assayed by peroxidase antiperoxidase technique.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Interaction between beta-endorphin, steroids and peptide hormones in fibrocystic lesions of the female breast]. 164 46

We studied the serum levels and peritoneal transport of prolactin in 13 CAPD patients and compared with 8 patients on hemodialysis and 10 normal subjects matched by age (30-78 years), sex, body mass index and serum glucose concentrations. CAPD and hemodialysis patients were matched also by hematocrit, serum creatinine, albumin concentrations and duration and dialysis (0-79 months), the prolactin levels in serum and in effluent were measured by RIA and NB2 bioassay. CAPD patients had higher serum prolactin levels than did hemodialysis-treated patients and control subjects. The bioactive/immunoactive ratio of serum prolactin in CAPD patients was 0.7 +/- 0.1 versus 0.9 +/- 0.1 in the control subjects (P less than 0.05) and 0.8 +/- 0.04 in the hemodialysis patients, mean +/- SEM. A significant linear correlation was demonstrated between serum levels and 8 hr peritoneal mass transfer of this hormone. A notable drop of prolactin took place after the first hour of dialysis. Serum prolactin was not influenced by peritoneal protein loss, glucose absorption rate or duration of CAPD. From this study we may conclude that hyperprolactinemia associated with CAPD is not affected by continuous peritoneal loss of prolactin, demonstrating only a slight decrease in bioactivity.
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PMID:Serum levels and peritoneal loss of prolactin in CAPD patients. 168 Apr 37

The pathophysiological role of the central dopaminergic mechanism in human essential hypertension (EHT) is still unknown, so we investigated a possible relationship between the central dopaminergic activity and salt sensitivity to blood pressure in patients with EHT. We divided 22 inpatients with EHT into salt-sensitive (SS, n = 11) and non-salt-sensitive (NSS, n = 11) groups according to an 8% increase of mean blood pressure (MBP) when dietary salt intake was increased from 2 g/day to 20 g/day for two periods of 7 days each. The change of central dopaminergic activity by salt load was evaluated as the percentage change of plasma prolactin (PRL) response to a small dose (25 micrograms) of thyrotropin-releasing hormone (TRH) administered intravenously. The mean percentage change of PRL response by salt load in the SS group was -9.4 +/- 8.5% (mean +/- SEM), which was remarkably lower than the 26.8 +/- 5.5% in the NSS group (P less than .01). There was a significant negative correlation between the percentage change of PRL response and that of MBP by salt load (r = -0.456, P less than .05). These results suggest that a lack of activation of the central dopaminergic system by salt load may contribute in part to a rise in blood pressure in SS patients with EHT.
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PMID:Salt sensitivity and central dopaminergic activity in patients with essential hypertension. 168 22

Arginine vasopressin, oxytocin and ACTH are released from the pituitary gland in response to acute hypoglycemia. To investigate the role of alpha-adrenergic mechanisms in mediating this response, 6 non-diabetic subjects were studied during hypoglycemia induced by 0.15 IU/kg i.v. insulin under control conditions, and during non-selective alpha-adrenergic blockade with phentolamine. In the control study plasma arginine vasopressin rose from 1.6 +/- 0.8 pmol/l (mean +/- SEM) basally to a maximum of 2.5 +/- 0.8 pmol/l following hypoglycemia (p less than 0.05). An exaggerated response was found during phentolamine blockade, with a maximum plasma vasopressin of 11.5 +/- 0.4 pmol/l (by analysis of variance, p less than 0.05). The plasma oxytocin response to hypoglycemia was similarly increased during phentolamine compared to control. Plasma growth hormone rose to 94 +/- 19 mU/l, and during blockade with phentolamine the response was significantly reduced reaching a peak of 34 +/- 7 mU/l (by analysis of variance, p less than 0.05). ACTH and prolactin both increased in response to hypoglycemia, but the increases were not affected by phentolamine. An alpha-adrenergic mechanism appears to inhibit the release of arginine vasopressin and oxytocin in response to hypoglycemia, but does not appear to affect the secretion of ACTH.
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PMID:Effect of alpha-adrenergic blockade on pituitary hormonal responses to insulin-induced hypoglycemia in humans. 168 2

Plasma prolactin and rectal temperature show a circadian rhythm in newborn sheep raised under continuous light. Melatonin lowers the concentration of plasma prolactin but it is not known if it affects its circadian rhythm. To detect whether melatonin acts on the circadian system we studied the effect of a subcutaneous melatonin implant in the circadian rhythms of prolactin and rectal temperature in newborn lambs raised under continuous light. We placed catheters in the pedal artery and vein in 9 newborn lambs (2-5 days of age). A subcutaneous melatonin implant was placed in 4 of the lambs at 9-12 days of age. Blood samples and rectal temperature measurements were obtained hourly for a period of 24 h, 11-15 days after the implant, at 20-27 days of age. To avoid interferences of heparin in our melatonin assay, serum melatonin concentration was measured before and during the implant in three additional newborns. Prolactin and melatonin were measured by RIA. Melatonin concentrations were 52.8 +/- 45.9 pg/ml (day) and 315.5 +/- 77.0 pg/ml (night) before treatment (SEM, P less than 0.001), and increased to 594.1 +/- 54.5 pg/ml after placing the implant (there was no difference in melatonin concentration between day and night during the time that the implant was in place). Melatonin had no effect on rectal temperature or its rhythm, but decreased basal plasma prolactin concentration (control: 97.5 +/- 11.3 ng/ml; treated: 25.1 +/- 2.4 ng/ml, P less than 0.001) and abolished the prolactin circadian rhythm, (Cosinor analysis): control: log prolactin (ng/ml) = 1.8 + 0.26 cos 15 (t - 11.16), p = 0.05; treated: log prolactin (ng/ml) = 1.2 + 0.14 cos 15 (t - 9.43), P = 0.36.
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PMID:Effect of a melatonin implant on the circadian variation of plasma prolactin and rectal temperature in newborn sheep. 178 66

In this prospective multicenter trial, 61 patients presenting with a macroprolactinoma were studied over a 1 month-period following a single 50 mg intragluteal injection of the long-acting repeatable (L.A.R.) form of bromocriptine. The effects of the drug were evaluated mainly by repetitive plasma prolactin measurements on days 1, 3, 7, 14 and 28 after injection, and by repeated visual-field and computed tomography scanning examinations. Normalization of PRL levels was obtained in 23% of patients during the first month following injection. In 6 patients (9.8%), PRL values remained within normal range on day 28 after injection. In these latter patients, PRL levels were significantly lower than in the patients whose PRL values were not normal on day 28 (312 +/- 111 vs 2454 +/- 484 ng/ml [m +/- SEM]). The mean lowest PRL levels were achieved on day 3. The mean percent maximal decrease in PRL levels ranged between 70 and 72% from days 3 to 14 but constantly remained below 50% in 6 patients. An improvement in visual field was observed by day 7 in 45% of patients presenting initially with visual field defects. In particular, in half of the patients with bilateral quadranopsia or hemianopsia, such visual impairments had disappeared after 1 month of treatment. Computed tomography scanning examinations showed in 11% of the patients a more than 20% reduction in tumor mass by day 7 following injection. On day 28, the percent reduction in tumor size was 20-40% in 28% and above 40% in 10% of the patients. Most adverse effects (digestive symptoms, dizziness, postural hypotension) were observed during the first 24 hours of treatment. Local and systemic tolerability was in general good. In macroprolactinoma patients, a single 50 mg injection of bromocriptine LAR was thus able to achieve in the short-term a clear cut reduction in tumor size in 2/5 patients and normalization of PRL levels in 1/10 of patients. A study of the effects of monthly administration of bromocriptine LAR is currently under progress to assess the long-term efficacy of this drug.
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PMID:[Short-term effect of delayed-action injectable bromocriptine in macroprolactinoma. French multicenter study]. 181 31

We determined the effect of 13 days of treatment with 2.0 mg/kg haloperidol, 30.0 mg/kg metoclopramide or 4.0 mg/kg domperidone on the number of tumor cells of mice bearing Ehrlich ascites carcinoma. The three dopaminergic blockers significantly reduced the number of tumor cells of experimental mice. The mean +/- SEM number of tumor cells x 10(6)/ml saline lavage was 25.5 +/- 5.9 for the haloperidol group, 36.8 +/- 4.7 for the metoclopramide group, 25.3 +/- 3.5 for the domperidone group and 54.0 +/- 9.0 for the control mice (treated with 0.9% NaCl). In a second experiment, treatment with 0.5 and 2.0 mg/kg haloperidol showed that the antitumor effect of this drug was dose dependent. The possible mechanisms underlying these results (such as an increase in prolactin levels or a direct action of these drugs on lymphocytes) are discussed in light of the specific pharmacological properties of each dopaminergic blocker.
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PMID:Antitumor effects of dopaminergic blockers in mice bearing Ehrlich tumors. 182 79

Seasonally anestrous Suffolk ewes (n = 28) were randomly divided into 5 groups and treated with varying doses of melatonin as follows; Groups C (n = 4), M1 (n = 6), M2 (n = 6), M3 (n = 6), M4 (n = 6) of ewes were fed pellets containing 0, 1, 2, 3 and 4 mg melatonin, respectively, daily for 60 days from May 17 (Day 0). Following feeding of the pellets at 13.00 hr plasma levels of melatonin rapidly increased reaching the peak values within 30 min, which ranged from 92.0 to 292.7 pg/ml and were highly correlated with the dose of melatonin administered (r = 0.986, P less than 0.01). Maximum dose of melatonin (4 mg) produced an increase of plasma melatonin similar in magnitude to nocturnal peaks of endogenous secretion. The onset of ovulatory cyclicity, assessed from plasma progesterone profiles, was advanced by melatonin administration. The mean +/- SEM intervals from the commencement of melatonin treatment until the onset of ovulatory cyclicity were 53.0 +/- 5.8, 53.6 +/- 2.5, 42.0 +/- 5.6 and 44.3 +/- 4.3 days for the Groups M1, M2, M3 and M4, respectively, which were shorter (M1, P less than 0.05; M2, M3 & M4, P less than 0.01) than that for the Group C (72.5 +/- 1.4 days). The melatonin treatment also suppressed, in a dose related manner, the rise in plasma prolactin under the lengthening photoperiod. We conclude that the dose-related efficacy of melatonin could be ascribed to the difference in the diurnal profiles of circulating melatonin.
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PMID:Diurnal changes in plasma melatonin and the timing of reproductive onset in anestrous sheep fed melatonin. 183 33


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