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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several pieces of evidence suggest the existence of a relationship between neuroendocrine and immune systems. Prolactin (PRL) has been demonstrated to modulate some immune responses and its influence seems to be permissive or inhibitory depending on its concentration. Previous studies have reported a reduced natural killer (NK) cell function in patients with hyperprolactinemia. In 36 patients (34 females and 2 males, aged 14-46 years) with hyperprolactinemia (mean +/- SEM PRL 142.2 +/- 42.1 micrograms/l) of tumorous (19 patients) and functional (17 patients) origins, NK activity of peripheral blood lymphocytes (PBL) was studied. Patients had NK cell activity against the K562 cell line which did not differ from that of lymphocytes from 36 age- and sex-matched healthy donors (mean +/- SEM lytic units (LU) 619.0 +/- 103.0 and 531.9 +/- 52.6 respectively). No correlation between PRL levels and LU values was found (r = 0.28). When patients with tumors or functional hyperprolactinemia were separately analysed no difference was found between these two groups (mean +/- SEM LU 690.0 +/- 117.7 vs. 606.0 +/- 148.8). In conclusion, our data demonstrate that neither the elevated PRL levels nor the PRL-secreting tumor per se interfere with the NK system of hyperprolactinemic patients.
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PMID:Natural killer activity in hyperprolactinemic patients. 280 74

Prolactin levels were measured by radioimmunoassay in paired breast milk and plasma samples of 11 hyperprolactinemic women with galactorrhea and various menstrual disorders (amenorrhea, n = 8; oligomenorrhea, n = 2; luteal phase defect, n = 1) before and during treatment with bromocriptine (Parlodel, Sandoz). Pretreatment levels of prolactin in the milk and plasma were 80 +/- 13 ng/mL (mean +/- SEM) and 47 +/- 7 ng/mL (P less than 0.05), respectively. While on treatment, the concentration gradient for prolactin remained in favour of the milk, with values for milk and plasma 59 +/- 11 and 29 +/- 3 ng/mL (P less than 0.01), respectively. Thus, bromocriptine lowered the prolactin concentrations in both breast milk and plasma. Since prolactin in milk is biologically active, these findings may be relevant to the initiation and maintenance of lactation in women with abnormal lactogenesis.
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PMID:Immunoreactive prolactin in breast milk and plasma of women with hyperprolactinemia, galactorrhea and menstrual dysfunction. 290 79

Prolactin-secreting pituitary adenomas were selectively removed through a transsphenoidal approach from 120 women. Basal serum PRL levels (measured one to six months after surgery) were normal in 96 patients and decreased appreciably but not to normal in the remaining 24 patients. Dynamics of PRL secretion were studied at three to four months in 81 patients who had normal basal PRL level. Two different patterns of response to provocative stimuli were noted in these patients. In one group (group I, n = 65), patients had greater than 100% rise in serum PRL following TRH or perphenazine (Pz) administration. However, when analyzed as a group, the mean +/- SEM incremental responses (delta PRL) to TRH and Pz in these patients (29.9 +/- 1.9, 20.4 +/- 1.5 ng/mL) were significantly less (P less than 0.005 and P less than 0.001) than those of normal women (38.8 +/- 5, 33 +/- 5 ng/mL, respectively). Nineteen of these patients were restudied 12 to 72 months after surgery. The responses to provocative stimulation at that time were improved and similar to normal women. In contrast, in the second group (n = 16) of patients (group II), the responses to stimulation with the same agents were blunted or absent and remained so during subsequent studies. Recurrence of the hyperprolactinemia was noted in 11 of the 16 patients in group II and in only two of 65 patients in group I. The daily serum PRL levels in the immediate postoperative period were higher in patients from group II than those from group I. We conclude that transsphenoidal surgery is an optimal form of therapy for patients with PRL-secreting adenomas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gradual recovery of lactotroph responsiveness to dynamic stimulation following surgical removal of prolactinomas: long-term follow-up studies. 309 97

The concentrations of prolactin in the milk of nine postpartum lactating mothers were determined by radioimmunoassay between days 3 to 280 of the puerperium (n = 324 samples). In addition, prolactin in milk was also determined at the beginning and the end of suckling in three of the same women, who provided 21 paired samples of foremilk and hindmilk between days 7 and 88 of the puerperium. Prolactin content was highest at 43.1 +/- 4 ng/ml (mean +/- SEM) in the early transition milk immediately after the colostrum phase during the first postpartum week, decreasing to 11.0 +/- 1.4 ng/ml in the mature milk (p less than 0.01) when weaning occurred in those mothers who breastfed for up to 40 weeks post partum. During suckling, the foremilk contained significantly more prolactin as compared with the hindmilk (29.5 +/- 2.7 versus 21.0 +/- 3.2 ng/ml; p less than 0.01). These findings, taken together with the known biologic potency of prolactin in breast milk, the osmoregulatory influence of the hormone in mammary and intestinal function, and its absorption by the newborn experimental animal, suggest that the presence of prolactin in milk may play some role in both lactation and the intestinal absorptive function of the suckling newborn.
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PMID:Prolactin in human milk: the influence of nursing and the duration of postpartum lactation. 334 20

Prolactin secretion and biological activity have been investigated in 20 females with persistent idiopathic galactorrhoea who had normal resting serum prolactin levels at presentation. Results were compared with those in 34 normal controls. Hyperprolactinaemia, which was persistent in one and intermittent in the other, developed in two patients over an observation period of 1.5 to 8.5 years. Resting prolactin levels stayed normal in the remaining eighteen who were further investigated. Menstruation was disordered in only six of the 18, while ovulation occurred (serum progesterone greater than 20 nmol/l) in all seven patients who were studied over a 5 week period. Serum prolactin concentrations over 24 h were similar in patients and controls (24 h mean +/- SEM prolactin, 288 +/- 36 mU/l, patients, n = 7; 291 +/- 21 mU/l, controls, n = 9) as were prolactin levels estimated twice weekly for 5 weeks. Prolactin responses to thyrotrophin-releasing hormone, 200 micrograms (at 20 min, 2417 +/- 658 mU/l, patients, n = 7; 2113 +/- 424 mU/l, controls, n = 8), the dopamine antagonist, domperidone, 10 mg (at 30 min, 5949 +/- 536 mU/l, patients, n = 7; 5858 +/- 460 mU/l, controls, n = 8) and insulin-induced hypoglycaemia (at 60 min, 1441 +/- 551 mU/l, patients, n = 7; 1298 +/- 183 mU/l, controls, n = 7) were similar in patients and controls. Two different radioimmunoassays using two different antisera gave similar estimates of serum prolactin levels and prolactin bioactivity in serum was normal in an in-vitro bioassay based on the ability of prolactin to stimulate proliferation of Nb2 node rat lymphoma cells (basal bioassayable prolactin, patients 355 +/- 43 mU/l, n = 10; controls 348 +/- 64 mU/l, n = 7). Metabolic abnormalities similar to those previously noted in hyperprolactinaemia were observed in the patients' 24 h profiles. These included mild hyperglycaemia (24 h mean +/- SEM glucose, 5.47 +/- 0.08 mmol/l, patients; 5.05 +/- 0.14 mmol/l, controls; P less than 0.05) and elevations in circulating lactate, pyruvate and alanine. Blood glycerol was decreased (24 h mean +/- SEM, 0.044 +/- 0.004 versus 0.058 +/- 0.004 mmol/l, P less than 0.05). In the majority of patients with idiopathic galactorrhoea, prolactin concentrations, regulation of secretion and bioactivity in vitro are normal. The galactorrhoea and metabolic abnormalities suggest increased tissue sensitivity to the lactogenic and metabolic actions of prolactin, while ovarian cyclical function is relatively spared.
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PMID:Prolactin secretion and biological activity in females with galactorrhoea and normal circulating prolactin concentrations at rest. 392 10

This study was performed to establish the dynamics of human chorionic gonadotropin, prolactin, and growth hormone throughout pregnancy in serum and amniotic fluid. Two hundred fifty healthy women at 8 to 42 weeks' gestation were studied. The highest serum human chorionic gonadotropin level was measured between weeks 8 to 12 (53,715 +/- 3574 mIU/ml, mean +/- SEM), with a decline to a mean plateau of 11,806 +/- 1250 mIU/ml from week 18. Amniotic fluid human chorionic gonadotropin had a similar pattern with a mean of 68,100 +/- 8422 mIU/ml at weeks 8 to 10, declining from week 18 to a plateau of 2005 +/- 260 mIU/ml. Human chorionic gonadotropin showed a significant correlation (r = 0.85, p less than 0.001) between levels of both compartments demonstrating an even distribution. Prolactin levels showed a dichotomy of patterns and levels. Serum prolactin showed a continuous rise from 45.3 +/- 14 ng/ml at week 8 to 224 +/- 20 ng/ml at week 36. In contrast, amniotic fluid prolactin remained low until week 14 (33.1 +/- 0.8 ng/ml), followed by a sharp and significant (p less than 0.001) increase to a plateau of 3750 +/- 200 ng/ml between weeks 18 to 26, declining to a second plateau of 500 +/- 50 ng/ml at week 36. Serum growth hormone increased from a mean of 3.5 +/- 1.4 ng/ml seen at weeks 8 to 10 to a mean of 14 +/- 2.0 ng/ml at weeks 28 to 30, followed by a plateau of similar levels. The pattern of growth hormone secretion in amniotic fluid demonstrated a sharp increase during the 14-16 interval with a maximum mean level of 15.5 +/- 1.5 ng/ml and a slow steady decline thereafter. In conclusion, the similar pattern and concentration of human chorionic gonadotropin throughout pregnancy in both maternal and amniotic fluid are probably the result of direct human chorionic gonadotropin diffusion from the placenta. The dissimilar pattern and concentration of prolactin are the result of two different sources of prolactin secretion during pregnancy. Serum prolactin originates from the pituitary and amniotic fluid prolactin from the decidua. Since the pattern of growth hormone secretion resembles that of prolactin, it is possible that growth hormone, like prolactin, is secreted by the same sources.
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PMID:Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy. 398 54

Temporal changes of circulating serum hormones were measured to compare the reproductive endocrinology of laying and nonlaying mallards. In this study all sixteen control mallards left with their mates laid eggs, while only one of sixteen mallards stressed by daily movement into new pens, laid eggs. Serum levels of luteinizing hormone (LH), prolactin, estradiol, and progesterone were significantly lower (P less than 0.05) in stressed nonlaying mallards than in laying mallards over the 7-week period. Within 1 week of the rotation treatment, LH concentrations in stressed mallards averaged (means +/- SEM) 2.72 +/- 0.19 ng/ml and were significantly lower (P less than 0.05) than LH levels in the controls (3.62 +/- 0.18 ng/ml). After 7 weeks, injections of luteinizing hormone releasing hormone (LHRH) induced a greater change in circulating LH levels in stressed mallards (2.1 +/- 0.3 ng/ml) than in breeding control mallards (0.9 +/- 0.2 ng/ml). These data demonstrate that the lack of reproduction in stressed mallards was associated with LHRH-sensitive pituitary pools of LH, despite their low concentrations of serum LH. These data suggest that the block in reproduction is a failure of the hypothalamus to produce or release releasing hormones. The serum hormone levels of the control mallards varied temporally with stages in the nesting cycle. LH levels increased with the onset of nesting activity, and showed marked fluctuations during the laying period. LH levels fell at the onset of incubation but increased after loss of clutch. Estradiol levels were highest prior to the laying of the first egg and their peak coincided with the initial nest building behavior of the females. Progesterone levels increased sharply with the laying of the 2nd-4th eggs, decreased sharply with the laying of the 6th egg, and then increased slightly at the end of the nesting cycle. Prolactin levels were initially low but gradually increased with laying and incubation activity, declined with loss of clutch, and increased again with renesting activity. Prolactin levels in the stressed mallards also increased (P less than 0.01) over the 7-week period, but significantly less (P less than 0.05) than in layers.
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PMID:Serum levels of luteinizing hormone, prolactin, estradiol and progesterone in laying and nonlaying mallards (Anas platyrhynchos). 634 Jul 45

Prolactin (PRL) synthesis and its release following thyrotropin-releasing hormone (TRH) administration during pregnancy and puerperium was studied in 45 women. Mean baseline E2 increased from 1,900 +/- 384 (SEM) pg/ml in the first trimester to 3,520 +/- 849 in the second trimester (P less than 0.05) and 43,057 +/- 5,765 pg/ml in the third trimester (P less than 0.001) of pregnancy. Mean baseline progesterone increased from 27.6 +/- 3.2 ng/ml in the first trimester to 41.9 +/- 6.6 in the second trimester (P less than 0.01) and 109.3 +/- 11.2 ng/ml in the third trimester (P less than 0.001) of pregnancy. Ten days after delivery, mean E2 dropped to 13 +/- 2.9 pg/ml and progesterone dropped to 0.56 +/- 0.07 ng/ml in the lactating women; in the nonlactating women, mean E2 level was 100 +/- 44 pg/ml and mean progesterone was 0.63 +/- 0.09 ng/ml. Baseline PRL increased from 27 +/- 15 ng/ml in the third trimester (P less than 0.002). The increased synthesis of PRL with increasing gestation was thought to be due to the stimulatory effects of E2 and progesterone, resulting in hyperplasia of the lactotrophs. In response to TRH, PRL demonstrated a significant increase from the first trimester to the second, with no further increase in the third. Therefore, it appears that the PRL reserve increases only during the first and second trimesters of pregnancy. Ten days after delivery, baseline PRL in response to TRH decreased to levels found in the first and second trimesters. However, the lactating women released less PRL than the nonlactating subjects (P less than 0.01), since PRL is released with each lactating episode which in turn probably reduces the PRL reserve.
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PMID:Prolactin synthesis and release during pregnancy and puerperium. 676 68

Seventeen infertile normoprolactinemic women with luteal phase defects were treated with epimestrol. In ten patients, normalization of the impaired luteal phase was achieved. Under epimestrol treatment, periovulatory estradiol concentrations (1077.3 +/- 121.5 pmoles/liter versus 612.7 +/- 64.2 pmoles/liter; mean +/- SEM; P < 0.01) and cervical scores (10.8 +/- 0.3 versus 7.9 +/- 0.38; mean +/- SEM; P < 0.01) were improved, and luteal progesterone (60.0 +/- 9.1 nmoles/liter versus 19.98 +/- 3.14 nmoles/liter; mean +/- SEM; P < 0.001) and estradiol secretioon (813.1 +/- 101.1 pmoles/liter versus 581.9 +/- 73.7 pmoles/liter; mean +/- SEM; P < 0.05) were significantly increased in those women with normalization of the luteal phase as compared with the seven patients in whom epimesterol was without effect. Prolactin levels were elevated in all patients after epimestrol therapy (P < 0.05). Basal LH levels and LH-RH stimulated levels improved following administration of epimestrol (P < 0.01) in the 10 women with normal luteal phases. FSH levels were not significantly affected. Two patients became pregnant. No side effects were noted.
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PMID:Epimestrol in treatment of inadequate luteal progesterone secretion. 677 95

The serum prolactin response to acute hypercalcemia during calcium infusion was studied in 7 normal subjects. Prolactin, and calcium levels were determined at 30 minute intervals during the 210 minutes of the infusion. The infusion performed consisted of either normal saline at 3 ml/min for 210 minutes, or 15 mg calcium/kg at 3 ml/min for 180 minutes followed by normal saline infusion for the final 30 minutes. Calcium concentration increased from a base line of 10.0 +/- 0.26 (mean +/- SEM) to a maximal level of 13.6 +/- 0.26 (mean +/- SEM) mg/100 ml, in response to calcium level in response to normal saline infusion. Prolactin level decreased significantly (P less than 0.05) from 9.5 +/- 1.45 (mean +/- SEM) to 3.7 +/- 0.2 (mean +/- SEM) ng/ml at 180 minutes.
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PMID:The effect of acute hypercalcemia on prolactin release in man. 726 25


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