Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 30 normal subjects, the mean (+/- SEM) plasma concentration of PRL was 5.90 +/- 0.40 ng/ml and that of PTH was 0.51 +/- 0.03 ng/ml. There was no significant difference in plasma hormone levels according to age or sex. Ten cases of primary hyperparathyroidism showed PRL concentrations (8.90 +/- 1.80 ng/ml) significantly (P less than 0.01) higher than those of the normal subjects. After adenomectomy, the PRL concentration decreased (5.35 +/- 0.50 ng/ml). However, this decrease was only significant in the 5 of 10 patients who had preoperative plasma PRL levels of 10 ng/ml or more (P less than 0.01). The increase in PRL concentration in 10 cases of secondary hyperparathyroidism with normal glomerular function was also significant (14.25 +/- 3.9 ng/ml; P less than 0.001). Fourteen patients with prolactinoma showed PTH plasma levels (1.25 +/- 0.15 ng/ml) significantly higher than those of normal subjects (P less than 0.001). Eight of the 14 patients received 7.5 mg/24 h of bromocriptine for 3 months; their mean plasma PTH level decreased significantly from 1.60 +/- 0.35 to 0.50 +/- 0.11 ng/ml (P less than 0.01). In 9 cases of secondary hyperprolactinemia, the increase in PTH (0.80 +/- 0.16 ng/ml) was significant compared to the plasma PTH levels in the normal group (P less than 0.05). These results show that an excess of plasma PRL is associated with an excess of plasma PTH and vice versa. The mechanisms of these relationships remain unclear.
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PMID:Comparison between the plasma concentrations of prolactin and parathyroid hormone in normal subjects and in patients with hyperparathyroidism or hyperprolactinemia. 713 Mar 42

It has been reported that administration of nomifensine (Nom) or of L-dopa + carbidopa (L-dopa + Carb) potentiates central dopaminergic tonus, resulting in decreased prolactin (PRL) secretion. It has been proposed that these drugs would help to discriminate patients with PRL-secreting pituitary tumours from those with so-called 'functional' hyperprolactinaemia. In this study, oral Nom (200 mg) was given to forty-three hyperprolactinaemic patients and L-dopa + Carb (50 mg Carb every 6 h for four doses followed by L-dopa 100 mg and Carb 35 mg) to thirty of them and both treatment to ten normal subjects. The hyperprolactinaemic patients were divided into four clinical groups. Group A, twenty patients with proven PRL-secreting pituitary tumours; Group B, thirteen women with elevated PRL levels (less than 100 ng/ml) without any radiological evidence of a pituitary tumour (hyperprolactinaemia of unknown aetiology or 'functional' hyperprolactinaemia); Group C, four women with polycystic ovarian disease and mildly elevated serum PRL; Group D, six patients with various other disorders associated with hyperprolactinaemia. PRL levels decreased in the normal controls below the basal values by 61.3% +/- 6.2 (SEM) after Nom and 77.6% +/- 4.2 after L-dopa + Carb. Decreases in serum PRL of at least 50% (in three consecutive determinations) were found in group A in 20% of patients after Nom and in 25% after L-dopa + Carb; in group B in 15% and 40% of cases; in most of the hyperprolactinaemic women in group C; and some in group D. In conclusion, these two treatments did not discriminate between tumorous and non-tumorous cases of PRL hypersecretion.
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PMID:Evaluation of two inhibitory tests (nomifensine and L-dopa + carbidopa) for the diagnosis of hyperprolactinaemic states. 722 70

Experiments have been carried out in order to clarify to what extent the absence of PRL renal catabolism in experimental renal insufficiency is responsible for the high PRL circulating levels. Furthermore, the relative contribution of the glomerular filtration rate and peritubular degradation to PRL renal clearance have been assessed. Circulating PRL basal levels were measured by RIA in sham-operated and intact control rats and in three uremic rat models: urine autoinfusion, bilateral ureteral ligation, and bilateral nephrectomy. Plasma PRL basal levels (nanograms per ml; mean +/- SEM) were increased in sham-operated rats (30.3 +/- 5.1) with respect to control animals (18.5 +/- 2.7; P less than 0.05). Bilaterally nephrectomized animals (66.4 +/- 16.4) and those with bilateral ureteral ligation (69.3 +/- 15.9) developed similar hyperprolactinemia, in contrast to urine-autoinfused rats (20.2 +/- 2.1; P less than 0.005) whose hormone levels were similar to those of control animals. Creatinine levels were markedly elevated and comparable in the three uremic rat groups. The results suggest that: 1) hyperprolactinemia in rats in acute renal insufficiency is due primarily to reduced renal function; 2) PRL renal catabolism in the rat requires a certain rate of glomerular filtration; and 3) PRL peritubular degradation does not seem to be relevant in PRL catabolism by rat kidney.
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PMID:Pathogenesis of hyperprolactinemia in uremic rats. 722 7

Plasma human prolactin (hPRL) was measured in 73 untreated acromegalic patients and was found to be elevated in 32% of the total population. Hyperprolactinemia was present in 40% of the females and in 27% of the male patients. In both groups, plasma hPRL correlated with plasma human growth hormone (hGH) levels with correlation coefficients of 0.38 (P less than 0.05) for females and 0.41 (P less than 0.005) for males. Forty-five patients were treated with conventional supervoltage pituitary irradiation and evaluated 2, 5, and 10 yr after treatment. The patients with hyperprolactinemia before irradiation showed a decrease in plasma hPRL at the most recent follow-up (mean +/- SEM, 125 +/- 34 vs. 67 +/- 15 ng/ml; P less than 0.01), although, in general, they did not achieve normal values. The patients who had normal plasma hPRL before irradiation (mean +/- SEM, 14 +/- 2 ng/ml) had increased levels after therapy (23 +/- ng/ml; P less than 0.005) but remained in the normal range during long term follow-up. In 10 patients followed for 1-10 yr without treatment, there was a tendency for plasma hPRL to rise progressively (mean increment, 122% above the initial value), with individual changes in hPRL strikingly parallel to the changes in plasma hGH. When serum hPRL was initially elevated, similar responses in both hormones were also seen in a small group of patients treated with surgical hypophysectomy. Galactorrhea was present in 5 of the 25 female patients; in 4 of the 5, plasma hPRL was within the normal range. Overall, these data suggest a closer relationship between hGH and hPRL in acromegaly than had been suspected, not only at the level of pituitary secretion but possibly also at the target cell.
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PMID:Plasma prolactin in acromegaly before and after treatment. 725 17

Hyperprolactinaemia may be associated with functional amenorrhoea. In order to evaluate the possible role of abnormal spontaneous LH secretion in hyperprolactinaemic amenorrhoeic women, plasma LH was measured at 15 min intervals for 300 min in 12 normal women during the early follicular phase of the menstrual cycle and compared to that observed in 11 hyperprolactinaemic amenorrhoeic subjects. Mean plasma prolactin was 9.1 +/- 3.6 ng/ml (X +/- SEM) in the euprolactinaemic and 168 +/- 32 ng/ml in the hyperprolactinaemic group. Sex steroids including oestrone, oestradiol, progesterone and 17-hydroxyprogesterone were similar in the 2 groups. Mean plasma LH levels over the 300 min sampling period were 9.4 +/- 1.6 mIU/ml in the normal subjects and 7.5 +/- 1.0 mIU/ml in the hyperprolactinaemic patients (P greater than 0.10). Every normal woman exhibited at least one LH spike in excess of 10 mIU/ml. Five hyperprolactinaemic patients failed to exhibit any LH spikes above 10 mIU/ml (P less than 0.02 compared to controls). Thus, hyperprolactinaemia was associated with an absence of LH spike activity in 45% of patients studied and this abnormality may play an aetiologic role in the hypogonadism observed in these subjects; in those hyperprolactinaemic subjects with pulsatile LH secretion, however, other explanations for their amenorrhoea should be considered.
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PMID:Patterns of spontaneous LH release in normo- and hyperprolactinaemic women. 725 98

In six patients with "empty sella" syndrome (ESS), three primary (pESS) and three secndary (sESS), the ratio of serum to cerebrospinal fluid (CSF) concentrations of prolactin (PRL) was 6.6 +/- 0.7 (mean +/- SEM) (range 5.5--9.6), with a significant correlation between serum and CSF levels of PRL (r = 0.93 p less than 0.01). A control group of ten normal subjects showed similar values. The hyperprolactinemia found in two cases of pESS did not change the serum/ CSF ratio of PRL. The acute release of PRL into the serum following TRH i.v. did not increase the PRL level in CSF either in control subjects or ESS, with one exception. In a case of sESS consecutive to the treatment with bromocriptine (for 6 months) of an invasive prolactinoma, TRH i. v. released PRL into the CSF but not into the blood, and the serum/ CSF ratio of PRL was very low, until a new cure with bromocriptine (for 3 months) mormalised it. It is suggested that the blood-CSF barrier for PRL is similar in ESS and in normal subjects, with the exception of sESS following incomplete remission of some invasive prolactinomas, in which the high permeability of BCB may be explained both by hemodynamic changes in the pituitary portal vascular system and by a new source of PRL which release it directly into the CSF, bypassing the blood route.
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PMID:Blood-cerebrospinal fluid barrier for prolactin in empty sella syndrome. 729 47

The effect of 100 mg im sulpiride on plasma Prl levels was studied in 10 normal females, 21 patients with galactorrhoea and normal plasma Prl, 10 women with puerperal hyperprolactinaemia and 27 patients with amenorrhoea-galactorrhoea and high plasma Prl levels. The response to sulpiride in patients with galactorrhoea but normal PRL was slightly higher (P < 0.05) than that observed in normal women, but only if expressed in per cent. Women with puerperal hyperprolactinaemia respond to the drug with a marked increase in Prl (mean +/- SEM: 563.0 +/- 142.8%), even though their baseline values are already very high (mean +/- SEM: 133.6 +/- 23.8 ng/ml). By contrast, there is a lower or no response to sulpiride in 13 women with pituitary tumour. The same was true in 11 patients with hyperprolactinaemia of uncertain aetiology but also 10 of these subjects presented signs suggestive of a tumour. In the last 3 patients with pathological hyperprolactinaemia in whom a consistent Prl increase after sulpiride was observed, hyperprolactinaemia was probably not of tumourous origin. On the basis of these results, the sulpiride test appears promising for discriminating between organic and 'functional' cases of enhanced Prl secretion.
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PMID:Effect of sulpiride on plasma prolactin levels in women with puerperal or pathological hyperprolactinaemia. 743 13

The effects of the intravenous administration of a calcium channel blocker, verapamil (0.0833 mg/min for 2-3 h after a 5 mg bolus) on prolactin (PRL) and thyrotropin (TSH) circulating levels were assessed in 7 normal subjects and in 17 patients with hyperprolactinemia (11 with prolactinoma and 6 sulpriride-induced). In the normal group a non-significant increase in PRL levels occurred (mean +/- SEM = 11.7 +/- 2.9 micrograms/l verapamil vs. 8.5 +/- 1.4 micrograms/l saline). In this control group the peak response of PRL and TSH to TRH (thyrotrophin releasing hormone) during verapamil or saline was also determined: PRL = 112.0 +/- 27.0 micrograms/l on verapamil vs. 53.6 micrograms/l on saline, p = 0.02; TSH 7.1 +/- 0.7 microU/l on verapamil vs. 9.0 +/- 0.6 mU/l on saline, p = 0.01. In the hyperprolactinemic subjects verapamil induced opposite effects on PRL levels, the prolactinoma group exhibiting an increase in the mean values (168.5 +/- 22.3 micrograms/l vs. 150.8 +/- 23.6 micrograms/l on saline, p = 0.04) whereas in the sulpiride-induced there was a reduction in the mean PRL levels (61.1 +/- 13.8 micrograms/l vs. 78.5 +/- 19.3 micrograms/l on saline, p = 0.002). In both groups of hyperprolactinemic patients no effects on TSH levels were observed. The authors discuss the possibility that the divergent effects of verapamil in hyperprolactinemia of different etiologies could be related to the balance between dopamine and calcium channel effects on hypothalamus and/or pituitary.
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PMID:Calcium and prolactin secretion in humans: effects of the channel blocker, verapamil, in the spontaneous and drug-induced hyperprolactinemia. 785 73

Somatuline, in common with other SRIH analogues, exerts antiproliferative and antisecretory activities on various tumors. Our purpose was to test the effectiveness of a slow-release formulation of somatuline on lactotroph hyperplasia and PRL hypersecretion induced by estrogens (17 beta E2) in rats. Female rats were primed with 17 beta E2 for 6 weeks before receiving somatuline (2 mg/kg) intramuscular injections every 10 days for one month. The mean anterior pituitary weight was 11.22 +/- 0.32 mg (mean +/- SEM) in non-estrogenized rats, 29.62 +/- 1.63 mg in 17 beta E2-primed rats and 23.58 +/- 1.26 mg in 17 beta E2-primed somatuline-treated rats. Mean plasma PRL level was 5.63 +/- 0.97 ng/ml, 182.37 +/- 27.55 ng/ml and 113.89 +/- 15.07 ng/ml in the same groups respectively. Thus, the 17 beta E2-induced pituitary enlargement and hyperprolactinemia were 20% and 38% lower respectively when animals were treated with somatuline during the last month of estrogenization. The 17 beta E2-induced increase in PRL cell density was also reduced by somatuline treatment. We conclude that the slow-release formulation of somatuline impedes 17 beta E2-induced hyperprolactinemia and pituitary enlargement concomittantly, at least in part by acting on lactotroph proliferation.
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PMID:Effect of the slow-release formulation of somatuline (BIM 23014) on estrogen-induced hyperprolactinemia and lactotroph hyperplasia in the female rat. 793 26

Both growth hormone (GH) and prolactin (PRL) modulate immune responses in vitro. We studied chemotaxis under agarose of polymorphonuclear cells from patients with acromegaly or hyperprolactinemia. Polymorphonuclear cells were purified by dextran sedimentation and subjected to stimulation with N-formylmethionyl-phenylalanine. The results showed a decrease in both directed migration (acromegaly: 971 +/- 155 microns; hyperprolactinemia: 1123 +/- 137 microns, expressed as mean +/- SEM) and spontaneous migration (acromegaly: 270 +/- 77 microns; hyperprolactinemia: 298 +/- 77 microns) when compared to similar features from normal controls (directed migration: 2019 +/- 99 microns; spontaneous migration: 590 +/- 49 microns) and from patients with non-GH/PRL-secreting pituitary tumours (directed migration: 1633 +/- 282 microns; spontaneous migration: 562 +/- 116 microns), suggesting that this defect is selective for acromegaly and hyperprolactinemia. Our results point to a putative direct or indirect effect of GH and PRL on polymorphonuclear cell chemotaxis.
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PMID:Decreased chemotaxis of neutrophils in acromegaly and hyperprolactinemia. 818 Jun 73


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