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Obesity and osteoporosis seem to have a common pathogenesis, especially because bone and adipose tissue have common origins. Since early weaning (EW) decreases adipogenesis and osteogenesis in neonate, further programming for obesity and hyperleptinemia, we hypothesized that these changes in adipogenesis could affect bone metabolism.
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Caffeine and its first-stage metabolites (paraxanthine, theophylline and theobromine) caused a significant potentiation of the locomotor activity induced by bromocriptine, 5 mg/kg, in mice pretreated with reserpine, 5 mg/kg (4h prior to the start of motor activity recordings). None of these substances significantly enhanced locomotor activity in reserpinized mice when administered alone. The rank order of potency was caffeine greater than paraxanthine greater than theophylline greater than theobromine. A high dose of a D-2 antagonist (sulpiride 100 mg/kg) caused a marked inhibition of the locomotor activity induced by bromocriptine, 5 mg/kg, plus 25 mg/kg of caffeine, paraxanthine or theophylline. However, a high dose of a D-1 antagonist (SCH-23390 1 mg/kg) caused a significant decrease of the locomotor activity induced by bromocriptine 5 mg/kg, plus 25 mg/kg of caffeine or paraxanthine, but did not change the locomotor activity caused by bromocriptine, 5 mg/kg, plus theophylline 25 mg/kg. The inhibitory effect of 5'-(N-ethyl)carboxamido-adenosine (NECA), 0.025 mg/kg, on bromocriptine-induced locomotor activation in reserpinized mice was reversed by the simultaneous administration of 10, 25 and 50 mg/kg of caffeine, paraxanthine or theophylline. The rank order of potency for reversal was theophylline greater than paraxanthine = caffeine. We suggest that methylxanthines act postsynaptically by potentiating the effects of D-2 stimulation and that this potentiation can be produced by D-1 agonism (paraxanthine or caffeine) and by adenosine antagonism (theophylline, paraxanthine or caffeine), most probably involving A-2 receptors.
We present the case of a 42-year-old male with a history of schizophrenia who developed signs and symptoms consistent with Neuroleptic Malignant Syndrome (NMS) after 3 weeks of treatment with Olanzapine. The patient presented with hyperpyrexia, tremors, labile blood pressure, and mental status changes that had progressed over the preceding 24 h. Laboratory data revealed a metabolic acidosis and an escalating creatinine phosphokinase. Olanzapine is a relatively new atypical anti-psychotic agent first introduced in November of 1996 under the trade name of zyprexa. Olanzapine differs from typical anti-psychotic agents in that it has a lower affinity for dopaminergic receptors and binds antagonistically to serotonin receptors in the nigrostriatal pathway. These unique properties result in relatively fewer extra-pyramidal symptoms when compared to traditional anti-psychotics. Because of olanzapine's favorable side-effect profile, it has quickly gained popularity in the psychiatric community. Although NMS is a recognized complication of anti-psychotic use, there has been only one case of olanzapine induced NMS reported in the literature. The POISON-INDEX system, used by toxicologists throughout the United States, does not list NMS as a potential reaction to olanzapine. The pharmacists at our institution were also unaware that NMS was a possible complication of olanzapine. We present this case to make clinicians aware of the potential for Olanzapine induced NMS.
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To study the effects of dopamin receptors-2 (DR2) on myocardial ischemic postconditioning and explore its underlying mechanisms.
Dopamine agonist therapy using selected drugs at particular dosage levels has been found to have therapeutic benefit in certain dyskinetic syndromes. Two ergot derivatives with dopamine agonist properties were administered at relatively low doses to eight neuroleptic-free schizophrenic patients with tardive dyskinesia. Neither agent significantly improved dyskinetic symptoms; no symptoms worsened. Dopamine agonists likely vary in their selective activation of functionally distinct dopamine receptors.
Data from 80 patients with IPs treated in our institutions were reviewed retrospectively. The criteria utilized included: (1) invasion of the cavernous sinus by tumor, corresponding to Grade III-IV according to the classification of Knosp; (2) serum prolactin level > 9.1 nmol/L; (3) clinical signs of hyperprolactinemia and mass effect. Among the 80 patients who met the criteria: 21 patients received bromocriptine as primary treatment (Group A); 21 patients initially received bromocriptine and then accepted microsurgery or irradiation (Group B); 38 patients had initially undergone transcranial or transsphenoidal microsurgery and then received bromocriptine or adjuvant radiotherapy (Group C). Eleven patients underwent gamma knife radiotherapy.
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Pituitary adenomas are benign intracranial endocrine tumors, accounting for ~10% of intracranial tumors. The aim of the present study was to analyze the effects of preoperative treatment with bromocriptine on the surgical treatment and postoperative complications of prolactin-secreting pituitary adenomas (prolactinomas). Data from 102 patients whose prolactinomas were surgically treated between March 2006 and March 2010 were retrospectively reviewed in the present study. The study group included 54 patients who had been treated preoperatively with bromocriptine. The patients were examined by magnetic resonance imaging (MRI) of the head and coronal computed tomography (CT) scanning, after which the pathological diagnosis of prolactinoma was confirmed. A total of 64 patients underwent total resection surgery through the nose and sphenoid sinus, and 25 patients underwent subtotal resection surgery or excision of a large portion of the tumor, leaving only a small quantity of residual tumor or tumor capsule. Patients were followed up for 1-9 months using MRI and measurements of serum prolactin levels. Seven patients were lost to follow-up. The results of the present study demonstrated that patients who were treated with large doses of bromocriptine or used bromocriptine chronically suffered from an increased rate of surgical difficulties and postoperative complications, as compared with the patents who had not been pre-treated with bromocriptine. In conclusion, oral administration of bromocriptine is important in the treatment of prolactinoma tumors. However, large doses or long-term use of bromocriptine may increase difficulties in surgery or postoperative complications, and reduce its ability to treat prolactinonas, as it can lead to hardening of the tumor tissue and capsules, and aggravate pituitary stalk adhesions.
Serum cortisol values were measured throughout the day over 10.5 hours. Thyroid hormones and cortisol binding globulin (CBG) were measured in the baseline sample. Comparisons of the serum cortisol peak after receiving the first dose of hydrocortisone, the time when the serum cortisol peak was obtained, the area under the curve (AUC) for the cortisol values and the levels of unbound cortisol on and off GH therapy were made. The results are expressed as mean +/- SEM. Comparisons were carried out within individuals, using the Wilcoxon signed rank test. A P-value less than 0.05 was considered statistically significant.
Reports of pregnancy in acromegalic women are uncommon, numbering less than 100, in which a case of acromegaly first diagnosed in pregnancy is rare.
Acromegaly is a rare disease which can significantly reduce life expectancy. Clinical features are diverse and the patient may consult a variety of medical and surgical specialists before the diagnosis is suspected. However, the disease is easily confirmed by the appropriate laboratory tests, namely GH and IGF1 measurements. In most cases, acromegaly is secondary to a micro or macrosomatotrope pituitary adenoma. Those lesions are easily visualized by a pituitary CT Scan or Magnetic Resonance Imaging. Visual fields have to be evaluated by a neuro-ophthalmologist, and a thorough evaluation of other pituitary functions have to be performed. Selective removal of the adenoma by the transsphenoidal route is the treatment of choice for acromegaly. When performed by an experienced neurosurgeon, normalization of GH secretion can be expected in approximately 75% of cases. The surgical outcome is modulated by the volume, the extension of the tumor and the preoperative GH level. Octreotide, radiotherapy or bromocriptine are indicated whenever the patient remains with an elevated level of GH with persistency of symptoms.
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The pattern of androgen dependent enzyme activities of epididymis was studied after the administration of prolactin and bromocriptine in albino rats. Prolactin activated the glycogenolysis and hexose mono and diphosphate pathways, which would be essential for sperm maturation. But bromocriptine inhibited these activities of epididymis. Hence role of bromocriptine in decreasing epididymal function has been suggested.
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After being suspected in the presence of galactorrhoea, it is now easy to prove hyperprolactinism thanks to radioimmunoassay of prolactin. The repercussions of hyperprolactinism on gonad function are now well known, especially in women where they lead to anovulation then amenorrhoea, whereas in man there occurs hypoandrogenism with loss of libido. Hyperprolactinemia may occur in numerous circumstances and may be deduced logically from the mechanism of secretory regulation of this hormone. Among the latter, one cause dominates the others by its therapeutic consequences, I.e. the presence of an adenoma or microadenoma secreting prolactin discovered thanks to tomography of the sella turcica. The treatment of hyperprolactinism has advanced in recent years with the introduction of dopamineric drugs such as bromcriptin which permits one to normalise prolactinemia and thus restore gonad function. It's use requires however certain precautions and neurological and ophthalmic supervision when htere is a microadenoma.
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The potassium and sodium currents in acutely isolated neostriatal neurons are modulated by activation of both D1- and D2-class receptors. The amplification of mRNA in individual neurons supports this conclusion and has shown that striatonigral neurons express not only D1 and D2 receptors, but D3 receptors as well. The characteristics of the modulations produced by these receptors provide a foundation for both antagonistic and synergistic actions of D1 and D2 agonists in the neostriatum. Understanding precisely how these modulations interact in shaping excitability, however, will require a better characterization of spatial domains in which they operate.
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Two hyperprolactinemic infertile women, one with and one without a pituitary adenoma, who were resistant to bromocriptine treatment, were treated orally with Hachimijiogan, a Chinese herbal medicine. This treatment reduced the serum prolactin level, resulting in a normal ovulatory cycle and pregnancy, without side effects.
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The present study was undertaken with the aim of exploring the role that opiate systems may have in neuroendocrine control in acromegaly. The effects of naloxone (0.4 mg, i.m.), of 2-Br-alpha-ergocryptine (CB154, 2.5 mg, p.o.) and of the interaction between CB154 and naloxone on growth hormone (GH) and prolactin (PRL) secretion were studied in 11 acromegalic patients. CB154 reduced both GH and PRL serum levels, naloxone only GH serum levels. The latter effect deserves further study aimed at a possible new therapeutic approach to GH hypersecretion observed in acromegaly. Naloxone also interfered with the lowering effects of CB154 and GH and PRL serum levels, pointing to the existence of an interaction between dopaminergic and opiate control of GH and PRL secretion in acromegaly.
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Huntington's chorea (HC) was studied in 14 untreated patients, in six patients receiving long-term neuroleptic treatment, and in four patients after drug withdrawal. Our results showed that patients with HC may be divided into three groups, otherwise clinically indistinguishable, on the basis of growth hormone responsiveness to dopaminergic stimuli. The existence of subpopulations of patients with HC must be considered in further studies on these subjects.
We have previously shown that using agonist affinity at recombinant receptors selectively expressed in clonal cells as the dependent variable in three-dimensional quantitative structure-activity relationship studies (3D-QSAR) presents a unique opportunity for accuracy and precision in measurement. Thus, a comparison of affinity's structural determinants for a set of compounds at two different recombinant dopamine receptors represents an attainable goal for 3D-QSAR. A molecular database of bound conformations of 16 structurally diverse agonists was established by alignment with a high-affinity template compound for the D1 receptor, 3-allyl-6-bromo-7,8-dihydroxy-1-phenyl-2,3,4, 5-tetrahydro-1H-benzazepin. A second molecular database of the bound conformations of the same compounds was established against a second template for the D2 receptor, bromocriptine. These aligned structures suggested three-point pharmacophore maps (one cationic nitrogen and two electronegative centers) for the two dopamine receptors, which differed primarily in the height of the nitrogen above the plane of the catechol ring and in the nature of the hydrogen-bonding region. The ln(1/KL) values for the low-affinity agonist binding conformation at recombinant D1 and D2 dopamine receptors stably expressed in C6 glioma cells were used as the target property for the CoMFA (comparative molecular field analysis) of the 16 aligned structures. The resulting CoMFA models yielded cross-validated R2 (q2) values (standard error of prediction) of 0. 879 (1.471, with five principal components) and 0.834 (1.652, with five principal components) for D1 and D2 affinity, respectively. The simple R2 values (standard error of the estimate) were 0.994 (0.323) and 0.999 (0.116), respectively, for D1 and D2 receptor. F values were 341 and 2465 for D1 and D2 models, respectively, with 5 and 10 df. The predictive utility of the CoMFA model was evaluated at both receptors using the dopamine agonists, apomorphine and 7-OH-DPAT. Predictions of KL were accurate at both receptors. Flexible 3D searches of several chemical databases (NCI, MDDR, CMC, ACD, and Maybridge) were done using basic pharmacophore models at each receptor to determine the similarity of hit lists between the two models. The D1 and D2 models yielded different lists of lead compounds. Several of the lead compounds closely resembled high-affinity training set compounds. Finally, homology modeling of agonist binding to the D2 receptor revealed some consistencies and inconsistencies with the CoMFA-derived D2 model and provided a possible rationale for features of the D2 CoMFA contour map. Together these results suggest that CoMFA-homology based models may provide useful insights concerning differential agonist-receptor interactions at related receptors. The results also suggest that comparisons of CoMFA models for two structurally related receptors may be a fruitful approach for differential QSAR.
This paper analyses the different therapeutic approaches that can be used for the treatment of benign breast diseases. These different options vary according to our understanding of the pathophysiology of the disease. It is very important to know exactly what sort of benign breast disease is being treated in terms of pathological abnormalities in order to obtain objective evaluations of the efficiency of any given hormone treatment (mainly progestogens, Danazol and Bromocriptine). It is also very important to know whether the treatment can change some of the cellular abnormalities that carry a high risk of breast cancer. These are: various forms of lobular hyperplasia. Last of all, it is important to know whether hormone treatment of benign breast disease can be considered as a way of preventing breast cancer. It is only by carrying out a large epidemiological study on patients who have been correctly matched and have been treated under the same protocol that such speculative questions can be answered.
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Pituitary prolactinoma patients should continue the original dose of bromocriptine for at least 4 months instead of immediate withdrawal during pregnancy. For those with large adenoma, bromocriptine should be taken throughout pregnancy. Blood levels of prolactin, progesterone, human chorionic gonadotropin (HCG) and visual dysfunction should be monitored every 2 weeks. If the levels of progesterone and HCG are low, they should be timely supplemented.If prolactin rises too rapidly and visual dysfunction worsens, the dose of bromocriptine should be appropriately increased. Taking bromocriptine during pregnancy can significantly reduce the rate of embryo stopping without improving the rate of embryo deformity. Thus use of bromocriptine is both safe and necessary.
The neonatal rat cardiomyocytes injury and apoptosis caused by hypoxia/reperfusion can be inhibited with DR2 activation, which mechanism is related to scavenging oxygen radical.
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Investigations were carried out with a dopamine agonist compound GYKI-32 887 to compare its binding capacity towards D2, 5-HT1 and 5-HT2 receptors. Synaptosomal membranes were prepared from corpus striatum, hippocampus and frontal cortex of rats. The tritiated ligands used were: 3H-spiperone for D2 and 5-HT2 receptors and 3H-5-HT for 5-HT1 receptors. Comparing the results obtained, IC50 and Ki values, one can conclude that GYKI-32 887 has higher affinity towards D2 receptors than serotonin ones and shows better selectivity than bromocriptine, the reference substance.
This is an 11 center German trial with a prospective randomized controlled open-label design. The trial enrolls females with newly diagnosed PPCM according to European Society of Cardiology criteria with a LV ejection fraction (LVEF) <35 %. Patients are randomized 1:1 to either best supportive care (BSC) including standard heart failure therapy plus 8 weeks of bromocriptine therapy (2.5 mg b.i.d. for 14 days and 2.5 mg q.d. from day 15 to 56) or to BSC plus 1 week of low-dose bromocriptine (2.5 mg q.d.) with anticoagulant therapy at a prophylactic dose administered during the period of bromocriptine treatment in both groups. The primary endpoint is change in LVEF from baseline to 6 months follow-up as assessed by cardiac magnetic resonance imaging (or echocardiography if CMR is not tolerated). The secondary endpoints are hospitalization for worsening heart failure, heart transplantation, and all-cause mortality during follow-up or a combination of these endpoints. A total of 60 patients will be recruited (including 6 potential dropouts) giving a power of 0.9 for an expected LVEF change of 10.8 % between treatment groups at 6 months.
Twenty-three patients with polycystic ovary syndrome and anovulatory infertility have been treated with bromocriptine. All had previously failed to respond to clomiphene. Twenty had normal serum prolactin concentrations and, of these, four (20%) developed regular ovulatory cycles. All three women with moderate hyperprolactinaemia ovulated regularly on bromocriptine so that, overall, seven of 23(30%) responded, which was a significantly higher proportion than that observed during a control period of no treatment. A further eight women ovulated at least once during the study period but these occasional ovulations were no more common during bromocriptine than with either clomiphene or no treatment. No suppression of LH was noted except during the luteal phase of ovulatory cycles and there was no change in the pattern of pulsatile release of LH. Testosterone and androstenedione concentrations remained elevated and unchanged. We conclude that bromocriptine may be expected to induce ovulation in hyperprolactinaemic women with polycystic ovary syndrome but that there is no clear indication for its use in clomiphene-resistant patients with normal serum prolactin concentrations.
The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
The motor effects of selective D-1 dopamine receptor stimulation in Parkinson's disease have been explored in a limited number of studies with partial D-1 agonists only and the results were unsatisfactory. Four 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-exposed parkinsonian monkeys already exhibiting levodopa- and dopamine agonist-induced dyskinesia received selective D-1 agonists ([2,3,4,5-tetrahydro-7-8-dihydroxy-1-phenyl-1-H-3-benzazepine- HCI] (SKF 38393), [(+-)6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro- 1H-3-benzazepine hydrobromide] (SKF 82958), [(1R, 3S)3-(1'-adamantyl)-1-aminomethyl-3,4-dihydro-5,6- dihydroxy-1H-2-benzopyran hydrochloride] (A-77636) and [(-)-(6aR)(12bR)-4,6,6a,7,8,12b-hexahydro-7-methyli ndolo (4,3-ab)-phenanthridine] (CY 208-243)) to compare these drugs with selective D-2 agonists (LY 171555, (+)-4-propyl-9- hydroxynaphthoxazine and bromocriptine) and levodopa in terms of antiparkinsonian efficacy and side effects. The D-1 class of compounds was as efficacious as the D-2 agents in alleviating parkinsonism in these animals. However, D-1 agonists were, in general, less likely to reproduce dyskinesia. In addition, D-1 agonists occasionally improved motor symptoms without concomitant dyskinesia, unlike D-2 agonists or levodopa (which always produced some dyskinesia with improvement in motor function). These preliminary results do not support the hypothesis that preferential D-1 receptor stimulation facilitates dyskinesia in primates.(ABSTRACT TRUNCATED AT 250 WORDS)
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Randomised trials evaluating the effectiveness of treatments used for suppression of postpartum lactation.
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Three cases of cerebral hemorrhage that occurred in the puerperium in normotensive women who used bromocriptine for milk suppression postpartum are described. Unlike in some other instances reported in the past, the extent of the bleeding was limited in these patients and the long range outcome was relatively benign. All episodes were associated with the development of hypertension. These incidents occurred between the 10th and 17th days postpartum; somewhat later than the usually observed peak time period (6th to 8th day) for the development of severe bromocriptine related side effects.