A case of infertility associated initially with amenorrhoea only and then with amenorrhoea and galactorrhoea following a successfully induced pregnancy is reported. In a period of eight years of continuous investigation and treatment this subject's infertility first responded to sequential clomiphene and human chorionic gonadotrophin (HCG) therapy resulting in a normal pregnancy. Subsequently she became refractory to this therapy. The availability of specific prolactin assays and a prolactin inhibitor (2-Br-α-ergocryptine, bromocriptine Sandoz) identified the aetiology of her amenorrhoea/galactorrhoea/infertility and provided a new mode of therapy. Planned conception has been achieved on three occasions, producing two normal males and a normal female child.
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The objective of this review was to assess the effects of bromocriptine on pregnancy rates among couples where subfertility has been attributed to idiopathic oligo- and/or asthenospermia.
We investigated causes of hyperprolactinemia in 11 children and adolescents (6 females and 5 males), aged from 1.5 to 17.5 years. Children with primary hypothyroidism, iatrogenic hyperprolactinemia and adolescents with polycystic ovaries were excluded.
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Prospective clinical study.
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The term gigantomastia has been used to describe breast enlargement to extreme size, with sloughing, haemorrhage and infection. The condition is rare and a case of pregnancy-related gigantomastia is reported.
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One of the characteristics of obesity-associated diabetes is an elevated fasting plasma insulin concentration with a weak insulin secretory response to subsequent glucose stimulation. Evidence suggests that hyperglycemia and hyperlipidemia may contribute to the initiation and progression of this disordered islet glucose sensing. It has been proposed that reducing hyperglycemia and hyperlipidemia per se may improve islet glucose sensing. Here we studied glucose-dependent insulin release in islets isolated from ob/ob mice treated with dopamine agonists (bromocriptine and SKF38393, BC/SKF) which significantly reduced circulating glucose and lipid levels of ob/ob mice. Islets from BC/SKF-treated mice showed a marked decrease of the elevated basal insulin release to levels similar to lean mice. Such treatment also induced a higher secretory response to glucose stimulation compared with that in ob/ob mice with sustained hyperglycemia and hyperlipidemia. Similarly, when islets from untreated ob/ob mice were cultured for 7 days in 11 mM glucose in the absence of free fatty acid, the basal insulin release was significantly decreased and high glucose stimulated insulin release increased compared with that from islets cultured in medium containing 30 mM glucose and 2 mM oleate. The BC/SKF-induced reduction of elevated basal insulin release was associated with decreased hexokinase activity and basal cyclic AMP content in islet tissue. Our results demonstrate that dopamine agonist treatment improves basal insulin release in ob/ob mice and this effect may be mediated, in part, by a reduction of hyperglycemia and hyperlipidemia.
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Ten chronic schizophrenic patients were given bromocriptine in doses increasing from 1.25 to 5 mg over 6 days (the low-dose therapy) and then up to 40 mg over 15 days (the high-dose therapy). Psychopathological status was assessed using the Brief Psychiatric Rating Scale, twice daily the first 6 days, and every 2 days thereafter. The prolactin (PRL) response to haloperidol stimulation (1 mg i.v.) was measured in five cases before and 3 days after the end of high-dose therapy, and in one patient before and 3 days after the end of low-dose therapy. Electroencephalographic sleep studies were carried out before therapy and every 2 nights during low-dose therapy in five patients, and in two cases during high-dose therapy. Bromocriptine therapy modified neither clinical symptomatology nor sleep patterns. The PRL response to haloperidol after therapy was markedly lower than that before therapy in the five patients treated with high doses, and markedly higher in the single patient tested who was treated only with low-dose therapy.
An effect of dialysis therapy on baseline prolactinemia and prolactinemia following suppression test with alpha-bromocriptine was determined in 34 patients with chronic renal failure. Gradual decrease in hyperprolactinemia with the duration of dialysis therapy has been observed. Prolactinemia baseline values in patients dialysed for 100 months did not differ from those determined in healthy individuals.
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In the treatment group bromocriptine was given intramuscularly to 22 patients after their first kidney transplantation along with conventional immunosuppression (cyclosporin A, glucocorticoids). Twenty-three patients receiving only conventional immunosuppression served as control subjects. The incidence of acute graft rejections, graft losses, and infections was evaluated.
The medical history of 37 women with nonpuerperal mastitis, who had been treated between January 1980 and July 1983 at the Dept. of Obstetrics and Gynaecology of the University of Tübingen, was reviewed because of the increasing prevalence of this disease. Defined by different history and clinical symptoms, two groups of patients were seen: 25 women with acute nonpuerperal mastitis and 12 women with chronic recurring nonpuerperal mastitis. The average age of the patients was 30 years. The inflammation was located mostly subareolar and around the nipple. The main symptoms were pain, erythema and swelling, in acute cases accompanied by fever and abscess formation. This process was strongly related to the interval between the onset of symptoms and the initiation of treatment. Anaerobes and Staphylococcus aureus could be cultured mainly from women with acute nonpuerperal mastitis. In females with chronic recurrent mastitis, mostly anaerobes were found. Women were treated with a prolactin inhibitor (bromocriptine), if abscess formation, leukocytosis or fever were absent. In patients with leukocytosis and/or fever this regimen was combined with antibiotics. Abscesses were treated surgically, in some cases in combination with prolactin inhibition and antibiotic administration. The results show that an early conservative treatment is important to prevent abscess formation. It seems that this treatment can reduce the rate of recurrences.
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Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 0.5 mg/animal i.v. once or twice) to common marmosets induced persistent parkinsonian motor deficits. The postsynaptic dopamine D2 receptor agonist properties of talipexole (B-HT 920, 2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]-azepine), which is believed to be a dopamine autoreceptor agonist, were examined using normal and MPTP-treated marmosets and were compared to these properties of bromocriptine, a selective dopamine D2 receptor agonist. Talipexole (20-160 micrograms/kg i.p.) dose dependently increased motor activity and reversed the akinesia and incoordination of movement in MPTP-treated marmosets. In normal marmosets, higher doses of talipexole (80-160 micrograms/kg i.p.) produced a dose-dependent increase in motor activity, while the lowest dose (20 micrograms/kg i.p.) depressed this activity. These data for talipexole were very similar to those for bromocriptine. Talipexole had, however, several properties different from those of bromocriptine; it had a rapid onset of antiparkinsonian activity compared to bromocriptine; it had more than 25 times as much activity potency as bromocriptine; a dose of talipexole (80 micrograms/kg i.p.) sufficient to produce the activity did not induce emesis as strongly as an insufficient dose of bromocriptine (0.5 mg/kg i.p.). These results suggest that talipexole has postsynaptic dopamine D2 receptor agonist properties and that these properties of talipexole may be favorable in the treatment of Parkinson's disease.
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Chronic administration of iminodipropionitrile (IDPN), a neurotoxin, to rats produces a persistent behavioral syndrome characterized by lateral and vertical head twitching, random circling and hyperactivity. Conventionally, this IDPN-induced dyskinesia has been considered to be due to abnormalities in the serotonin neuronal system. However, the present study also demonstrated marked alterations in the dopamine (DA) and acetylcholine (ACh) neuronal systems. These were activation of DA neurons in the nucleus accumbens and thalamus + midbrain, decreased activity in the other brain areas and a decrease in D1 DA receptors. ACh contents were decreased in most brain areas while muscarinic ACh receptors were increased in the striatum, superior colliculus and geniculate nucleus. These alterations in the ACh neuronal system may be secondary to abnormalities in the DA neuronal system. IDPN-induced dyskinesia was enhanced by administration of L-dopa, which increases DA concentration, but was completely inhibited by ceruletide, which inhibits DA release. The dyskinesia was also inhibited by sulpiride, a central antagonist of D2 DA receptors. Interestingly, apomorphine and bromocriptine, which are DA receptor agonists, did not aggravate, but decreased dyskinesia in the IDPN-treated rats. These results strongly suggest that dyskinesia is caused not by abnormality of postsynaptic receptors in the DA neuronal system but by abnormally enhanced function of the presynaptic DA neurons themselves. In addition, ceruletide may be useful in the treatment of dyskinesia, and bromocriptine alone or in combination with L-dopa may be effective in Parkinson's disease without the development of dyskinesia. Thus, the IDPN-treated rat model is useful for clarifying the biochemical pathophysiology of dyskinesia and developing drugs for its treatment.
Quantified ultrastructural observations of the pars intermedia (PI) of the murine hypophysis enable evaluation and kinetic study of relatively fine secretory changes in the gland. Changes in volume of rER and newly formed dense secretory granules (Golgi granules) appear to best translate functional variations in the PI, as shown by the morphological effects of drugs affecting the dopaminergic control of the gland. Our morphometric results show that the PI is stimulated, but only briefly (no longer than 8-12 days), by both salt-loading and Na deprivation. However, the PI displays different secretory patterns in salt-loaded and Na-deprived mice; moreover, bromocriptine, which abolishes PI stimulation in Na-deprived mice, has only a slight inhibitory effect in salt-treated animals. Thus, it appears that the stimulation of the PI under both experimental conditions is triggered by different mechanisms. These results underline the plurifactorial control of the PI and show that the gland may have complex effects on hydromineral regulation.
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In the crested newt, permanent lesions to the anterior preoptic area brought about an enhancement of triiodothyronine (T3) production. This was not mediated by prolactin, since the effect was demonstrable also in ergocryptine (CB 154)-treated animals. The observed rise in circulating T3 levels in the ergocryptine-treated surgical animals confirms that lesions to the anterior preoptic area stimulate pituitary thyrotrophic activity, resulting in the activation of the thyroid gland.
Recent studies on the neurobiology of cognition have focused on the ability of the prefrontal cortex (PFC) to support processes of working memory, i.e, mnemonic processes by which information relevant for a correct response is temporarily maintained to be reevaluated or updated on a trial-by-trial basis. Of most recent interest is the role played by dopamine (DA) in spatial working memory processes of the principal sulcal region of the PFC. Although D1 DA receptors appear to modulate these mnemonic processes in monkeys, several lines of research suggest that D2 DA receptors could also be relevant to cognitive functions. Therefore, we assessed the effects of a specific D2 receptor agonist (bromocriptine) and placebo on visuospatial delayed response performance in human subjects. During delay periods of 0 or 8 sec, subjects were required to remember the spatial location of rapidly presented visual cues displayed in peripheral vision within a 360° circumference. The extent to which D2 receptor activation by bromocriptine facilitated working memory in the 8-sec delay condition relative to placebo performance was assessed. As a means of providing validation of bromocriptine's D2 receptor effect, maximum inhibition of prolactin (PRL) secretion, which is inhibited specifically by activation of D2 receptor sites, was determined. Additionally, tasks having no working memory component were administered to rule out nonspecific effects of bromocriptine on sensory, arousal, attentional, and motor factors. Results demonstrated a significant facilitatory effect of bromocriptine on spatial delayed response performance (i.e., 8-sec delay performance). Results could not be explained by nonspecific effects of bromocriptine. Thus, findings of this study suggest that spatial working memory is facilitated by D2 receptor activation. The role that DA may play in human cognitive processes is discussed within the larger theoretical framework of DA's general role in the facilitation of goal-directed behavior. In the case of cognition, DA may facilitate processes that serve to guide motivated behavior through complex environments.
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Deficiency of dopaminergic activity in menopause is induced by hypoestrogenemia correlating with serum levels of prolactin. This deficiency was identified in hypertensive menopausal women by the results of acute and prolonged tests with dopamine mimetic--parlodel.
To make evidence-based treatment recommendations for the medical and surgical treatment of patients with Parkinson disease (PD) with levodopa-induced motor fluctuations and dyskinesia. To that end, five questions were addressed. 1. Which medications reduce off time? 2. What is the relative efficacy of medications in reducing off time? 3. Which medications reduce dyskinesia? 4. Does deep brain stimulation (DBS) of the subthalamic nucleus (STN), globus pallidus interna (GPi), or ventral intermediate (VIM) nucleus of the thalamus reduce off time, dyskinesia, and antiparkinsonian medication usage and improve motor function? 5. Which factors predict improvement after DBS?
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The mammary gland is a good model to study the hormonal regulation of amino acid uptake. Danazol, which decreases gonadotrophin release, causes a fall in gamma-glutamyltranspeptidase (GGT) and in amino acid uptake by the gland. Treatment of the rats with estrogens and progesterone partially reverts this effect. Treatment with gonadotrophins completely reverts it. gamma-Glutamyl-amino acids (GAA) increase the uptake of amino acids by the mammary gland in rats previously treated with bromocriptine. We suggest that GAA may act as signals to stimulate amino acid uptake and that the role of GGT may be to generate that signal.
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Renal function was assessed in 8 males at reproductive age suffering from lupus nephritis (LN). Normal renal function was registered in 5 patients, hypofunction in 3 males. Endocrinological examinations (evaluation of secondary sexual characters, of hypophyseal and sex hormone profile, sexological questionnaires, spermograms) failed to distinguish significant differences between SLE males and renal patients without SLE suffering from hypogonadism (13 males with uremic hypogonadism, 10 males with azoospermia induced by cytostatics). Endocrinological changes revealed may result from uremia and immunodepressive therapy. In 5 patients these abnormalities were corrected by parlodel and zinc sulfate. The authors came to the conclusion that feminization is not universal in LN males.
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We investigated whether the immunosuppressive effect of bromocriptine in mice is due to its direct effect on lymphocyte functions or through inhibition of prolactin secretion. Incubation of mouse Babl/c splenic lymphocytes with bromocriptine in vitro at a concentration of around 0.5 to 1 microgram/mL causes an inhibition of antigen- or mitogen-induced proliferation. However, bromocriptine in vitro has no effect on lymphokine production (gamma-interferon and interleukin-2), expression of interleukin-2 receptor or lymphocyte cytotoxic function. Furthermore, treatment of Babl/c mice with bromocriptine inhibits the mixed lymphocyte reaction and mitogen stimulation, as well as primary and secondary antibody production. However, we postulated that the inhibition of ex vivo functional activity could not account for a direct cytostatic or cytotoxic effect of bromocriptine. This is supported by the in vitro data, which shows that bromocriptine has no effect on proliferating P-815 mastocytoma tumor cells. Finally, (NZB/NZW) F1 mice spontaneously develop a disease similar to systemic lupus erythematosus. In both non-autoimmune Babl/c mice and (NZB/NZW) F1 lupus-mice, the serum level of bromocriptine achieved by a treatment with 5 mg/kg on average is 2-6 ng/mL. On the one hand, this dose is sufficient to significantly alter the ex vivo functional tests in Babl/c mice and to show a beneficial effect in the in vivo model of female lupus-mice. On the other hand, the lowest concentration which could have an inhibitory effect on antigen- and mitogen-induced proliferation in vitro is 200 ng/mL, ie 50 times more than that required in vivo to obtain significant reductions of proteinurea, glomerular membrane proliferation and immune deposits in lupus-mice. The serum levels of gamma-interferon and interleukin-2 are reduced in lupus-mice when compared with Babl/c mice. The treatment with bromocriptine does not influence these parameters. In conclusion, our data demonstrate that the major immunosuppressive activity of bromocriptine is probably dependent on its hypoprolactinemic effect.
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In rats with unilateral 6-hydroxydopamine lesions of the substantia nigra, a specific D1 dopamine receptor agonist, SKF 38393A, at a dose that does not itself produce turning, significantly increased the contralateral rotation observed following a low dose of the specific D2 agonist LY 171555. Doses of SKF 38393A or the D2 agonist bromocriptine, which would themselves not induce turning, in combination produced a high rate of turning. These results suggest a synergistic interaction between D1 and D2 dopamine receptors in this system.