Great strides have been made in the understanding of anatomy, physiology, pathology, diagnosis, and treatment of pituitary adenomas. The single greatest credit should probably be given to the rapid advancement in surgical techniques that ushered in a new era of multispecialty interest in the pituitary and its disorders. The fate of patients with pituitary adenomas was thus greatly improved. Surgical treatment can offer a cure in a vast majority of patients. The morbidity and mortality following transsphenoidal surgery are low. In patients with certain hormonally active pituitary macroadenomas, multidisciplinary therapy including pre- and postoperative medical management with bromocriptine and postoperative radiation therapy have decreased the recurrence rate to a respectable 10 per cent.
No link has been found between lisuride use and fibrotic cardiac valvulopathy, in agreement with the 5-HT(2B) receptor antagonist effect of this drug. The very low incidence of spontaneous reports of any other fibrosis could be even compatible with an association by chance in the population exposed to lisuride. Although close monitoring for this kind of side effects is still to be recommended in the therapy with lisuride, our data do not support the concept of a class effect suggesting that all ergot-derived drugs and especially DA receptor agonists with some chemical similarity to the ergot structure will cause or facilitate cardiac valvulopathies as observed with pergolide.
Here we investigated roles of the pituitary bone morphogenetic protein (BMP) system in modulating GH production regulated by a somatostatin analog, octreotide (OCT) and a dopamine agonist, bromocriptine (BRC) in rat pituitary somatolactotrope tumor GH3 cells. The GH3 cells were found to express BMP ligands, including BMP-4 and BMP-6; BMP type-1 and type-2 receptors (except the type-1 receptor, activin receptor-like kinase (ALK)-6); and Smad signaling molecules. Forskolin stimulated GH production in accordance with cAMP synthesis. BRC, but not OCT, suppressed forskolin-induced cAMP synthesis by GH3 cells. Individual treatment with OCT and BRC reduced forskolin-induced GH secretion. A low concentration (0.1 microM) of OCT in combination with BRC (1-100 microM) exhibited additive effects on reducing GH and cAMP production induced by forskolin. However, a high concentration (10 microM) of OCT in combination with BRC failed to suppress GH and cAMP production. BMP-4 specifically enhanced GH secretion and cAMP production induced by forskolin in GH3 cells. BRC, but not OCT, inhibited BMP-4-induced activation of Smad1,5,8 phosphorylation and Id-1 transcription and decreased ALK-3 expression. Of note, in the presence of a high concentration of OCT, the BRC effects suppressing BMP-4-Smad1,5,8 signaling were significantly impaired. In the presence of BMP-4, a high concentration of OCT also attenuated the BRC effects suppressing forskolin-induced GH and cAMP production. Collectively, a high concentration of OCT interferes with BRC effects by reducing cAMP production and suppressing BMP-4 signaling in GH3 cells. These findings may explain the mechanism of resistance of GH reduction to a combination therapy with OCT and BRC for GH-producing pituitary adenomas.
Neuroleptic malignant syndrome (NMS) is a possible cause of fever of unknown origin (FUO) and is a potentially fatal adverse effect of various drugs, especially of neuroleptics. First generation antipsychotics, such as received by the patient described in this article, are more likely to cause NMS than second generation antipsychotics. The key symptoms are the development of severe muscle rigidity and elevated temperature associated with the use of neuroleptic medication. Malignant catatonia (MC) is an important differential diagnosis of NMS. While neuroleptics can trigger NMS and must be immediately discontinued if NMS occurs, neuroleptic therapy represents the first line treatment for MC. This article describes the case of a patient with schizoaffective disorder where initially the diagnosis of NMS was not clear. Eventually, fever and a markedly elevated serum creatine kinase (CK) led to the correct diagnosis and the appropriate therapy with dantrolene, bromocriptine and amantadine. Furthermore, a thorough review of the currently available literature on NMS is provided.
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This review describes the pharmacologic and pharmacokinetic properties of selected DAs and relates these characteristics to clinical outcomes, with an emphasis on adverse events.
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Activin A is a homodimer of inhibin beta A subunits, and was first isolated from gonadal fluids on the basis of its ability to stimulate FSH secretion by rat pituitary cells in vitro. The beta A subunits of activin and their mRNAs have been found in many cell types, in several species and at different stages of development, suggesting that activin A has a wide range of diverse biological roles. Apart from the modulation of gonadotroph function, in-vitro studies have demonstrated inhibitory effects of activin A on GH synthesis, GH secretion and possibly somatotroph proliferation. We have therefore investigated the potential role of activin A in the pathophysiological regulation of GH secretion by human somatotrophinoma cells using in-vitro techniques. Cell cultures were established by enzyme dispersion of adenoma tissue obtained from six patients with acromegaly, and treated for 72 h with 0.01-10 nmol recombinant human activin A/l followed by a 2-h stimulation test with 10 nmol GH-releasing factor (GRF)/l. Medium was collected at 24, 48 and 72 h, as well as after GRF treatment, and GH concentrations were measured by immunoradiometric assay. Basal GH secretion from the cells of two tumours was significantly stimulated 12-63% above control values during treatment with 0.01-10 nmol activin A/l, whereas the peptide had no effect on GH release from cells of the remainder of the tumours. GRF significantly stimulated GH release from the cells of two different adenomas, and pretreatment with 0.01-1 nmol activin A/1 partially but significantly blocked GRF-stimulated GH release from the cells of one of these.(ABSTRACT TRUNCATED AT 250 WORDS)
To assess the effectiveness of dopamine agonist bromocriptine in reducing the incidence and severity of OHSS in patients undergoing assisted reproduction and its effect on pregnancy rates.
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Miscarriage clinic, Yokohama City University Hospital, Yokohama, Japan.
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Recent literature has suggested that late recurrence of pituitary adenoma after radiotherapy is common. We hypothesized that late failures might be a result of inadequate dose (less than 4500 cGy). To investigate, we analyzed 105 patients treated at our institution between 1965 and 1986 (analysis, 2/89). The minimum observation time was greater than or equal to 5 years in 58% and greater than or equal to 10 years in 30% of the patients. All patients received megavoltage radiotherapy (range, 4200-5500 cGy; mean, 4821 cGy) at a mean dose per fraction of 172 cGy; 100 patients received greater than or equal to 4500 cGy tumor dose. Twenty-nine patients received radiotherapy alone, and 76 had postoperative radiotherapy after frontal craniotomy (20 patients) or transsphenoidal hypophysectomy (56 patients). At presentation, 71% of patients had extrasellar disease, 57% had visual field deficits, and 50% had endocrinopathy. Of patients treated postoperatively, 74% had gross residual disease. Four local failures occurred at 13, 16, 57, and 64 months after postoperative radiotherapy, all within the irradiated volume (tumor doses of 4700, 4715, 5000, and 5100 cGy). All four patients had presented with moderate to extensive extrasellar disease with visual field defects. Two of the four remain free of second recurrence at 7 and 13 years after salvage transsphenoidal hypophysectomy. The local control rate with radiotherapy (product-limit method) at 10 years was 100% in the radiotherapy-alone group and 92% in the postoperative radiotherapy group (95% for all patients). To prevent bias, seven patients who received bromocriptine, none of whom demonstrated a recurrence, were censored from the local control analysis at the initiation of the drug. No patient in this study suffered recurrence greater than 64 months after radiotherapy, with 31 patients (none with bromocriptine) observed 10 to 21 years. We conclude that treatment of pituitary adenoma with greater than or equal to 4500 cGy in 25 fractions can result in a high (greater than or equal to 90%) probability of stable long-term control.
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Secreting pituitary adenomas are usually not considered a disease of older people. However, in male patients, prolactin-secreting pituitary tumours occur at a similar frequency throughout the entire life span, giving the opportunity to study in this gender the influence of age on the clinical presentation and response to treatment of these tumours.
Previous studies in patients with idiopathic hyperprolactinemia (IH) that have suggested the presence of decreased central dopaminergic tone have assumed normal responsiveness of lactotrophs to dopamine (DA). We have examined DA sensitivity in 17 women with IH and 19 female controls by evaluating the plasma PRL responses to successive infusions of increasing concentrations of DA (4, 40, and 400 ng/kg . min) as well as to a dopaminergic agonist, bromocriptine (2.5 mg, orally), and to a dopaminergic agonist, bromocriptine (2.5 mg, orally), and to a dopaminergic receptor blocker, domperidone (2 mg, iv). PRL levels in controls were unchanged during a saline infusion, but decreased by 34 +/- 7% (mean +/- SE) at the end of the lowest DA infusion (P less than 0.05 vs. saline). Progressive PRL suppression was produced with each increasing dose. In contrast, in patients with IH, the lowest dose produced no significant suppression from basal PRL levels (P less than 0.001 vs. controls); at 40 ng/kg . min DA, fractional suppression was evident but was less than that in controls (P less than 0.01); at 400 ng/kg . min, fractional PRL suppression in IH patients was indistinguishable from that in controls (70 +/- 6% vs. 73 +/- 4%). Patients with IH also exhibited markedly reduced and delayed PRL response to domperidone (P less than 0.02 vs. controls). Significant impairment of the PRL-lowering effect of bromocriptine was observed in the IH patients between 1 and 2 h (P less than 0.02 vs. controls), and their responses to bromocriptine were again delayed. The results indicate the presence of a relative resistance to DA in patients with IH. This resistance is compatible with a decrease in the number or affinity of lactotroph DA receptors.
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Early stage Parkinson's disease may be better left untreated if it does not limit motor function. Once limitation of function is present levodopa-dopa decarboxylase inhibitor combinations are the most effective therapy, although amantadine may be satisfactory for a time in milder cases. The optimal independent roles of the ergot derivatives bromocriptine and pergolide, and the MAOb inhibitor selegiline, are not yet generally agreed although they are accepted as useful in supplementing the effects of levodopa. With prolonged levodopa use various late-stage treatment problems may appear. The pathogenesis of these is poorly understood and no completely satisfactory ways of managing them are available.
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It is note that hyperprolactinemia is frequently associated to chronic renal failure (CRF). The etiopathogenesis of this endocrine disorder is not clearly understood, trying to evaluate the possible hypothalamic-pituitary cause we have evaluated the Prl levels under some pharmacological tests: TRH (200 mcg i.v.),Domperidone (DOM)(10 mg i.v.),Nomifensine (NOM)(200 mg p.o.)and Bromocriptine (BRC)(2.5 mg p.o.) in 3 groups of patients: CRF(8 cases), dysfunctional (8 cases) and tumoral (9 cases) hyperPrl. Prl plasma levels have been evaluated by RIA (kits,Biodata,Roma). In patients affected by CRF either direct (BRC) than indirect (NOM) agonist acting dopaminergic drugs failed to induce a reduction in Prl plasma levels, like to tumoral patients for NOM, and in contrast to the significant decrease after BRC (-70%) in tumoral and (-74%) in dysfunctional and NOM (-50%) observed in dysfunctional patients. CRF and dysfunctional patients showed significant response to TRH and DOM, being prolactinoma bearing patients unresponsive to these tests. These results show an hyporesponsivity of pituitary Prl secreting cells to dopaminergic control suggesting the existence of central etiopathological factor in inducing hyperprolactinemia in CRF patients.
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This study examines the role of dopaminergic mechanisms in the regulation of human pancreatic polypeptide (hPP) secretion in 11 normal male volunteers. Administration of domperidone (20 mg iv), an extracerebral inhibitor of dopamine receptors, resulted in a hPP rise (p less than 0.05) within 10 min and a peak response (p less than 0.01) at 15 min after drug administration. Administration of the dopaminergic agonist, bromocriptine, 2.5 mg tid for 4 days eliminated hPP responses to isometric handgrip exercise in these 11 volunteers. These results suggest that dopaminergic mechanisms may exert a tonic inhibitory effect on hPP secretion in normal subjects.
Bruxism is a diurnal or nocturnal parafunctional activity that includes tooth clenching, bracing, gnashing, and grinding. The dopaminergic system seems to be the key pathophysiology of bruxism and diminution of dopaminergic transmission at the prefrontal cortex seems to induce it. We report two patients with diurnal bruxism in whom a bilateral frontal lobe injury resulted from hemorrhagic stroke or traumatic brain injury. These patients' bruxism was refractory to bromocriptine but responded to low-dose metoclopramide therapy. We propose that administering low doses of metoclopramide is possibly a sound method for treating bruxism in a brain injury patient with frontal lobe hypoperfusion on positron emission tomography imaging.
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Dopamine agonists have been reported to increase the risk of cardiac valve regurgitation in patients with Parkinson's disease. However, it is unknown whether these drugs might be harmful for patients with hyperprolactinaemia (HyperPRL). The aim of the study was to evaluate whether HyperPRL patients treated with dopamine agonists had a higher prevalence of cardiac valves regurgitation than that of general population.
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Three trials evaluated the efficacy and safety of pergolide. Eighty-six de novo patients and 314 patients already receiving levodopa were enrolled in an open-label study. Of the de novo patients, 47.5% showed a marked or moderate improvement and 32% showed a mild improvement. In the levodopa add-on group, 53.8% showed marked or moderate improvement and 36.3% showed mild improvement. In a short-term, double-blind study, the efficacy of pergolide was compared with that of bromocriptine. One hundred seventy-two patients were randomized to receive pergolide, and 173 were randomized to receive bromocriptine. In de novo patients, bromocriptine (n = 49) and pergolide (n = 49) demonstrated similar efficacy. However, significantly more levodopa-treated patients in the pergolide group, compared with the bromocriptine group, demonstrated marked or moderate improvements in several items of the rating scale score. In a long-term study, 151 of 314 patients receiving pergolide in combination with levodopa remained in the study for 3 years, and 127 for 4 years, and in these patients the initial improvement was maintained. In 18 of 62 de novo patients, the initial improvement was maintained for up to 3 years. These trials indicate that pergolide has efficacy in patients with Parkinson's disease, either as monotherapy or in combination with levodopa.
Groups of newborn rabbits were treated with exogenous prolactin, with fluphenazine (a stimulant of endogenous prolactin secretion) with bromocriptine (a blocker of endogenous prolactin secretion), or with bromocriptine plus exogenous prolactin, and lean body hydration in these animals was compared with that of untreated controls. Animals treated with prolactin or fluphenazine retained more water than did the controls. Bromocriptine-treated animals retained less water than did the controls. Exogenous prolactin abolished the effect of bromocriptine.
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Three experiments were performed in order to add further support to the hypothesis that the exaggerated aggressiveness elicited by apomorphine in REM sleep deprived rats was due to a state of supersensitivity of post-synaptic dopaminergic receptors in brain. In the first experiment, REM deprived rats displayed much aggressiveness when challenged with 10 and 20 mg/kg of bromocriptine and piribedil. Thus, the intensification of responses by REM sleep deprivation is not restricted to apomorphine, as it was also obtained with two other dopaminergic agonists. In the second experiment, the association of REM deprivation with an injection of haloperidol 24 h before apomorphine administration induced still more aggressive behavior when compared to the rats that were only sleep deprived. It has been claimed that 24 h after haloperidol a state of supersensitivity to dopamine agonists occurs in the brain; therefore, it is probable that REM deprivation could also act similarly. The third experiment showed that haloperidol administered 2 h before apomorphine administration blocked the aggressive behavior in rats either submitted to REM deprivation alone or to REM deprivation plus a previous injection of haloperidol 24 h before. This also favors the proposed hypothesis. Alternative possibilities for explaining the observed hyperresponsiveness of REM deprived rats to apomorphine and other dopaminergic agonists are also analysed.
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The treatment of a slowly growing invasive prolactinoma with bromocriptine for 8 months resulted in a substantial decrease in plasma prolactin levels despite rapid suprasellar tumor expansion. On exploration, this uncommon observation could be attributed to hematogenous metastasis from an occult gastric adenocarcinoma to the pituitary tumor. Apart from infiltration of neighboring parts of the hypothalamus, autopsy revealed no other hematogenous metastases. This extraordinary type of neoplasm-to-neoplasm metastasis was not shown by computed tomography. This possibility should be considered whenever progressive growth of a pituitary mass is accompanied by a decrease in hormonal overproduction.
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To examine whether high serum prolactin levels inhibit follicular maturation, prolactin was injected during diestrus of intact female rats or endogenous prolactin levels were raised by applying a suckling stimulus. Injections of rat prolactin (100 micrograms per injection) given 2 and 1 days before proestrus resulted in a lower estradiol production by proestrous follicles during a 4-h incubation period than follicles isolated from control rats. In 4 out of 7 animals this occurred without a change in serum progesterone and luteinizing hormone (LH) concentrations. In the 3 remaining animals corpus luteum function was activated. In these animals serum LH concentrations were decreased and follicular estradiol production was further suppressed. To study follicular development in the presence of suckling-induced hyperprolactinemia, the following experiment was performed. Removal of a 5-pup litter at Day 13 (0900 h) of lactation (Day 1 = day of parturition) resulted in ovulation at Day 16. Replacement of a new litter 24 h after litter removal did not interfere with ovulation on Day 16. This procedure allowed the study of follicular development between Days 14 and 15 in the presence of raised serum prolactin levels. It appeared that this treatment did not affect follicular growth, but in vitro estradiol production by preovulatory follicles isolated at Day 15 was lower than in follicles isolated from nonlactating animals. In 3 out of 13 animals corpus luteum function was reactivated. In these animals LH levels and follicular estradiol production were significantly suppressed. Treatment with bromocriptine (1 mg per injection) on Days 13 and 14, in addition to litter replacement, restored the high estradiol production at Day 15 without affecting serum LH concentrations. The results of this study demonstrate that in the presence of high prolactin levels, follicular estradiol production is low. The inverse relation between prolactin and follicular estradiol production in the presence of unchanged serum LH levels suggests that prolactin can have a direct action on estrogen biosynthesis of follicle cells.
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A 14-year-old girl presented with a rapidly growing, invasive prolactin-producing pituitary tumor that failed to respond to dopamine agonist medication. Histological, immunocytochemical, and ultrastructural studies of the surgically removed tissue revealed a pleomorphic, chromophobic, or slightly acidophilic pituitary tumor that was immunoreactive for prolactin and that, according to electron microscopy, consisted of atypical lactotrophs showing no evidence of cell shrinkage. In situ hybridization demonstrated large amounts of prolactin messenger ribonucleic acid (mRNA), moderate amounts of estrogen receptor mRNA and dopamine (D2) receptor mRNA, and an absence of growth hormone mRNA in the tumor cells. Because D2 receptor mRNA was present in the tumor, causes other than D2 receptor loss may have been responsible for the resistance of the lactotrophs to dopamine agonist administration.
To review evidence for the treatment of neuroleptic malignant syndrome (NMS) and to discuss how to rechallenge patients with neuroleptics when continued pharmacotherapy for chronic psychological illness is required.
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We have studied a women who presented at the age of 51 with a large FSH and alpha-subunit producing pituitary adenoma. Following insertion of ventriculo-peritoneal shunts and external pituitary irradiation there was no change in the elevated serum concentrations of FSH, and alpha-subunit over a four year period although she developed both ACTH and TSH deficiency. Various drugs, however, did alter the FSH and alpha-subunit concentrations and these changes suggest possible mechanisms controlling FSH secretion. Ethinyloestradiol 0.03 mg daily for three weeks suppressed serum FSH to 77% of the basal level (240 +/- 35 i.u./l to 184 +/- 20 i.u./l) but alpha-subunit rose to 130% of basal level (281 +/- 50 ng/ml to 366 +/- 40 ng/ml). On ethinyloestradiol 0.1 mg daily, FSH suppressed to 17% of basal (40 +/- 11 i.u./l) with no change in alpha-subunit concentration, while on 0.2 mg daily suppression of FSH was similar but alpha-subunit fell to 59% of basal (190 +/- 28 ng/ml). Dexamethasone, 3 mg daily for one week reduced FSH to 53% of the initial concentration and alpha-subunit to 74% while bromocriptine 7.5 mg daily for three months, reduced FSH to 39% and alpha-subunit to 66% of basal. Neither thyroxine, 0.2 mg daily for four weeks, nor an LHRH analogue, (Buserelin, Hoechst) 200 micrograms, three times daily for three months elicited any effect. Chromatography on Sephadex G100 showed that serum FSH and alpha-subunit both had Kav values somewhat lower than those of their standard counterparts (FSH, 0.20 vs 0.25; alpha-subunit 0.35 vs 0.45).(ABSTRACT TRUNCATED AT 250 WORDS)
Serious ADRs reported between 1994 and 2010 in association with bromocriptine used for lactation inhibition in France.
In 32 patients with macroprolactinomas or functionless pituitary macroadenomas biochemical and clinical data were correlated with PRL immunocytochemistry. Serum PRL levels revealed a positive correlation with tumour PRL content. Hyperprolactinaemia of 3000 mU/l or more was found only in patients with PRL-positive tumours. In 15 patients with borderline hyperprolactinaemia (below 3000 mU/l), 7 PRL-positive and 8 PRL-negative macroadenomas were found, and in 9 normoprolactinaemic patients 4 PRL-positive and 5 PRL-negative macroadenomas. Patients with PRL-immunostainable tumours had significantly higher median basal serum PRL (P less than or equal to 0.05) than patients with PRL-negative tumours. PRL stimulation after TRH, basal and GnRH-stimulated FSH and LH did not show significant differences between the two groups. A discriminant analysis using 6 biochemical variables was attempted to differentiate between PRL-negative and -positive tumours, which would be helpful in patients with borderline hyperprolactinaemia. Dopamine agonist therapy led to suppression of serum PRL with few exceptions in patients with PRL-positive and -negative tumours, whereas shrinkage was only observed in PRL-immunostainable tumours with high serum PRL levels (over 18,000 mU/l). All patients with PRL-negative tumours showed no change or even growth of the tumour despite dopamine agonist therapy. Our observations indicate that a pituitary macroadenoma associated with serum PRL of more than 3000 mU/l is most probably a prolactinoma (tumour immunostainable for PRL). Dopamine agonist therapy is effective in PRL suppression and tumour shrinkage in most of these patients. Macroadenomas without hormone hypersecretion or with borderline hyperprolactinaemia below 3000 mU/l may or may not contain PRL-immunostainable cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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Patients were studied in an academic environment.
The combination treatment with bromocriptine and clomiphene citrate was applied to 11 normoprolactinemic anovulatory patients who did not respond to clomiphene citrate alone. This combination treatment restored ovulation in 8 of these patients (72.7%). Conception was observed in 2 patients (18.1%) out of 11. The patients who responded to combination treatment showed a significant increase in the serum level of estradiol in the preovulatory phase, of progesterone in the mid-luteal phase, and a significant decrease of serum prolactin. They also showed significant increase in the frequency of luteinizing hormone (LH) pulsatility on day 12 of the cycle from 1.38 +/- 0.86 to 3.75 +/- 0.83 pulses/4h. The 3 patients who did not respond to combination treatment showed no increase in the serum level of estradiol or progesterone, but showed increase in the frequency of LH pulsatility in spite of continuous anovulation. These results indicate that the combination treatment with bromocriptine and clomiphene citrate is effective for treatment of patients with normoprolactinemic anovulation who do not respond to clomiphene alone, and suggest that the mechanism of the effect of combination treatment is related to an increase in the frequency of LH pulsatility caused by bromocriptine, which in turn stimulates follicular maturation.
HVA and 5-HIAA levels were determined in the lumbar CSF of 17 patients affected by endogenous depression. The modification of the amine metabolites after treatment (tryciclics, bromocriptine, trazodone, ECT) were not related to the specific therapy nor to the clinical improvement. In 11 patients, HVA and 5-HIAA showed opposite modificatons. The possible role of interactions between dopaminergic and serotoninergic systems in the pathogenesis of endogenous depression is discussed.
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1. The effects of bromocriptine (BC) on choreiform movement were compared with those of bromperidol (BP) and fluphenazine (FLZ) in a patient with Huntington disease. The patient (male, 42 years old) was treated with BP (15 mg/day, 4 weeks), FLZ (3 mg/day, 4 weeks), low dose of BC (5 mg/day, 4 weeks) and relatively high dose of BC (10 mg/day, 8 weeks). The CSF content of homovanilic acid (HVA) was assayed at last day of the each drug trial. The efficacy of the drugs was evaluated by electromyography. 2. Although BP and FLZ did not succeed to ameliorate the choreiform movement, both low dose and high dose BC showed rapid improvement of the involuntary movement. The CSF HVA concentration was 35.0 ng/ml before beginning treatment. Whereas FLZ and high dose of BC substantially increased the levels of HVA after the dosage (49.3 and 53.1 ng/ml, respectively), moderate increase of HVA (41.5 ng/ml) was observed when the low dose of BC was administered. These observations suggest that increase of CSF HVA might be necessary for clinical improvement of choreiform movement but not correlate with the degree of improvement and dopamine agonists could be useful drug for the treatment of choreiform movement which is refractory to the administration of neuroleptics.
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Neuroprotection in Parkinson's disease is defined as halting or slowing of the progression of neurodegeneration. Neuroprotective properties of dopamine agonists may be mediated via several mechanisms, (levodopa-sparing effect, decreased dopamine turnover, antioxidant activity or inhibition of the subthalamic nucleus). Many preclinical studies demonstrate that bromocriptine, pergolide, pramipexole, ropinirole and other dopamine agonists provide significant protection against neuronal loss in experimental models. Only a few studies have investigated the potential neuroprotective effect of dopamine agonists at the clinical level. Several recent trials have used neuroimaging biomarkers to assess the rate of dopamine neuron loss in dopamine agonist-treated versus levodopa-treated patients using fluoro-dopa PET or beta-CIT SPECT. Ropinirole slowed the decline of putaminal dopamine storage capacity and pramipexole reduced decline in striatal beta-CIT uptake to a similar extent, compared to levodopa. It is not possible to exclude, however, some pharmacologic or pharmacodynamic effects of drugs on imaging markers in these studies, as well as symptomatic effects of dopamine agonist treatment in clinical outcomes.
The role of dopamine (DA) input on the activity of glutamate neurons was investigated on rat striatal and cortical tissue using the measurement of sodium-dependent high affinity glutamate uptake (HAGU) as an index. Incubation of the tissue in the presence of DA, apomorphine or bromocriptine produced marked inhibition of 3H-glutamate uptake from rat striatal homogenates. No change occurred with samples from the frontal cortex. Dopaminergic inhibition of HAGU in striatal homogenates was shown to be reversed in the presence of haloperidol or domperidone which act by blocking dopaminergic receptor sites. These results are consistent with the existence of an inhibitory control of the neuronal activity of the glutamatergic neurons in the striatum by the nigro-striatal dopaminergic input. The effects could be due to the activation of D2-like DA receptors located at pre-synaptic levels on cortico-striatal glutamatergic nerve endings.