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Parlodel

Generic Parlodel is the most effective preparation in struggle against female diseases as persistent breast milk production, infertility, amenorrhea (lack of a menstrual period) and other disorders caused by prolactin-secreting tumors. Generic Parlodel can also be helpful for patients with Parkinson`s disease and its symptoms caused by low levels of dopamine in the brain. Generic Parlodel acts as up-to-date remedy reducing prolactin level.

Other names for this medication:

Similar Products:
Apokyn, Mirapex, Requip

 

Also known as:  Bromocriptine.

Description

Generic Parlodel is created using perfect medical formula which is a magnificent weapon against women problems such as persistent breast milk production, infertility, amenorrhea (lack of a menstrual period) and other disorders caused by prolactin-secreting tumors. Target of Generic Parlodel is to reduce prolactin level and help to produce breast milk and fertility in women.

Generic Parlodel acts as up-to-date remedy reducing prolactin level. When it is used for treatment of Parkinson disease, it works by stimulating dopamine receptors in some certain brain parts.

Parlodel is also known as Bromocriptine, Proctinal.

Generic Parlodel is a hormone (dopamine agonist).

Generic Parlodel can't lead to vaginal bleeding, uterine or breast cancer, breast tenderness.

Generic name of Generic Parlodel is Bromocriptine.

Brand name of Generic Parlodel is Parlodel.

Dosage

Generic Parlodel is available in the form of tablets (2.5 mg) which should be taken by mouth with meals or without it.

Take Generic Parlodel every day at the same time and remember that its dosage depends on patient's health state.

If you want to achieve most effective results do not stop taking Generic Parlodel suddenly.

Overdose

If you overdose Generic Parlodel and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store below 25 degrees C (77 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Parlodel are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Parlodel if you are allergic to Generic Parlodel components.

Do not take Generic Parlodel if you are pregnant, planning to become pregnant or breast-feeding.

Do not use Generic Parlodel in case of having uncontrolled high blood pressure, blood poisoning, having recently given birth or have coronary artery disease (chest pain) or any other severe heart disease.

In case you take Generic Parlodel while using birth control pills, remember that birth control pills become less effective

Patients under 15 years should be extremely careful with Generic Parlodel.

Avoid alcohol.

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It can be dangerous to stop Generic Parlodel taking suddenly.

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Hyperprolactinemia has been associated with impaired metabolism, including insulin resistance. However, the metabolic effects of elevated prolactin (PRL) levels are not completely clarified. The aim of this study was to obtain more insights of metabolic consequences in hyperprolactinemia patients. Fourteen consecutive patients, eight women and six men, aged 39.7 (±13.7) years with prolactinomas (median PRL 72 [49-131] μg/L in women and 1,260 [123-9,600] μg/L in men) were included. Anthropometric data and metabolic values were studied before and after 2 and 6 months on DA agonists (Bromocriptine [5.7 (±3.9) mg/day, n = 13] or Cabergoline [0.5 mg/week, n = 1]). Euglycemic hyperinsulinemic clamps were studied in six patients before and after 6 months of treatment. PRL normalized in all patients. Anthropometric data changed only in males with a significant decrease of median body weight (95.6 [80.7-110.1] to 83.4 [77.8-99.1] kg, P = 0.046), waist circumference and fat percentage after 6 months. LDL cholesterol was positively correlated to PRL at diagnosis (r = 0.62, P = 0.025) and decreased within 2 months (3.4 [±0.9] to 2.9 [±0.6] mmol/L, P = 0.003). Insulin, IGFBP-1 and total adiponectin levels did not change. Insulin sensitivity tended to improve after 6 months; M-value from 5.7 (±1.8) to 7.8 (±2.6) mg/kg/min, P = 0.083 and per cent improvement in M-value was correlated to per cent reduction in PRL levels (r = -0.85, P = 0.034). In conclusion, beneficial metabolic changes were seen in prolactinoma patients after treatment with DA agonists, underscoring the importance of an active treatment approach and to consider the metabolic profile in the clinical management of hyperprolactinemia patients.

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The effects of bromocriptine in patients with Parkinson's disease manifesting various problems in levodopa therapy were tested in a double-blind manner with the collaboration of 59 institutions. The slow and low principle was in part adopted. Either bromocriptine or placebo was added to levodopa. Twenty-nine % of the bromocriptine-treated patients (n = 108), in contrast to 14.8% of the placebo-treated (n = 108), showed either marked or moderate improvement (P less than 0.05). Twenty to 37% improvement was noted in most of the symptoms studied in those treated with bromocriptine. The significant superiority of bromocriptine was also noted in the effects on wearing-off phenomena and frozen gait. No irreversible side effects were noted. It is concluded that bromocriptine is useful in patients who are manifesting various difficulties in levodopa therapy. Our results are comparable to those using higher maintenance doses. Dopamine antagonistic actions were not observed. This is unlike the case with experimental animals.

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The clinical pharmacokinetics of ergotamine, dihydroergotamine, ergotoxine, bromocriptine, methysergide, and lergotrile are reviewed. Generally the new radioimmunoassay methods have partially resolved the problems involved in determining some of these ergot derivatives in biologic fluids after the low doses used clinically. However, our present knowledge of their pharmacokinetics is limited and much work remains to be done in this area. Many cases show a great difference between results produced with a radioactive drug and with radioimmunoassay. The longer half-lives measured by using a radioactive derivative are apparently due to the many metabolites of ergot alkaloids. However, we still do not know the clinical importance of these metabolites. For instance, the amount of dihydroergotamine reaching the systemic circulation remains below 1% (radioimmunoassay), but according to studies performed with a radioactive derivative the absorption quotient is about 30%. Further studies are needed to resolve the problem of an apparently high "first-pas" metabolism of this and other ergot alkaloids in the liver or gastrointestinal mucosa.

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This study focused on the three-dimensional imaging of hormone-secreting cells and their microvascular environment in estrogen-induced prolactinoma of the rat pituitary gland. Adult female Wistar-Imamichi rats were injected with estradiol dipropionate and killed 7 weeks later. Some rats given estrogen for 7 weeks also were injected with bromocriptine before killing. To obtain a detailed three-dimensional image of microvessels, dialyzed fluorescein isothiocyanate (FITC)-conjugated gelatin was injected into the left ventricle of the rat heart. After the perfusion, the pituitary glands were resected and subjected to immunohistochemistry (IHC). To evaluate the effects of estrogen and bromocriptine, IHC was performed with antibodies against prolactin (PRL), adrenocorticotropic hormone (ACTH), and growth hormone (GH). With the combination, microvessels and cells containing PRL, ACTH, and GH could be clearly identified by confocal laser scanning microscopy (CLSM). The PRL cells increased in number and became hypertrophic after prolonged exposure to estrogen. With bromocriptine administration after estrogen treatment, however, PRL cells decreased in number and became atrophic. The current study revealed that estrogen and bromocriptine had significant effects on PRL secretion and the microvascular environment. Therefore, this technique (FITC injection and IHC) with CLSM is suitable for the three-dimensional imaging of hormone-secreting mechanisms under various conditions.

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In parathyroid adenomas and experimentally in the normal rat pituitary gland, cell replication and secretory activity were previously shown to be correlated. A similar relationship has now been investigated in human pituitary tumours, since this could have relevance to their growth and aetiology. The effect of bromocriptine on the two variables was examined.

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Two hundred and thirty patients with acromegaly were diagnosed and treated in a prospective cooperative study in twelve university clinics. Primary treatment was: trans-sphenoidal surgery (152 patients), trans-sphenoidal surgery with additional cryotherapy (eighteen patients), Yttrium-90-implantation (thirty patients), bromocriptine (thirty patients). The results of endocrine assessment before treatment and 6 months after operation, 90-Y implantation or commencement of bromocriptine therapy are reported. The best results (low GH, no or little deterioration of pituitary function, low complication rate) were achieved by trans-sphenoidal surgery, especially in patients with intrasellar tumours (basal GH less than 5 ng/ml in 59.7%). Results were less good with increasing tumour size. Additional cryosurgery was accompanied by a high rate of anterior pituitary insufficiency and is no longer employed. Yttrium-90-implantation resulted in less improvement in GH levels (basal GH less than 5 ng/ml in 51.7% of patients with intrasellar tumours), a high rate of pituitary insufficiency and more complications. Bromocriptine treatment was least effective in lowering GH concentrations (basal GH less than 5 ng/ml in 33% of patients with intrasellar tumours). Different criteria for treatment success were compared. In the entire group, basal GH concentrations below 5 ng/ml were attained in 51.7% of all patients whose values were higher than this prior to treatment. Suppressibility of GH below 2 ng/ml during glucose loading occurred in only 34.9%. An abnormal GH response to TRH/LHRH was present in 47.2% before and in 43.4% after/during treatment. The prognostic significance of this latter finding must be evaluated by further study.

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We, and others, have previously described the histological changes that occur in the prostate gland of intact Noble (NBL) rats following prolonged hormonal treatment. Dysplasia, a pre-neoplastic lesion, develops specifically in the dorsolateral prostates (DLPs) of NBL rats treated for 16 weeks with a combined regimen of testosterone (T) and estradiol-17beta (E2) (T + E2-treated rats). Concurrent with DLP dysplasia induction, the dual hormone regimen also elicits hyperprolactinemia, in addition to an elevation of nuclear type II estrogen binding sites (type II EBS), no alteration in estrogen receptors (ER), and marked epithelial cell proliferation in the dysplastic foci. The aim of this study was to investigate whether the dual hormone action is mediated via E2-induced hyperprolactinemia. Bromocriptine (Br), at a dose of 4 mg/kg body wt per day, was used to suppress pituitary prolactin (PRL) release. Serum PRL levels were lowered from values of 341 +/- 50 ng/ml in T + E2-treated rats to 32 +/- 10 ng/ml in Br co-treated animals. The latter values were comparable to those in untreated control rats. In addition, Br co-treatment effectively inhibited the evolution of dysplasia (six out of eight rats) and the often associated inflammation (five out of eight rats) in most animals. In contrast, Br co-treatment did not suppress the T + E2-induced type II EBS elevation nor alter ER levels in the DLPs of these rats, when compared with T + E2-treated rats. These data extend the many previous studies that have detailed marked influences of PRL on rat prostatic functions. However, the current study is the first to implicate PRL in prostatic dysplasia induction in vivo.

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Widespread use and abuse of cocaine have increased the frequency with which health professionals must manage acute and chronic intoxication and the complications stemming from drug ingestion. Acute intoxication from catecholamine excess progresses through three stages, affecting the cardiovascular, respiratory, and central nervous systems. Management is to support or return these systems to normal with sedation, beta blockade, and antiarrhythmics. Casual cocaine use is no longer considered benign, and numerous related medical complications are now recognized. Dopaminergic systems are the principal sites of reward and participate in abstinence symptomatology, putatively through depletion of dopamine and changes in receptor sensitivity and responsiveness. Long-term treatment approaches have focused on psychologic strategies of behavior modification and supportive psychotherapy. Pharmacotherapy with desipramine, amantadine, and bromocriptine was shown in preliminary studies to minimize the symptoms of cocaine withdrawal when used adjunctively with psychotherapy. The response to treatment may depend on the patient's premorbid psychiatric status.

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The "absolute safety" of bromocriptine as a drug of choice in suppression of lactation is questioned. Two cases of cerebrovascular events after the use of bromocriptine for lactation suppression are presented, and the available, pertinent literature is reviewed.

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Dopamine (DA) neurons participate in tonic inhibition of prolactin (PRL), whereas beta-endorphin (beta-End) and serotonin (5-HT) neurons appear to be important stimulatory links for nocturnal PRL surges that occur throughout the first half of pregnancy in the rat. The purpose of this study was to determine how these neuronal components might be organized within the pathway controlling PRL release during gestation. Maximal stimulation of DA receptors with the agonist bromocriptine mesylate (Bromo) completely blocked the PRL response to beta-End (100 ng/microliters/min for 15 min) given intracerebroventricularly (i.c.v.) on day 8 of pregnancy. DA receptor blockade, produced by implanting a 25 mg pellet of haloperidol (Hal) on day 7 of pregnancy, resulted in PRL levels of 500-600 ng/ml by the following morning. beta-End i.c.v. or 250 mg/ml/kg BW of the DA synthesis inhibitor, alpha-methyl-p-tyrosine (alpha-MPT), given during the intersurge period, were equally effective in significantly increasing PRL (p less than 0.01) above pretreatment levels. beta-End and alpha-MPT evoked similar increases in rats pretreated with Hal, suggesting the stimulatory effect of beta-End on nocturnal PRL surges may primarily be due to DA inhibition. The next objective was to determine how beta-End and 5-HT might interact to stimulate the nocturnal surge. Day 8 pregnant rats were infused continuously with the opioid receptor blocker, naloxone hydrochloride (Nal), at a rate of 2.0 mg/10 min from 1000-1300 h. The PRL response to an injection of 20 mg/kg BW 5-hydroxytryptophan (5-HTP) at 1200 h was greatly attenuated, compared to controls infused with saline instead of Nal. This suggests that 5-HT stimulates PRL, at least in part, by an action at opioid receptors. Distilled H2O or 10 mg/kg BW of the selective S2 receptor blocker, ketanserin tartrate (Ket), was given intraperitoneally (i.p.) during the intersurge period on day 8 of pregnancy. All animals demonstrated an identical response to beta-End given 2 hours later, regardless of the type of pretreatment. It appears that beta-End does not stimulate PRL by way of an S2 receptor. Although beta-End induced a significant increase in PRL on day 16 of pregnancy, the response was attenuated by more than 60% compared to the response on day 8 of pregnancy. This attenuation may involve placental lactogens, shown to be secreted during this time and to inhibit PRL secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

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Our findings emphasize the importance of PRL, locally produced by infiltrating T lymphocytes, for aberrant synovial cell functions in RA, and suggest possible clinical application of PRL inhibitors.

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Electronic searches of Cochrane Library, EMBASE, MEDLINE, PsycLIT, Biological Abstracts and LILACS; reference searching; personal communication; conference abstracts; unpublished trials from pharmaceutical industry; book chapters on treatment of cocaine dependence, was performed for the primary version of this review in 2001. Another search of the electronic databases was done in December of 2002 for this update. The specialised register of trials of the Cochrane Group on Drugs and Alcohol was searched until February 2003.

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The increased occurrence of levodopa adjunct in autonomically impaired PD suggests that there is a more rapid deterioration of functional performance in parkinsonian patients with early autonomic involvement.

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Hypothalamo-pituitary disconnection (HPD) in the sheep results in a two-fold increase in pituitary intermediate lobe (IL) immunoreactive (ir)-alpha-N-acetylated endorphin (NacEP) and ir-alpha-melanocyte-stimulating hormone (alpha MSH) content. The rise in IL NacEP content is accompanied by a markedly altered pattern of processing, in that NacEP1-27 becomes the dominant molecular species with a complementary fall in Nac alpha-EP and Nac gamma-EP. To determine if these effects reflect the loss of descending dopaminergic neuronal input to the IL, we have chronically treated two groups (n = 4 per group) of normal sheep with the dopamine antagonist haloperidol or the dopamine agonist bromocriptine; a group of HPD sheep were also treated with bromocriptine. Acid extracts of IL were diluted and ir-alpha-MSH and ir-NacEP content determined by radioimmunoassay; aliquots were submitted to reversed-phase HPLC and collected fractions similarly assayed. Bromocriptine lowered ir-NacEP and ir-alpha-MSH by about 30%; on HPLC the ir-NacEP profiles, and perhaps to a lesser extent those for ir-alpha-MSH were qualitatively similar to untreated controls. In contrast, haloperidol increased by about 45% both ir-NacEP and ir-alpha-MSH levels and produced a marked change in the ir-NacEP molecular profile, with NacEP1-27 becoming the predominant molecular form and other species representing only minor components in the chromatogram. In the treated HPD group, bromocriptine partially restored the processing profiles previously observed in HPD animals to those found in untreated intact animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cushing's syndrome is a serious endocrine condition for which no treatment has been proven fully satisfactory at least for its pituitary dependent form (Cushing's disease). Indeed, despite some advances in pharmacology (cyproheptadine, bromocriptine, lisuride) and in surgical and radiation procedures at pituitary level, a definitive cure is often delayed. The inhibitors of steroids synthesis (ketoconazole, aminoglutethimide, metyrapone, mitotane) are still very valuable tools in its management as a palliative treatment.

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Injection of prostaglandin F2 alpha (PGF2 alpha) initiated a significant increase in plasma prolactin levels in all goats except those in anoestrus. Luteolysis occurred in non-pregnant goats during the mid luteal phase when the goats were given PGF2 alpha either with or without the suppression of prolactin release by bromocryptine (CB154). Luteolysis and subsequent parturition also occurred in pregnant goats in mid and late gestation after PGF2 alpha injection, with an associated release of prolactin and decrease in plasma progesterone. Acute prolactin release in response to injection of thyrotrophin releasing factor may have had a transient effect on plasma progesterone levels, but did not appear to be luteolytic in either pregnant or non-pregnant goats.

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Experience with bromocriptine in 106 patients treated over nine years was reviewed. Most of the patients were already being treated with levodopa (combined with a peripheral decarboxylase inhibitor). These patients, after having initially achieved a good response to levodopa, were no longer responding satisfactorily. Most of the patients were also experiencing diurnal oscillations in performance: "wearing off" and "on-off" phenomena. In these patients previous attempts at changing the dose (increasing or decreasing) or changing the scheduling of levodopa had been unsuccessful. Bromocriptine was added to levodopa beginning at a dose of 5 mg/day, and each week was increased by another 5 mg/day. At a dose of bromocriptine of at least 25 mg/day, there was a decrease in disability in the majority of patients with a decrease in the severity of the diurnal oscillations in performance (especially "wearing off" phenomena). In most patients, the addition of bromocriptine resulted in an approximately 10% reduction in the dose of levodopa. The majority of patients sustained their improvement at least one year. In some patients improvement was sustained for up to five years. The therapeutic efficacy of bromocriptine was limited in many patients by the occurrence of adverse effects including mental changes, dyskinesias, orthostatic hypotension, and nausea. These adverse effects could often be minimized by reducing the dose of bromocriptine or levodopa. All adverse effects were reversible upon stopping the drug. We have found bromocriptine to be a valuable adjunct in the treatment of these patients.

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The on-off phenomenon is an almost invariable consequence of sustained levodopa treatment in patients with Parkinson's disease. Phases of immobility and incapacity associated with depression alternate with jubilant thaws. Both pharmacokinetic and pharmacodynamic factors are involved in its pathogenesis, but evidence is presented to indicate that the importance of levodopa handling has been underestimated and that progressive reduction in the storage capacity of surviving nigrostriatal dopamine terminals is not a critical factor. Re-distribution of levodopa dosage which may mean smaller, more frequent doses, or larger less frequent increments, may be helpful in controlling oscillations in some patients. Dietary protein restriction, the use of selegiline hydrochloride and bromocriptine may also temporarily improve motor fluctuations. New approaches to management include the use of subcutaneous apomorphine, controlled-release preparations of levodopa with a peripheral dopa decarboxylase inhibitor and the continuous intra-duodenal administration of levodopa.

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Treatment group received 150 mg of CC from day 5 to 9 and 7.5 mg bromocriptine continuously, with hCG 10,000 units on day 16 or 17. Control group received the same protocol of CC combined with placebo.

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At the end of the 1st month, 64% of the patients had PRL suppression of > 75% of baseline values. After 1 year, 88% of the cases had PRL suppression of > 90%. Persistent PRL normalization was seen in three cases. Tumor shrinkage was seen in 64% of the patients on day 5, in 73% on day 28, and in 90% after 6 months of treatment. Early visual field improvement was seen in 83% of the cases. All patients had improvement of clinical symptoms.

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In 21 patients with prolactinomas resistant to bromocriptine, we studied the effects of CV 205-502 on PRL hypersecretion and tumor mass, as assessed by consecutive computed tomography examinations. Cell culture studies were performed in 9 of such tumors. In 11 patients (group I; 52%) with a mean baseline plasma PRL level of 468 +/- 160 micrograms/L (+/- SE), normal PRL values were achieved after 1-6 months of treatment with 0.1-0.5 mg/day CV 205-502. Tumor size was reduced by 25% or more in 6 of 11 patients. In group II (n = 10), PRL levels (948 +/- 538 micrograms/L at baseline) were reduced by 48% after treatment with 0.1 mg/day CV 205-502. A progressive increase in the daily dose up to 0.5 mg did not further improve the partial reduction of PRL. No reduction in tumor size was observed in this group. The cell culture studies showed that 1) a brief exposure to both drugs provoked PRL suppression lasting 3 days; 2) in group I, CV 205-502 suppressed PRL release more efficiently than bromocriptine, with a maximal inhibition of 72% at 10(-9) mol/L; and 3) in group II, CV 205-502 only achieved a 26% inhibition of PRL release at 10(-8) mol/L, superimposable to that of bromocriptine. These data indicate that in at least half of such adenomas resistant to bromocriptine, CV 205-502, probably due to its higher affinity toward the D2 dopamine receptor, can overcome such resistance.

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The dopamine agonist bromocriptine and L-dopa significantly inhibited whereas dopamine antagonist haloperidol aggravated the gastric lesions induced by pylorus ligation in mice as found earlier for rats. Furthermore, the successful use of a dopamine antagonist alone for the induction of gastric lesions also in mice was demonstrated, since the gastric lesions were induced by a single dose of haloperidol without any additional noxious treatment. Bromocriptine successfully inhibited both the gastric lesion-potentiating as well as the gastric lesion-inducing effect of haloperidol.

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It is useful to divide Parkinsonian patients into those whose signs are confined to tremor, rigidity and akinesia, and those with evidence of a more diffuse disturbance. The treatment of choice in the former is levodopa combined with a peripheral decarboxylase inhibitor. At the onset of the disease, when disability is minimal, amantadine or anticholinergic drugs may suffice. Bromocriptine is useful in some patients who derive only short-lived benefit from each dose of levodopa. The role of stereotactic surgery is now confined to patients with an incapacitating unilateral tremor which has not improved with drug therapy. In elderly patients with evidence of diffuse cerebral dysfunction such as dementia, grasp reflex, hyper-reflexia or severe postural hypotension, the beneficial effect of these drugs is often outweighed by the side effects. Small doses of levodopa alone may be tried. Anticholinergic drugs and amantadine should be avoided in such patients.

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The role of GH was examined using an antiserum to rat GH (anti-rGH). When administered to lactating rats on day 2 of lactation it was without effect, whereas bromocriptine markedly suppressed milk production, with no additional effect of combined treatment. On day 6 of lactation, treatment with anti-rGH was also without effect, whilst bromocriptine again suppressed milk production. Combined treatment, however, suppressed milk synthesis completely, suggesting that GH was capable of maintaining about 50% of normal milk yield in the absence of prolactin at day 6 of lactation. By day 14 of lactation, anti-rGH treatment alone was capable of decreasing milk yield by about 20%, and again milk secretion only stopped completely when GH and prolactin were suppressed. These data suggest that the role of GH in supporting lactation increases as lactation progresses. The effects of GH in stimulating growth and in increasing milk yield in ruminants have been proposed to be mediated via insulin-like growth factor-I (IGF-I). In rats treated with anti-rGH, both IGF-I and IGF-II were decreased in serum. The concentration of the major IGF-binding protein (IGFBP-3) was not, however, affected by inhibition of GH or prolactin individually, but was decreased in animals treated with bromocriptine and anti-rGH. In animals given both bromocriptine and anti-rGH, concurrent treatment with recombinant bovine GH maintained milk yield at 50% of control values and normalized serum IGF-I, IGF-II and IGFBP-3 concentrations. By contrast, concurrent treatment with IGF-I or IGF-II, despite normalizing their respective concentrations in serum, failed to affect milk yield.(ABSTRACT TRUNCATED AT 250 WORDS)

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The long term efficacy and safety of transsphenoidal resection for preoperative diagnosis of PRL-secreting pituitary adenomas in a large series of women have not been described. Four hundred and nine consecutive women at this university tertiary referral center undergoing transsphenoidal resection for preoperative diagnosis of PRL-secreting pituitary adenoma were followed for a minimum of 4 yr. The objective was to determine the efficacy and morbidity of this procedure and to identify features correlating with the resolution of hyperprolactinemia. Outcome measures included referral, preoperative, surgical, postoperative hospitalization, and long-term follow-up information, including recent PRL concentration. Follow-up was ascertained in 83% of patients who were followed for a mean of 9.2 yr. Recurrence of hyperprolactinemia occurred in 47% of total patients, but in only 16% with a single surgical procedure, histological diagnosis of prolactinoma, and postoperative PRL concentration of 5 ng/mL or less. The best single predictor of cure was postoperative day 1 PRL concentration of 5 ng/mL or less. Eighty-eight percent of women desiring conception conceived within 1 yr. Glucocorticoid-dependent hypopituitarism occurred in 23% of patients undergoing postoperative radiotherapy. There was no operative mortality. Operative morbidity was low. Our experience demonstrates that women undergoing transsphenoidal surgery for diagnosis of PRL-secreting adenoma form a heterogeneous patient population. The best long term results are achieved in the pure prolactinoma group, for whom transsphenoidal resection is generally safe and effective.

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A 24-year-old woman (G1P0) presented at 24 weeks gestation with massive hypertrophy of her breasts. A decision to operate was made by a multidisciplinary team. At 30 weeks gestation, bilateral mastectomies were performed, with removal of more than 8 kg per side. Reconstruction was started 10 months after delivery using tissue expanders followed by definitive implants.

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parlodel medication 2015-12-28

124 patients with sleep events were found in 20 publications. Overall, 6.6% of patients taking dopamine agonists who attended movement disorder centres had sleep events. Men were over-represented. Sleep events occurred at both high and low doses of the drugs, with different durations of treatment (0-20 years), and with or without preceding signs of tiredness. Sleep attacks are a class effect, having been found in patients taking the following dopamine agonists: levodopa (monotherapy in 8 patients), ergot agonists (apomorphine in 2 patients, bromocriptine in 13, cabergoline in 1, lisuride or piribedil in 23 buy parlodel , pergolide in 5,) and non-ergot agonists (pramipexole in 32, ropinirole in 38). Reports suggest two distinct types of events: those of sudden onset without warning and those of slow onset with prodrome drowsiness.

parlodel online 2015-06-20

The involvement of central dopamine (DA) neurons in the rewarding action of cocaine is well established. Cocaine euphoria depends on DA activation, and cocaine increases DA neurotransmission by blocking synaptic reuptake. Chronic cocaine use, however, appears to deplete brain DA, and perhaps leads to cocaine craving and withdrawal states. Bromocriptine, a specific DA receptor agonist, appears to ameliorate buy parlodel cocaine craving. Possible clinical roles for bromocriptine, and for DA receptor antagonists, are outlined.

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Nelson's syndrome is a severe complication of bilateral adrenalectomy performed in the treatment of some Cushing's diseases, and its management remains difficult. Trough the observation of a patient suffering from a severe form of Nelson's syndrome for more than 10 years, the authors review the literature buy parlodel and discuss the main current therapeutic possibilities.

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To investigate the effect of prolactin on CD40 and CD154 expressions on the surface of peripheral blood mononuclear cells in patients with systemic buy parlodel lupus erythematosus (SLE) and explore the role of prolactin in the pathogenesis of SLE.

parlodel drug study 2016-07-12

The authors report clinical observations in 12 acromegalic patients treated with long-acting octreotide (Sandostatin LAR, Novartis, 20 mg intramuscular injection per 28 days administered for 6-36 months). Clinically and hormonally active acromegaly was evidenced in all patients by the presence of typical clinical symptoms, increased serum growth hormone and insulin-like growth factor I concentrations, and by non-suppressible serum growth hormone levels after oral glucose administration. In all patients previous treatments (transsphenoidal surgery, pituitary irradiation and bromocriptine therapy) were uneffective or contraindicated, or they were refused by the patients. Octreotide test (Sandostatin, Novartis, 100 g subcutaneously) performed in all patients before treatment precisely predicted the hormonal effectiveness of long-acting octreotide treatment. Three-six months after therapy serum growth hormone levels buy parlodel decreased from 13.6 +/- 3.9 ng/ml (mean +/- SD) to 3.4 +/- 1.7 ng/ml, while insulin-like growth factor I concentrations decreased from 483 +/- 127 ng/ml to 248 +/- ng/ml. Of the 12 patients 7 (58%) had serum growth hormone levels considered as safe values (< 2.5 ng/ml), whereas in 9 patients (75%) serum insulin-like growth factor I concentrations returned to age- and sex-matched normals. Repeat pituitary magnetic resonance imaging performed in 8 patients treated longer than 1 year revealed a decrease of tumor size in 3 patients (37%). There was a considerable clinical improvement during treatment: severe headache, which was present in most patients, as well as perspiration, joint pain, swelling of extremities, and weakness markedly decreased or disappeared. These results indicate that long-acting octreotide offers a very effective treatment of choice in acromegalic patients in whom other previous therapies were ineffective, contraindicated, or refused.

parlodel dosage used 2016-11-28

A 34-year-old woman was hospitalized for exploration of amenorrhea and galactorrhea. She had experienced primary sterility, diagnosed 11 years earlier. Endocrine tests demonstrated hyperprolactinemia (serum prolactin 594 ng/ml). Magnetic resonance imaging (MRI) showed a soft tissue mass located within the posterior part of the sphenoidal sinus. The pituitary gland appeared normal. Medical treatment with bromocriptine was unsuccessful. Transsphenoidal tumor resection was performed. Histology reported adenoma, which was consistent with prolactin-producing tumor demonstrated by immunohistochemical staining for prolactin. Because of the persistence of hyperprolactinemia related to an intra-sphenoidal tumor remnant, bromocriptine (15 mg/d) was initiated. Menses ensued and prolactin level declined (49 ng/ml). One year later, the tumor remnant had disappeared on the MRI and the patient became pregnant. Ectopic buy parlodel adenomas of the sphenoidal sinus are of particular interest due to the diagnostic difficulties encountered. Nevertheless, the nature of the lesion can be determined from the endocrine manifestations. Some of these tumors respond to medical treatment, similar to intra sellar tumors. Surgery remains however the only means of obtaining definitive diagnosis and cure.

parlodel maximum dose 2015-05-15

The return of menses in amenorrheic normoprolactinemic women after treatment with bromocriptine is well documented. To determine whether an buy parlodel increased pituitary prolactin-secreting capacity may be the underlying mechanism, 14 women with amenorrhea were studied. None complained of galactorrhea, but in all 14 it was possible to express a few drops of milk from the nipple. All women were normoprolactinemic and had normal sellar tomography. A standard thyrotropin-releasing hormone (TRH) test was performed and bromocriptine (2.5 mg twice daily) was administered. Within 8 weeks, 9 of 14 patients had return of menses. The second group of five patients did not respond to bromocriptine. The mean prolactin response to TRH was significantly greater in those women who experienced return of menses, although there was individual overlap between both groups. This finding suggests that enhanced prolactin secretory capacity may account for amenorrhea is some apparently normoprolactinemic patients. The TRH test may serve to identify those patients who may benefit from bromocriptine.

bromocriptine parlodel dosage 2015-05-26

Preclinical models of behavioral and toxic effects of cocaine are reviewed and their potential for predicting compounds with efficacy and safety buy parlodel in the medical management of cocaine abuse and toxicity is assessed. Many of the existing models appear to be good predictors of the effects of compounds against specific behavioral or toxicological actions of cocaine. However, the utility of the models for prediction of the efficacy of new therapeutic entities must await clinical validation as no accepted or standard pharmacotherapy currently exists. Preclinical data generated by these models with drugs currently under clinical investigation for cocaine abuse treatment as well as with other compounds are reviewed. These compounds include buprenorphine, bromocriptine, desmethylimipramine, carbamazepine, dopaminergic agonists, antagonists and partial agonists, dopamine reuptake inhibitors, sigma ligands, serotonin antagonists, and excitatory amino acid antagonists. Preclinical information on several drug classes appears sufficiently promising to warrant further evaluation. These include dopamine agonists and partial agonists, D1 receptor antagonists, selective sigma ligands, and modulators of the N-methyl-D-aspartate subtype glutamate receptor.

parlodel brand name 2016-06-07

The on-off phenomenon is an almost invariable consequence of sustained levodopa treatment in patients with Parkinson's disease. Phases of buy parlodel immobility and incapacity associated with depression alternate with jubilant thaws. Both pharmacokinetic and pharmacodynamic factors are involved in its pathogenesis, but evidence is presented to indicate that the importance of levodopa handling has been underestimated and that progressive reduction in the storage capacity of surviving nigrostriatal dopamine terminals is not a critical factor. Re-distribution of levodopa dosage which may mean smaller, more frequent doses, or larger less frequent increments, may be helpful in controlling oscillations in some patients. Dietary protein restriction, the use of selegiline hydrochloride and bromocriptine may also temporarily improve motor fluctuations. New approaches to management include the use of subcutaneous apomorphine, controlled-release preparations of levodopa with a peripheral dopa decarboxylase inhibitor and the continuous intra-duodenal administration of levodopa.

parlodel tablet uses 2017-04-22

Introduccion. El mutismo buy parlodel acinetico se considera una alteracion del estado motivacional de la persona, por el cual el paciente es incapaz de iniciar respuestas verbales o motoras de caracter voluntario, aun teniendo preservadas las funciones sensomotoras y de vigilancia. Caso clinico. Varon de 43 años, intervenido de una fistula arteriovenosa del cerebelo complicada con hidrocefalia, que respondio espectacularmente al tratamiento con bromocriptina. Conclusion. Tipicamente se ha descrito el mutismo acinetico como una complicacion transitoria de las cirugias de la fosa posterior. Sin embargo, tambien puede aparecer tras multiples fallos valvulares en pacientes con hidrocefalia.

parlodel alcohol 2016-06-21

An effective systematic approach for the management buy parlodel of prolactin-secreting pituitary adenomas is described. This methodology has stood the test of time and has been modified in accordance with experience. The primary goals are to obtain satisfactory control of the tumor and to avoid undesirable side effects related to dopamine agonist-based therapeutic agents.

parlodel tablets 2017-01-26

Six patients with primary amenorrhea and hyperprolactinemia are presented. The patients had normal secondary characteristics and normal body proportions. In four patients a tumour of the hypophysis was diagnosed radiologically, while in two patients the cause of hyperprolactinemia remained unknown. The gonadotropin concentration in the serum was normal. Reaction to Gn-RH was the same as that in women with the normal cycle in the follicular phase. In all the patients with function of the thyroid was normal. Primary amenorrhea was found in 14.6% of women with a disturbed cycle and hyperprolactinemia. In all the patients the administration of bromocryptin normalized buy parlodel prolactin concentrations, induced ovulation, and four patients became pregnant.

parlodel drug uses 2015-10-27

In this study, we evaluated the importance of the determination of buy parlodel serum prolactin levels in postpill amenorrheic patients.

parlodel drug classification 2015-03-19

The study was buy parlodel conducted double blind and subjects' order of dose exposure was randomized.

parlodel tabs 2016-06-30

The influence of a dopaminergic antagonist, metoclopramide (MET), and an agonist, bromocriptine (BROMO), on reproductive status was examined in female frogs, Rana temporaria. MET induced advanced ovulation during hibernation, suggesting dopaminergic inhibition of gonadotropin (LH) release during this period. Claritin D Generic BROMO did not decrease plasma LH in intact females in comparison with vehicle (VEH)-treated controls (VEH: 11 +/- 6 vs BROMO: 5 +/- 4 ng/ml) or in sham-lesioned (SL) females (SL; 12 +/- 5 vs SL + BROMO: 9 +/- 8 ng/ml). However, BROMO significantly depressed the rise in plasma LH following lesioning (L) which disconnected the hypothalamus from the medium eminence-pituitary complex (L + BROMO: 29 +/- 10 vs L: 74 +/- 30 ng/ml; P < 0.002). Taken together with previous results of lesion studies, these data point to an important role of dopaminergic inhibition in the regulation of seasonal reproduction in this frog.

parlodel generic name 2015-10-30

Using a two-lever operant task rats were trained to discriminate 40 mg/kg IP of bupropion from saline. Despite bupropion's established dopaminergic activity in vitro and in vivo, it was found that the bupropion cue was neither mimicked by the dopaminergic drugs L-DOPA and bromocriptine nor blocked by a variety of neuroleptics (haloperidol, thioridazine, and thiothixene). In addition, bupropion was active in attenuating the behavior-suppressing effects of haloperidol, unlike amphetamine and the atypical antidepressants, nomifensine and viloxazine. The bupropion cue was not mimicked or disrupted by adrenergic or serotonergic drugs, but it did generalize to some stimulants (amphetamine, cocaine and caffeine) as well as to nomifensine and viloxazine. The generalizations were blocked by neuroleptics. These data Clomid Online Prescription indicate that bupropion's cue properties may not be based on its ability to modulate dopaminergic receptor activity. The possible involvement of phenylethylamine in the bupropion cue is also discussed.

parlodel 10 mg 2017-04-29

A man of 38 years of age was found to have a type I endocrine polyadenomatosis in 1969. He was operated upon for removal of tumor of the islets of Langerhans with lymph gland metastases, and the head of the pancreas was removed. This was followed at a later date by ablation of two parathyroid adenomas. A clinically silent adenoma of the left adrenal was not removed and a silent and enclosed pituitary tumore was discovered. There were no clinical or hormonal signs Cleocin Dosage of progression of the pancreatic tumor ten years later, but hypertension and behavioural disorders had developed. Catecholamine levels were normal. Selective blood aldosterone levels were just within significant values. A massive increase in prolactin secretion (more than 100 times the normal) was noted. This could be reduced by bromocriptine, and the possible role of prolactin in the behavioural disorders present is discussed.

parlodel and alcohol 2016-12-06

This study was designed to investigate the effects of 1.25 mg of the dopamine D(2) agonist bromocriptine on Deltasone Dosage spatial working memory, planning and discrimination reversal learning in young healthy volunteers.

parlodel reviews 2016-04-22

ClinicalTrials. Lipitor Replacement Drugs gov Identifier: NCT00998556.

parlodel cost 2015-12-26

Malnutrition during lactation is associated with hypoprolactinemia and failure in milk production. Adult rats whose mothers were malnourished presented higher body weight and serum tri-iodothyronine (T(3)). Maternal hypoprolactinemia at the end of lactation caused higher body weight in adult life, suggesting an association between maternal prolactin (PRL) level and programming of the offspring's adult body weight. Here, we studied the consequences Cipro 500mg Dosage of the maternal PRL inhibition at the end of lactation by bromocriptine (BRO) injection, a dopaminergic agonist, upon serum TSH and thyroid hormones, thyroid iodide uptake, liver mitochondrial alpha-glycerophosphate dehydrogenase (mGPD), liver and pituitary de-iodinase activities (D1 and/or D2), and in vitro post-TRH TSH release in the adult offspring. Wistar lactating rats were divided into BRO - injected with 1 mg/twice a day, daily for the last 3 days of lactation, and C - control, saline-injected with the same frequency. At 180 days of age, the offspring were injected with (125)I i.p. and after 2 h, they were killed. Adult animals whose mothers were treated with BRO at the end of lactation presented lower serum TSH (-51%), T(3) (-23%), and thyroxine (-21%), lower thyroid (125)I uptake (-41%), liver mGPD (-55%), and pituitary D2 (-51%) activities, without changes in the in vitro post-TRH TSH release. We show that maternal PRL suppression at the end of lactation programs a hypometabolic state in adulthood, in part due to a thyroid hypofunction, caused by a central hypothyroidism, probably due to decreased TRH secretion. We suggest that PRL during lactation can regulate the hypothalamus-pituitary-thyroid axis and programs its function.

parlodel dosing 2016-10-21

This study was done to elucidate the relationship between the hormones beta-estradiol, progesterone, prolactin and beta-endorphin and nest-building behavior in rabbit does during the periparturient period. Beta-estradiol increased as parturition approached with a significant increase starting 2 days before parturition (day -2). Progesterone decreased with the progress of gestation, but a significant decrease was observed starting on day -2. Prolactin concentration started to increase on day -2 prepartum but a significant increase in prolactin concentration was not noted until the last day of pregnancy. The concentration of beta-endorphin was highly variable during the sampling period and could not be correlated with the other hormones or nest-building behavior. To assess the role of prolactin in nest-building behavior, groups of rabbits were treated with bromocryptine, bromocryptine plus prolactin or saline (controls). Treatment with 4 mg bromocryptine or 4 mg bromocryptine + 1.5 mg bovine prolactin on days 25 and 27 of pregnancy did not affect the number of live kits born or the gestation length. The mean nest scores, a measure of the nest quality, were not affected by bromocryptine treatment, but treatment with bromocryptine plus prolactin resulted in lower nest scores (P < 0.05). Injection of 8 mg bromocryptine from day 28 of gestation to kindling resulted in an extended gestation (P < 0.05). Injection of 4 or 8 mg bromocryptine resulted in fewer live kits born (P < 0.05), reduced nest scores (P < 0.01) and blocked milk production, as determined from the palpable mammary tissue. These results indicate that prolactin has less influence on nest-building behavior than on milk production. The hormones most likely to influence nest building are beta-estradiol and Anafranil Ocd Reviews progesterone because the levels of these hormones started to change at the time when the rabbits started to prepare nests. Further study is required to determine the influence of these hormones on nest-building behavior.

parlodel pills 2017-12-27

We have studied the contribution of neuronal and postjunctional dopamine (DA) receptors and of the DA1 and DA2 receptor subtypes to the blood pressure effects of DA and bromocriptine in the rabbit. The norepinephrine release rate, i.e., the rate of entry of endogenous norepinephrine into the plasma, was derived from the plasma level of endogenous norepinephrine and the plasma [3H]norepinephrine clearance. Bromocriptine (40 micrograms kg-1) lowered the norepinephrine release rate and the arterial blood pressure both in anesthetized rabbits and in pithed rabbits with electrically stimulated sympathetic outflow. These effects were antagonized by the selective DA2 antagonist domperidone but not by the selective DA1 antagonist SCH 23390. DA (10-160 micrograms kg-1 min-1) dose-dependently increased the norepinephrine release rate and caused only transient hypotension in anesthetized rabbits. However, after treatment with desipramine, DA did not change the norepinephrine release rate and produced a persistent fall in blood pressure. When DA and domperidone were given simultaneously to desipramine-treated rabbits, the hypotensive effect of DA was unchanged, Bactrim Ds Alcohol but now DA increased the norepinephrine release rate. When DA and SCH 23390 were given simultaneously to desipramine-treated rabbits, DA failed to lower blood pressure and decreased the norepinephrine release rate. Propranolol did not change the effects of DA in desipramine-treated rabbits. These results suggest that bromocriptine decreases blood pressure by activating ganglionic and/or prejunctional, inhibitory DA2 receptors in the peripheral sympathetic nervous system. DA also activates these receptors, but in addition releases norepinephrine in the manner of an indirectly acting sympathomimetic amine and activates postjunctional vascular DA1 receptors, and the latter seems to be the main component in DA-induced hypotension.