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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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Patients with pituitary adenomas were examined with positron emission tomography (PET) with the administration of the 11C-labelled dopamine-D2 antagonists N-methylspiperone and raclopride. The studies were repeated after protection of the D2-receptors with Haloperidol to enable a separation of specific and unspecific receptor binding. The receptor binding was evaluated by visual inspection and with the application of a kinetic model. The results showed marked specific dopamine-D2 receptor binding in the prolactinomas and minimal or no such binding in the hormonally inactive adenomas. The two tracers 11C-raclopride and 11C-N-methylspiperone showed qualitatively the same result although raclopride resulted in a higher tumor to normal brain ratio. In conclusion, PET is a valuable complement to other radiologic techniques like computed tomography and magnetic resonance imaging in the evaluation of pituitary adenomas. An assessment of the dopamine-D2 receptors in the adenomas has a direct influence on the choice of treatment because adenomas with high amounts of receptors are in most cases effectively treated with dopamine agonists like bromocriptine.

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PRL receptors have been previously identified in purified rat liver plasma membrane and Golgi vesicle preparations. In this study, we report on PRL receptors located in highly purified lysosome preparations. These lysosomal PRL receptors were characterized using Scatchard analysis and compared to other intracellular and cell surface receptors. We have identified two classes of lysosomes. Lighter lysosome-like vesicles, which are greatly enriched in acid phosphatase activity (the marker enzyme of lysosomes), contain a great deal of binding activity. This PRL binding was only slightly increased by pretreatment of animals with the lysosomotropic agent chloroquine. In contrast, mature lysosomes showed very little binding activity in control animals, but chloroquine treatment increased binding 7- to 8-fold in these mature lysosomes. We suggest that the lysosome-like structures are immature lysosomes (namely prelysosomes) toward which the hormone-receptor complex is internalized: they appear to bear little proteolytic activity. These structures could play a role in PRL receptor recycling. Lysosomal PRL receptors showed curvilinear Scatchard plots, in contrast to plasma membrane and Golgi counterparts, which were linear over the same range of hormone concentrations. The high affinity site in lysosomes had a Kd comparable to the cell surface and Golgi receptors. The number of binding sites per mg protein in prelysosomes and lysosomes was 3 times greater than that in the homogenate, but Golgi preparations were 3 times as rich as lysosomes. The great number of PRL receptors in prelysosomes could be attributed, in large part, to the low affinity sites. The internalization of PRL into rat liver was examined after in vivo injection of [125I]iodoovine PRL. The labeled hormone was found initially in the plasma membrane fraction, after which it localized preferentially in the Golgi fraction, with maximum incorporation 15 min postinjection. Substantial radioactivity was observed in both classes of lysosomes (L-1 and L-2). In contrast to the Golgi fraction, maximum incorporation of [125I]iodoovine PRL in lysosomes occurred at 30 min. This suggests either that during internalization, PRL first reaches Golgi elements and is then transferred to the lysosomal compartment, or that there are two independent pathways of internalization, one rapid toward the Golgi complex (may be a path of receptor recycling) and the other toward lysosomes (probably leading to receptor degradation).

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Hyperprolactinemia is one of the causes of sterility. Cabergoline is indicated in cases resistant to bromocriptine, but, usually, its administration is interrupted at the beginning of the pregnancy. A case of prolonged treatment with cabergoline during pregnancy is reported, without teratogenic effects on the fetus.

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After single doses (100 to 400 microgram orally), pergolide, a synthetic ergot, reduced basal plasma prolactin levels in normal subjects in a dose-related manner. This effect persisted for more than 24 hr. Multiple doses of pergolide (150 to 250 microgram daily for 7 days) resulted in a plasma prolactin decrease of more than 80%. A single dose of pergolide (150 microgram orally) suppressed plasma prolactin and abolished the plasma prolactin diurnal rhythm, i.e., suppression of sleep-induced elevation in plasma prolactin during a 40-hr period. Perphenazine (5 mg intramuscularly)-induced plasma prolactin elevation was inhibited by pergolide; the effect was dose dependent. After single or multiple doses, pergolide had no effect on plasma follicle-stimulating hormone, luteinizing hormone, cortisol, growth hormone, and thyroid-stimulating hormone. Pergolide appears to have specificity at the pituitary level for the dopamine receptors that mediate prolactin secretion.

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Pituitary and testicular hormone secretion and sex-hormone binding globulin (SHBG) level were investigated in 15 males with active acromegaly in normal and hyperprolactinemic state. Basal serum folitropin (FSH) and lutropin (LH) levels did not change before and after the administration of bromocriptine and remained in normal range compared with those in healthy men. Serum total testosterone concentration and SHBG were decreased particularly in hyperprolactinemic patients, but their levels were significantly increased to the normal limits following bromocriptine application. Although slight changes in serum concentration of free testosterone (fT) and circadian rhythm of fT in saliva was observed before and following bromocriptine treatment, the statistical differences were not significant. The results of the present study suggest that in acromegaly the alterations in peripheral metabolism of sexual steroids may exist.

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Peripartum cardiomyopathy (PPCM) is a potentially life-threatening heart disease emerging toward the end of pregnancy or in the first postpartal months in previously healthy women. Recent data suggest a central role of unbalanced peri-/postpartum oxidative stress that triggers the proteolytic cleavage of the nursing hormone prolactin (PRL) into a potent antiangiogenic, proapoptotic, and proinflammatory 16-kDa PRL fragment. This notion is supported by the observation that inhibition of PRL secretion by bromocriptine, a dopamine D2-receptor agonist, prevented the onset of disease in an animal model of PPCM and by first clinical experiences where bromocriptine seem to exert positive effects with respect to prevention or treatment of PPCM patients. Here, we highlight the current state of knowledge on diagnosis of PPCM, provide insights into the biology and pathophysiology of 16-kDa PRL and bromocriptine, and outline potential consequences for the clinical management and treatment options for PPCM patients.

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Pergolide mesylate ((8 beta)-8-[(methylthio)methyl]-6-propylergoline monomethanesulfonate, LY 127,809, CAS 66104-23-2) is a novel and potent dopamine agonist marketed for treating the symptoms of Parkinson's disease. The potential secondary pharmacological effects of this agent on the cardiovascular, respiratory, and the autonomic nervous systems were examined. Pergolide exhibited significant pharmacological effects in cardiovascular and autonomic tests at high oral or intravenous doses. The reference dopamine agonist, bromocriptine, exhibited effects qualitatively similar to, but at doses generally higher than, pergolide, in parallel with its lower therapeutic potency relative to pergolide. In summary, these studies confirm the pharmacological selectivity of pergolide at low doses, and indicate the potential for secondary pharmacological side effects upon cardiovascular function at significant multiples of the clinical dose.

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After 1 month, 63% of the patients in both groups had normal PRL and 43% had menses. Side effects were similar. After 1 year all patients except one had normal PRL levels, and 89% were ovulating.

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The markedly increased well being in patients treated with CV 205-502 cannot be explained by its better tolerability and is probably caused by a specific central activity of CV 205-502. Further research into the antidepressive properties of this compound is warranted.

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In a 21-year-old woman with McCune-Albright syndrome, acromegaly and hyperprolactinemia with hypopituitarism developed secondary to a large pituitary tumor. Bromocriptine suppressed the secretion of growth hormone and prolactin, with a reduction in tumor size. However, at the age of 8, she already showed evidence of biochemical acromegaly, with a paradoxical rise of growth hormone levels during two glucose tolerance tests, in the presence of a radiologically normal pituitary fossa. These data support the hypothesis that long-standing hypothalamic stimulation may have been responsible for the later development of a pituitary tumor.

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Rats with a unilateral 6-hydroxydopamine lesion of substantia nigra were treated with the dopamine agonists SKF-82958 (D1 receptor selective) or bromocriptine (D2 receptor-selective) and their circling response recorded. Both of the compounds induced an acute episode of rotation directed away from the lesioned side. Consecutive daily treatments with either compound usually resulted in a significantly increased average response (sensitization) over a 3- to 6-day treatment period. But nearly all animals treated with low doses of either SKF-82958 or bromocriptine exhibited one or more days when they were totally unresponsive to drug treatment. Response fluctuations thus were not exclusively associated with D1 or D2 receptor agonist treatment. When subsequently tested, undrugged, in the drug-associated environment, 2, 4 and 10 weeks after their last drug treatment, rats that had previously been treated with SKF-82958 exhibited rapid contralateral rotation while rats that had previously been treated with bromocriptine showed no such undrugged rotation. This result is consistent with previous findings that the D1 receptor agonist, SKF-38393, but not the D2 receptor agonist, quinpirole, had long-term behavioral effect in nigral rats, and suggests that persistent motor consequences of limited treatment with dopamine receptor agonists are D1 receptor-related.

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The problem of hyperprolactinaemia is dominated by the search for an active pituitary adenoma, which, if it is at all large, requires neuro-surgical operation. In cases where a microadenoma is responsible or where the pathological secretion of prolactin is istrogenic, the most serious consequence is sterility. Hyperprolactinaemia in fact works at two levels: on cyclical gonadotrophic activity and on luteal function. Whatever the cause is, bromocriptine allows hyperprolactinaemia to be corrected together with the disturbances of ovulation resulting from it.

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Twenty-three patients with microprolactinoma (basal serum PRL levels 1620-18750 mU/l) and 16 patients with macroprolactinoma (basal serum PRL levels 4110-111000 mU/l), previously shown to be intolerant of bromocriptine. All patients had gonadal failure and 11 patients with macroprolactinoma had visual field defects. Five patients with macro- and one with microprolactinoma had previously undergone surgery.

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Results in 136 hyperprolactinaemic women who presented with infertility, amenorrhoea, menstrual irregularities and/or galactorrhoea are reported. There was radiographic evidence of pituitary microadenoma in 21 (15.4%) patients and 5 (3.7%) had macroadenoma. Four patients were taking antidepressants, 2 antihypertensive drugs and 7 had taken oral contraceptives for a period of 6 months to 5 years. The remaining patients had no obvious cause for elevated prolactin levels. Patients with pituitary adenoma had a significantly higher (p less than 0.001) baseline serum prolactin level (182 +/- 4.6 ng/ml) than those with no adenoma (59.2 +/- 4.2 ng/ml). All patients in the study were treated with bromocriptine (2.5-10 mg) to normalize serum prolactin or to achieve a pregnancy. The patients without an adenoma required a significantly smaller dose of bromocriptine (2.5-5.0 mg) (p less than 0.005) than those with an adenoma. Galactorrhoea disappeared in all 64 patients within 2-4 months of treatment, sixty-six (71%) of the 93 patients who desired pregnancy achieved it within 3 to 8 months of bromocriptine therapy; 32 of these patients received additional treatment with clomiphene and human chorionic gonadotrophins for induction of ovulation. In the remaining 70 patients menstruation became regular and ovulation was evident in 40% of them. There was no significant difference in the pregnancy rate between the patients with or without pituitary adenoma. Similarly, presence of galactorrhoea or a high level of prolactin did not influence the pregnancy rate. No complications were observed during pregnancy related to pituitary adenomas; 8 (12%) pregnancies ended in first trimester abortion. No lethal congenital fetal abnormalities were observed in the patients treated with bromocriptine.(ABSTRACT TRUNCATED AT 250 WORDS)

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Eleven patients with prolactin-producing pituitary adenomas were treated with the new non-ergot, long-acting dopamine agonist, CV 205-502, for a period of 2-18 months (mean 11 months). Tumour volumes ranged from 1.9 to 64 ml in seven patients who were newly diagnosed, and from 0.1 to 3.1 ml in four patients who had been treated for macroprolactinomas by oral bromocriptine or depot bromocriptine (Parlodel LAR). Plasma prolactin values ranged from 3.5 to 360 U/l before institution of CV 205-502 treatment in these 11 patients. The following observations were made: (1) plasma prolactin values fell dramatically in all patients, and values within the normal range were obtained in five patients at once-daily doses of CV 205-502 between 0.075 and 0.300 mg; (2) tumour size reduction was obtained in all patients with macroadenomas on pretreatment CT scans. Tumour reduction was associated with the development of a partial empty sella in five patients, and with visualization of the pituitary in six cases; (3) bitemporal hemianopia (five patients) disappeared in four patients and improved in one patient. Oculomotor palsy receded in one patient; (4) signs of anterior pituitary insufficiency improved or normalized in most cases affected; (5) mild nausea or dizziness during the first days of CV 205-502 treatment and/or during several days after a dose increase were observed in three patients. We conclude that CV 205-502 in a once daily dose is an effective and safe alternative in the long-term treatment of macroprolactinomas.

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In patients with early Parkinson's disease, ropinirole monotherapy was more efficacious than bromocriptine with regard to improvement in activities of daily living, and need for supplemental levodopa. Ropinirole recipients had a higher requirement for levodopa supplementation than levodopa recipients in a 5-year study, but the incidence of dyskinesia was significantly lower with ropinirole than with levodopa (markedly so in the one third of ropinirole recipients who were able to remain on monotherapy with no levodopa supplementation). Thus available data suggest that ropinirole may provide a means of treating early Parkinson's disease while minimising the risk of dyskinesia and delaying the need for supplemental levodopa in some patients. In addition, ropinirole is also efficacious in the management of more advanced Parkinson's disease in patients who are experiencing motor complications after long term levodopa use.

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The effects of intravenous infusions of dopamine (0.1 to 1 mg kg-1h-1) and bromocriptine (10 to 40 micrograms kg-1h-1) on colonic motility were investigated in fasted dogs fitted with permanent strain gauges on the ascending, transverse and descending colon. Infused at rates of 0.5 and 1 mg kg-1h-1 during 1 h, dopamine immediately stimulated the motility of the descending colon; after a delay of 40 to 60 min this effect was balanced by an inhibition of the motility of the ascending and transverse colon. Bromocriptine infused intravenously at doses of 10 to 40 micrograms kg-1h-1 stimulated the motility of the whole colon but these effects were limited to the duration of the infusion (60 min). Both propranolol (0.5 mg kg-1) and tolazoline (2 mg kg-1) failed to block the effects of dopamine and bromocriptine whereas phentolamine (0.1 mg kg-1) and prazosin (0.2 mg kg-1) partially reduced the inhibitory effects of dopamine on the proximal colon. Haloperidol at doses higher than 0.2 mg kg-1 and domperidone blocked the bromocriptine-induced stimulation of colonic motility which was unaffected by previous treatment with alpha- and beta-adrenoceptor blocking agents. These results suggest that in the dog, dopamine and bromocriptine stimulate colonic motility through specific dopamine receptors. However, they suggest that the inhibitory effects of dopamine on the proximal colon which are blocked by dopamine antagonists are also partially due to an effect on alpha 1-adrenoceptors.

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Administration of 4 mg of the antiprogestagen RU486 to 4-day-cyclic rats over 8 consecutive days starting on the day of estrus (Day 1) induced and anovulatory cystic ovarian condition with endocrine and morphological features similar to those exhibited in polycystic ovarian disease (PCO). To determine whether the RU486-treated rat responds in an analogous fashion to therapies similar to those that have been used to treat human PCO, RU486-treated rats were injection on Days 5 and 7 with 1) 1 mg of an LHRH antagonist (LHRHa), 2) 5 IU of human FSH (hFSH), 3) 2 mg of the antiandrogen flutamide (FLU), 4) 1 mg of the antiestrogen tamoxifen (TMX), or 5) 1 mg of the dopamine agonist bromocriptine (BRC). Controls were intact cyclic rats decapitated on estrus and rats injected with RU486 and the corresponding vehicles (saline or 70% ethanol) used with LHRHa, hFSH, FLU, TMX, and BRC injections. RU486-treated rats were decapitated on Day 9, and the serum concentrations of LH, FSH, prolactin (PRL), testosterone (T), and estradiol-17 beta (E2) were determined. Pituitary and ovary weight, number of follicular cysts, size of the corpora lutea, and rates of follicular growth and atresia were also noted. Finally, the ovulatory response to ovine LH (oLH) in rats treated with RU486 and injected with various doses of hFSH (5, 10, or 20 IU) was evaluated. While administration of LHRHa and of TMX decreased the serum concentrations of LH, T and E2 and the LH/FSH and T/E2, ratios, and injections of BRC and of FLU increased the serum concentration of LH and T, the administration of hFSH (10 IU) to RU486-treated rats increased only the serum levels of E2. All treatments decreased, though in different degrees, both the number of cysts and the rate of follicular atresia, and stimulated follicular growth. The positive effects on follicular growth and atresia were significantly higher in those rats injected with hFSH. Moreover, RU486-treated rats injected with different doses of hFSH ovulated in a dose-dependent manner in response to oLH. Rates deprived of the actions of progesterone through the administration of the antiprogestagen RU486 had 1) endocrine and morphologic alterations comparable to those observed in women with PCO, 2) analogous responses to therapies similar to those that have been used to treat human PCO, and 3) an ovulatory response to combined treatment with FSH and LH. These results establish the fundamental adequacy of using the RU486-treated rat as a PCO model.

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Twenty hyperprolactinemic women (median prolactin [PRL] 2,989 mU/L, range 1,149 to 11,910 mU/L), previously unsuccessfully treated with bromocriptine, were treated in a prospective study, for 3 to 24 months with the new, nonergot, long-acting, dopamine agonist, CV 205-502. Treatment resulted in normalization of PRL in 14 patients, in one daily dose of 0.075 to 0.150 mg of the drug. Three patients were treated in doses above 0.150 mg up to 0.300 mg, but PRL was not normalized during the study. Menstrual function was restored in 15 of 18 amenorrheic patients. Galactorrhea, present in 7 patients, disappeared in 5. Four patients became pregnant and gave birth to healthy children. In conclusion, we found CV 205-502 effective in one daily dose, with good tolerability; it is safe and provides a valuable alternative to the dopamine agonist drugs in use today.

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Forty migraineurs (10 males, 30 females) were randomized according to a two-period (3-month), two-treatment, crossover design. Efficacy was assessed using quantitative data recorded in the patient's headache diary. Data were evaluated using the Wallenstein's method.

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In normal rats, before Day 12 of pseudopregnancy, minimal levels of 20 alpha-HSD activity were detected in functional CL whereas those in the residue were 3-5 times higher. When ovulation was blocked for more than 2 weeks by placing rats in a continuously lit environment before the induction of pseudopregnancy, only minimal levels of 20 alpha-HSD activity were detectable in the functional CL and residue before Day 12. In normal pseudopregnant rats, there was a linear increase in 20 alpha-HSD activity from Day 12 to 15 in the functional CL and residue, but the rate of elevation was much higher in functional CL. This tendency was much more clear-cut in rats in the continuous lighting. In immature rats in which pseudopregnancy was induced by PMSG and hCG treatment, 20 alpha-HSD activity peaked twice. The first small peak was attributed to the early regression of some of the large number of corpora lutea, and the changes in 20 alpha-HSD activity in most of the corpora lutea paralleled those in rats in continuous lighting. Bromocriptine abolished the prolactin surges, and in normal pseudopregnant rats an increase in 20 alpha-HSD activity in functional CL started from 12 h and the rate of the increase was accelerated from 36 h afterwards, while a relatively small increase was observed in the residue at 18 h and later.(ABSTRACT TRUNCATED AT 250 WORDS)

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Two review authors independently assessed a single trial for inclusion, evaluated trial quality and extracted data. Data were checked for accuracy.

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Bilateral Vim stimulation suppressed both extremity and orolingual tremors which interfered with daily living activities such as eating and swallowing.

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The Cochrane Subfertility Review Group specialised register of controlled trials was searched.

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Secondary diabetes mellitus is known to occur in acromegaly due to insulin resistance caused by growth hormone excess. However, diabetes in acromegaly usually does not lead to ketosis. We describe an unusual case of a patient that presented with diabetic ketoacidosis in the emergency room with thirst, polyuria and dyspnoea. The patient was subsequently diagnosed with a growth hormone-secreting pitutary macroadenoma as the underlying pathology; after initial stabilisation with insulin and fluids, the patient was successfully treated with trans-sphenoidal surgery.

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Extracellular single-cell recording and microiontophoretic techniques were used to characterize the presynaptic dopamine (DA) receptors (autoreceptors) on A10 DA neurons in the rat ventral tegmental area. Thus, the ability of various agonists to inhibit the activity of A10 DA neurons was compared. DA and the DA agonists N-n-propylnorapomorphine (NPA), apomorphine, lisuride, pergolide, LY141865 and bromocriptine all suppressed the activity of A10DA neurons. NPA was the most potent exogenous agonist, exerting effects that were similar to an equimolar concentration of DA (0.01 M). When ejected at equimolar concentrations (0.01 M) and equivalent ejection currents, the rank order of potency for these agonists was DA = NPA greater than LY141865 greater than pergolide = lisuride = apomorphine greater than norepinephrine greater than bromocriptine. The alpha-2 adrenoceptor agonist clonidine, the beta adrenoceptor agonist isoproterenol, the D-1 specific DA agonist SKF 38393 and the hallucinogenic ergot lysergic acid diethylamide exerted only weak effects or were inactive. The D-2 specific DA antagonist sulpiride completely blocked the rate-suppressant effects of DA and DA agonists but not those of gamma-aminobutyric acid. The purported D-1 specific DA antagonist SCH 23390 failed to block the effects of either DA or the D-2 specific DA agonist LY141865. These results indicate that DA agonists suppress the activity of the majority of A10 DA neurons by acting directly on somatodendritic DA autoreceptors which exhibit the pharmacological characteristics of D-2 receptors.

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Using the MEDLINE and Cochrane Library Central databases, we selected clinical trials that allowed paired comparisons of bromocriptine with the most frequently prescribed dopamine receptor agonists in PD (ie, pergolide, piribedil, pramipexole, and ropinirole). From these data, we calculated dose equivalents of optimal daily doses for each pair of dopamine receptor agonists.

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parlodel ovulation drug 2016-11-19

Hyperprolactinemia may be due to various etiological factors and may present with different signs and buy parlodel symptoms. It is relatively less frequent in childhood than in adulthood. The aim of this study was to evaluate retrospectively the clinical course and outcome of hyperprolactinemia in pediatric patients.

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Patients with GH deficiency frequently have multiple hormone deficiencies and require hydrocortisone replacement. We have investigated whether GH treatment alters circulating cortisol buy parlodel levels in hypopituitary patients receiving stable replacement therapy.

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Healthy mature horses were treated using either PTU or BROM for 28 days. The effect of treatment on the thyroid axis was assessed by measuring T3, T4 buy parlodel , rT3 and e-TSH before and at +14 and +28 days. The effect of PTU and BROM on the response of T3, T4, rT3 and e-TSH to thyrotrophin-release hormone (TRH) administration was also assessed before and at +14 and +28 days of treatment.

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Transcription of the prolactin gene is suppressed by dopaminergic activation of D2 receptors in pituitary lactotrophs. The mechanism of signal transduction at the nuclear level and the cell surface was examined in the dopamine-responsive GH4ZR7 cell line. Dopamine treatment caused a 40-50% decrease in endogenous prolactin mRNA that was specifically blocked by addition of (-)-sulpiride. To define dopamine-responsive elements, plasmids containing 5'-regulatory buy parlodel regions of the prolactin gene fused to the coding sequences for luciferase were transiently or stably transfected into GH4ZR7 cells. Chimeric transcripts initiated at the authentic transcription start site were regulated in a promoter-selective manner; dopamine or the agonist bromocryptine inhibited prolactin promoter (position -422) activity by 70%, but had no regulatory effects on other cellular or viral promoters. A shorter prolactin promoter (position -78) or a prolactin TATAA box linked to heterologous binding sites for transcription factor Pit-1 was sufficient to confer dopamine inhibition (40%). In addition to the prolactin promoter, we found that dopamine inhibited transcriptional activity of the Pit-1 promoter (positions -258 to +8) by 60%. Surprisingly, deletion of two cAMP response elements in the Pit-1 promoter only partially eliminated dopamine responsiveness. These data suggest that sequences in the Pit-1 promoter between positions -92 and +8, which include an autoregulatory Pit-1-binding site and the TATAA box, are sufficient for negative regulation. In this study, we also examined the signal transduction pathways that link D2 receptor activation and the inhibition of prolactin gene transcription. We found, as suggested in earlier studies, that a dopamine-dependent decrease in cAMP may be important for mediating negative regulation of transcription. However, high extracellular K+ concentrations that prevent dopamine effects on membrane potential and [Ca2+]i, but not cAMP levels, completely blocked dopamine regulation of the prolactin promoter. This suggests that two distinct signaling pathways initiated at D2 receptors may be required for transcriptional regulation of the prolactin gene.

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Over recent years I have been studying whether dopamine agonist treatment alone, or in early combination with levodopa, might institute a better long-term treatment in Parkinson's disease than levodopa alone. Indeed, early combination of levodopa with bromocriptine, pergolide or lisuride has indicated that this kind of treatment results in better management of Parkinson's disease with fewer fluctuations in disability, especially end-of-dose disturbances and dyskinesias, than treatment with levodopa alone. Furthermore, similar results were obtained by using lisuride in combination with selegiline and levodopa. However, during long-term treatment the changes in parkinsonian disability were equal in all treatment groups with or without selegiline. Thus, the possible efficacy of selegiline in slowing down the progression of Parkinson's disease requires further investigations. As a new treatment strategy it appears advisable to initiate the dopaminergic treatment in early Parkinson's buy parlodel disease by using initially selegiline and a dopamine agonist and by adding levodopa when the therapeutic response is insufficient. Another alternative would be to start with selegiline alone, then add a dopamine agonist and, finally, levodopa.

parlodel drug class 2017-10-26

Hyperprolactinemia is commonly found in both female and male patients with abnormal sexual and/or reproductive function or with galactorrhea. If serum prolactin levels are above 200 microg/L, a prolactin-secreting pituitary adenoma (prolactinoma) is the underlying cause, but if levels are lower, differential diagnoses include the intake of various drugs, compression of the pituitary stalk by other pathology, hypothyroidism, renal failure, cirrhosis, chest wall lesions, or idiopathic hyperprolactinemia. When a pituitary tumor is present, patients often have pressure symptoms in addition to endocrine dysfunction, such as headaches, visual field defects, or cranial nerve deficits. The large majority of patients with prolactinomas, both micro- and macroprolactinomas, can be successfully treated with dopaminergic drugs as first-line treatment, with normalization of prolactin secretion and gonadal function, and with significant tumor shrinkage in a high percentage of cases. Surgical resection of the prolactinoma is the option for patients who may refuse or do not respond to long-term pharmacological therapy. Radiotherapy and/or estrogens are also reasonable choices if surgery fails. In patients with asymptomatic microprolactinoma no treatment needs to be given and a regular follow-up with serial prolactin measurements and pituitary imaging should be buy parlodel organized. Currently, the most commonly used dopamine agonists are bromocriptine, pergolide, quinagolide and cabergoline. When comparing the plasma half-life, efficacy and tolerability of these drugs, cabergoline seems to have the most favorable profile, followed by quinagolide. Ifprolactin levels are well controlled with dopamine agonist therapy, gradual tapering of the dose to the lowest effective amount is recommended, and in a number of cases medication can be stopped after several years. Evidence to date suggests that cabergoline and quinagolide appear to have a good safety profile for women who wish to conceive, but hard evidence proving that dopamine agonists do not provoke congenital malformations when taken during early pregnancy is currently only available for bromocriptine. Once pregnant, dopamine agonist therapy should be immediately stopped, unless growth of a macroprolactinoma is likely or pressure symptoms occur. At our institution patients with symptomatic prolactinomas, both micro- and macroadenomas, are treated with cabergoline as the first-line aproach. In the small group of patients who do not respond to this treatment, or who refuse long-term therapy, surgery is offered. Radiotherapy is given if both pharmacologic therapy and surgery fail.

parlodel buy 2016-01-30

A 50-yr-old man with a large goiter had elevated serum levels of T4 (22 micrograms/dl), T3 (228 ng/dl), and free T4 (6.6 ng/dl), a high 24-h 131I-thyroidal uptake (69%), and an elevated TSH level (3.6 microU/ml), as well as hyperresponsiveness of TSH to TRH (peak TSH, 47 microU/ml). Normal serum alpha-subunit concentrations and sella turcica films mitigated against the presence of a pituitary tumor. A normal basal metabolic rate and minimally elevated concentration of testosterone-estradiol binding globulin were consistent with generalized resistance to thyroid hormone. Mild lactotroph resistance was also present. buy parlodel The patient was given bromocriptine for 16 months (2.5-10 mg daily). Basal serum TSH levels decreased (less than 0.3-2 microU/ml), as did the TSH response to TRH; serum T4 levels (14-17 micrograms/dl); and 24-h 131I-thyroidal uptake (28%) were reduced. Serum T3 levels, however, changed little. The thyroid gland decreased to normal size, and the basal metabolic rate and testosterone-estradiol binding globulin remained normal. Bromocriptine was stopped for 4 months. Serum TSH increased to 4.5 microU/ml; T4 and T3 increased to 27 micrograms/dl and 328 ng/dl; the patient became clinically mildly hyperthyroid. Thus, bromocriptine in this patient was useful in decreasing TSH secretion and decreasing goiter size, while maintaining clinical euthyroidism. Only a small amount of TSH was necessary to maintain iodine uptake and thyroid hormone synthesis and secretion in a responsive thyroid gland. We speculate that this patient may be secreting a highly bioactive form of TSH and/or have increased thyroid sensitivity to TSH.

parlodel drug study 2015-01-24

Prolactin deficiency, induced by bromocryptine treatment, brought about reciprocal changes in the ability of adipocytes and acini isolated from lactating rats to synthesize lipids. The capacity to synthesize fatty acids and phospholipids decreased in the mammary gland and increased in adipocytes by bromocryptine treatment. In the mammary gland, the maximum buy parlodel potential activity of the pentose shunt as well as the specific activities of the pathway dehydrogenases were significantly reduced by bromocryptine treatment. Simultaneously, adipose tissue increased its lipogenic capacity but neither the maximum potential of the shunt nor the specific activities of the pentose phosphate shunt dehydrogenases were significantly changed with respect to the control lactating rats. Thus, a differential regulatory mechanism(s) of the pentose phosphate shunt activity appears to operate in these two tissues. Adipocytes from lactating rats showed a poor responsiveness to insulin in terms of lipid synthesis from glucose. In contrast, in adipocytes from bromocryptine treated rats insulin was able to increase lipid synthesis (105%). Sheep prolactin administration 'in vivo' partially reversed the effects of bromocryptine. These data suggest that prolactin mediates adipocytes resistance to insulin during lactation. Phospholipid synthesis, as occurred in fatty acid synthesis, is increased in adipose tissue and decreased in mammary gland by bromocryptine treatment. However, alpha 1-adrenergic stimulation increases phosphatidylinositol turnover to about the same percentages in both mammary gland acini and adipocytes from lactating rats independently of bromocryptine treatment.

parlodel 5 mg 2016-10-01

One hundred seven patients (46 men and 61 women) from 27 centers were included in the statistical analysis. All had previously been treated with a dopamine agonist (bromocriptine). Fifty-five patients had undergone surgery before being administered quinagolide: 17 of the patients had also received radiotherapy (before and after the initiation of treatment with quinagolide in 14 and 3 cases respectively). Quinagolide was given at doses ranging from 75 to 750 microg daily and continued for buy parlodel more than one year for 84 patients.

bromocriptine parlodel dosage 2016-03-28

In a previous publication, using human 5-hydroxytryptamine(7) (h5-HT(7)) receptor-expressing human embryonic kidney (HEK) 293 cells, we reported the rapid, potent inactivation of the h5-HT(7) receptor stimulation of cAMP production by three antagonists: risperidone, 9-OH-risperidone, and methiothepin (Smith et al., 2006). To better understand the drug-receptor interaction producing the inactivation, we 1) expanded the list of inactivating drugs, 2) determined the inactivating potencies and efficacies by performing concentration-response experiments, and 3) determined the potencies and efficacies of the inactivators as irreversible binding site inhibitors. Three new drugs were found to fully inactivate the h5-HT(7) receptor: lisuride, bromocryptine, and metergoline. As inactivators, these drugs displayed potencies of 1, 80, and 321 nM, respectively. Pretreatment of 5-HT(7)-expressing HEK cells with increasing concentrations of the inactivating drugs risperidone, 9-OH-risperidone, methiothepin, lisuride, bromocriptine, and metergoline potently inhibited radiolabeling of the h5-HT(7) receptor, with IC(50) values of 9, 5.5, 152, 3, 73, and 10 nM, respectively. We were surprised to find that maximal buy parlodel concentrations of risperidone and 9-OH-risperidone inhibited only 50% of the radiolabeling of h5-HT(7) receptors. These results indicate that risperidone and 9-OH risperidone may be producing 5-HT(7) receptor inactivation by different mechanisms than lisuride, bromocryptine, metergoline, and methiothepin. These results are not interpretable using the conventional model of G-protein-coupled receptor function. The complex seems capable of assuming a stable inactive conformation as a result of the interaction of certain antagonists. The rapid, potent inactivation of the receptor-G-protein complex by antagonists implies a constitutive, pre-existing complex between the h5-HT(7) receptor and a G-protein.

parlodel dosage hyperprolactinemia 2016-12-14

Bromocriptine treatment results in clinical improvement and inhibition of plasma GH levels in only part of the acromegalic patients. The possible role of the simultaneous presence of Prl and GH in GH-secreting pituitary adenomas was investigated with regard to the inhibitory action of bromocriptine on GH secretion and the paradoxical increase of GH release in reaction to TRH. Surgically obtained pituitary tumour tissue from 35 consecutive acromegalic patients was studied immunohistochemically. In 21 patients no Prl was present in the tumour tissue. These patients had normal plasma Prl levels. In the other 14 patients Prl was present in the tumour tissue. Hyperprolactinaemia was found in 10 of these buy parlodel 14 patient. Plasma GH levels from 2 till 10 h after the administration of 2.5 mg bromocriptine measured before operation were significantly more suppressed in the patients with mixed GH/Prl-containing than in those with pure GH-containing pituitary adenomas, being 38 +/- 4% and 65 +/- 4% of basal values, respectively (P less than 0.01). The response of GH to TRH, however, did not differ significantly between the two groups.

parlodel medicine 2015-07-13

These results highlight that acromegaly buy parlodel is not easily treated with surgery alone. The preoperative GH level was associated with the surgical outcome.

parlodel brand name 2016-11-18

Malignant neuroleptic syndrome (alteration of consciousness, muscle rigidity and hyperthermia) is a potentially lethal condition, due also to its life-threatening complications. In particular, hypokinetic and hyperkinetic arrhythmias can be rare and severe early manifestations of this illness, and they deserve a careful approach because of their drug-refractoriness. Arrhythmias associated with the malignant neuroleptic syndrome depend on various mechanisms: neurotransmitter receptor blockades typical of neuroleptic drugs, clustered lipid droplets among the cardiac myofibrils and possible electrolytic disorder due to diaphoresis. The two cases described here presented hypokinetic and hyperkinetic (supraventricular and ventricular) arrhythmias. The arrhythmias, which failed to buy parlodel respond to antiarrhythmic drugs, were temporarily suppressed by DC shock, over-drive pacing and correction of electrolytic imbalance. In case 1, prolonged bromocriptine treatment was required. Complete wash-out of the causative agents resulted in lasting regression of arrhythmias. In conclusion, a correct treatment and a favourable outcome of this syndrome can be achieved only through early diagnosis.

parlodel dosage 2016-07-15

To buy parlodel evaluate QOL in women with microprolactinomas treated with dopamine agonists, comparing the patients with normal versus those with elevated prolactin levels, and to identify clinical and biochemical influences on patients' QOL.

parlodel 10 mg 2017-08-07

The authors used 86Rb+ as a marker for K+ to study ouabain- Zyloprim And Alcohol insensitive, bumetanide-sensitive 86Rb+ uptake in cultured fetal human NPE monolayers.

parlodel maximum dose 2015-09-16

A double blind crossover trial of the prolactin inhibitor bromocriptine in painful benign breast disease is reported. Twenty-nine women with cyclical mastalgia and 11 with non-cyclical pain were treated with bromocriptine, 5 mg daily, and placebo over six menstrual cycels. Assessment of response to treatment was made by a linear analogue system and clinical examination together with plasma prolactin estimations. Bromocriptine produced a significant improvement in breast symptoms and a significant fall in prolactin levels in the cyclical pain group, but had no effect in the non-cyclical group. These results suggest that bromocriptine offers a new and effective approach in the management of cyclical breast Buspar Drug Class pain.

parlodel cost 2017-03-19

DNA synthesis was correlated (P < 0.05) with plasma hormone levels in cases of prolactinoma, both treated and not treated with bromocriptine, and in a group of putative FSH secreting tumours from male patients. The correlation was not significant in cases of acromegaly. Comparisons of mean values between groups treated and not treated with bromocriptine Avapro Pill Picture showed significantly lower DNA synthesis and mean nuclear diameter in prolactinomas under treatment but not in GH secreting tumours.

parlodel 5mg tablets 2015-06-24

This case suggests that, to exclude the alternative diagnosis of nonfunctioning pituitary adenoma or another mass lesion of the hypothalamic-pituitary region, repeat neuroimaging studies during long-term follow-up may Famvir Cost Uk be advisable in patients with presumed microprolactinoma who did not show reduction of the tumor during dopaminergic therapy.

parlodel tabs 2016-01-09

When investigations fail to reveal a cause for infertility, treatment must then be based on possible, but unproven, causes, and since there is a high spontaneous pregnancy rate in unexplained infertility the effect of any treatment is difficult to assess. Such treatment has included correction of anatomical variants such as uterine retroversion and the use of hormonal manipulation during the follicular and luteal phases of the menstrual cycle. Ovum entrapment, occult spontaneous abortion and faults in sperm fertilizing capacity have all been implicated, and it is likely that immunological factors play a substantial role in unexplained infertility. Evidence does not support the use of bromocriptine in the absence of hyperprolactinaemia. Successful treatment by intrauterine insemination is unlikely if there are circulating anti-sperm antibodies in the partner. Improving Zofran Dosing cervical mucus by treatment with oestrogens and clearing infections with antibiotics may have a modest place but it is very difficult to show that these treatments have more than a placebo effect. Endometriosis is often missed and the possibility of it having developed after initial investigation warrants repeat laparoscopy after 2 years. Three approaches are currently acceptable in the management of the couple with unexplained infertility: await spontaneous pregnancy, the empirical use of clomiphene and in-vitro fertilization.

buy parlodel online 2016-11-15

Malignant Hyperthermia is a specific potentially fatal condition which occurs in susceptible individuals in response to various triggering mechanisms, of which anesthetic agents have been found to be the Risperdal 1mg Medication most common offenders. Leading symptoms are generalized muscular rigidity and hyperpyrexia. The etiology seems to be associated with some inherited disturbance in muscle metabolism related to calcium regulation. This syndrome is known for 25 years, the mechanism of triggering, the genetics and the treatment have been able to get examined by animal model as malignant hyperthermia syndrome may occur in swine as well. Pharmacological in-vitro studies on biopsy specimen of muscle fragments are presently one of the most accepted means for pre-anesthetic diagnosis, the hydantoin derivate dantrolene sodium is the only known specific drug in treatment and prophylaxis. Neuroleptic Malignant Syndrome which occurs in patients treated with neuroleptics shows almost identical symptoms. Although the pathogenesis is still unknown, most authors believe a neuroleptic-induced alteration of central neuroregulatory mechanisms is involved. Alternative etiologic mechanisms are suggested by the striking similarities noted between the Neuroleptic Malignant Syndrome and Malignant Hyperthermia. Both disorders might be based on common pathophysiologic mechanisms and might be induced in susceptible patients by a variety of pharmacologic agents. The authors present and compare the actual knowledge concerning symptoms, course and therapy of both syndromes on the basis of 126 case studies of the Neuroleptic Malignant Syndrome from literature.

parlodel reviews 2015-09-23

Management of male infertility is always a difficult task. In recent years booming of artificial reproductive technologies (ART) has put infertologists and andrologists in front of a million dollar question whether to treat the person or the gametes. A basic andrology laboratory at present has become part and parcel of an infertility clinic. Hence treatment of male infertility has become institutional and collective for clinicians and basic scientists. The basic approach towards management of male infertility includes confirmation of diagnosis and to find out the cause for which pathological, endocrinological and biochemical tests are essential. In this series specific defects causing seminopathy has been found in 18% cases where treatment is Guduchi Dosage straightforward and towards the cause. The main bulk of idiopathic seminal defects (82%) really poses challenge to the infertologists so far management is concerned. In this study commonest seminal defect has been found to be oligoasthenozoospermia which amounts to 63% cases. For medical management purpose drugs commonly used are clomiphene, gonadotrophins, bromocriptine, L-thyroxine, vitamin E, B12, etc. When they fail the main approach remains to be intra-uterine insemination (IUI) and ART eg, in vitro fertilisation (IVF) and intracytoplasmic sperm injection (ICSI).

parlodel tablet price 2017-01-28

This study was designed to assess the effects of bromocriptine, a dopamine D2 receptor agonist, on sleep bruxism. Seven otherwise healthy patients with severe and frequent sleep bruxism participated in this randomized, double-blind, placebo-controlled study. The study used a crossover design that included 2 weeks of active treatment or placebo with a washout period of 1 week. To further evaluate whether bromocriptine influences striatal D2 receptor binding, we used iodine-123-iodobenzamide single photon emission computed tomography (SPECT) under both placebo and bromocriptine regimens. Bromocriptine did not reduce the frequency of episodes of bruxism during sleep (mean +/- SEM, 9.0 +/- 1.0 and 9.6 +/- 1.5 bruxism episodes per hour for placebo and bromocriptine, respectively) or the amplitude of masseter muscle contractions (root mean square values, 48.2 +/- 15.5 microV and 46.9 +/- 12.7 microV for placebo and bromocriptine, respectively). SPECT also failed to reveal that either treatment had any influence on striatal D2 binding (values for total binding in counts/pixel, 1.80 [1.72-1.93] and 1.79 [1.56-1.87] for placebo and bromocriptine, respectively). This study shows that a nightly dose of bromocriptine does not exacerbate or reduce sleep bruxism motor activity.

parlodel generic 2016-07-19

The clinical features of 65 patients with acromegaly (31 males, 34 females; mean age: 50+/-2 yr.) who were admitted to Tokyo Women's Medical University between 1990 and 1999 were analyzed retrospectively from medical records.

parlodel online 2017-01-02

Both antitumor and antisecretory efficacies of dopamine agonists (DA) make them the first-line treatment of macroprolactinomas. However, there is no guideline for MRI follow-up once prolactin is controlled. The aim of our study was to determine whether a regular MRI follow-up was necessary in patients with long-term normal prolactin levels under DA.