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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.


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.


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.


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


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.

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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.


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.

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Malignant neuroleptic syndrome is a complication of antipsychotic medication use. Clozapine use is also associated with polyserositis and eosinophilia. We report a 17 years old female treated with clozapine, valproic acid, lithium carbonate and lorazepam that consulted in the emergency room for confusion, lethargy, catatonia, rigidity, myalgya and fever. Complete blood count showed eosinophilia. An abdominal CAT scan showed ascites and pleural effusion. Clozapine was discontinued and bromocriptine was started. One week after admission, the patient remained febrile and liver enzymes were elevated. Valproic acid was discontinued. Inflammatory parameters stated to subside and the patient was discharged afebrile days after admission.

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Seventeen women with prolactin levels of 100 ng/ml and above suspected of harboring prolactin-secreting pituitary adenoma, from the basis of this study. Ten patients had radiological signs of an adenoma while in 7 the radiological criteria for such a diagnosis were not fulfilled. Ovulation and pregnancy were induced with bromocriptine in all 17 patients. They were carefully observed during pregnancy and following delivery. All gave birth to full-term babies after uneventful pregnancies, except for one patient who experienced intrauterine fetal death at 31 wk of gestation. It is our policy that women with suspected intrasellar prolactin-secreting pituitary adenoma be allowed to conceive and give birth without previous surgical intervention. The patient should be closely followed during pregnancy for clinical symptoms of enlargement of the tumor, including periodic visual field examinations. In cases of neurologic or ophthalmologic complications, surgery or bromocriptine administration without interruption of pregnancy is advocated, or if lung maturity is achieved, delivery should be induced.

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We performed this retrospective analysis to determine the efficacy of surgery and radiotherapy over hormonal and volumetric control of prolactinomas, many of which had failed during dopa-agonist therapy. In the same analysis, the efficiency of topical bromocriptine application as a preliminary study was compared with standard treatment modalities.

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36 women with postpartal breast engorgement were treated with a single oral dose of 2.5 mg bromocriptine (Pravidel). Significant relief was recorded in 28 patients, 6 patients required a second dose of 2.5 mg bromocriptine, whereas 2 patients failed to respond. Antibiotics were at first avoided in the treatment of puerperal mastitis. 26 patients with all characteristics of breast inflammation were treated exclusively with bromocriptine: for 3 days 2.5 mg t.i.d., for the following 11 days 2.5 mg twice daily. The temperature dropped below 37C in 25 patients within 12-24 hours, tension and pain disappearing simultaneously. One patient did not respond after 36 hours, so that an antibiotic was administered additionally; in another patient who had been admitted to the hospital six days after the onset of the clinical symptoms of breast inflammation, bromocriptine failed to prevent abscess formation. The results indicate that in most cases of puerperal breast inflammation no antibiotics are required. Puerperal mastitis can be treated effectively by the exclusive administration of bromocriptine.

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In 24-day-old rats the reappearance of ovarian HCG-receptors up to day 4 after the injection of 200 IU HCG was due only to receptors in non-luteal cells. The receptor capacity increase observed on days 6 and 7 after the hormone injecion resulted from newly synthesized binding sites in luteinizing ovaries. Bromocriptine or an antiestrogen inhibited this receptor synthesis.

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A 21-year-old woman had sterility due to amenorrhoea-galactorrhoea with hyperprolactinaemia and hypoplastic ovaries. The sella turcica was asymmetrical but tomograms were suggestive of a congenital appearance. There was no suprasellar expansion. Treatment with bromocriptine and HMG resulted in pregnancy. Acute pituitary failure occurred at the 10th week, revealing an adenoma. The pregnancy proceeded to term after hypophysectomy. This complication, the first reported under the effects of bromocriptine, may serve as a reminder of the precautions to be taken during pregnancy in a hyperprolactinaemic woman.

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The objective of the study was to study the acute effects of bromocriptine (a D2R agonist) on circadian leptin levels in obese women, whereas body weight and caloric intake remained constant.

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Bilateral microinjections of dopamine (DA, 0.3, 3.0 or 30.0 micrograms) or the DA-agonist, bromocriptine (3.0 micrograms) into the basolateral amygdala (BLA) dose-dependently attenuated cold restraint stress (3 h at 4 degrees C)-induced gastric ulcer formation in rats. On the other hand, intra-BLA injections of the neurotoxin, 6-hydroxydopamine (10 micrograms) of the DA-antagonist, haloperidol (0.1 or 1.0 micrograms) aggravated such stress ulcer formation. All these effects were seen only when the injection sites were localized in the posterior (and not the anterior) BLA. Further, pretreatment of rats with haloperidol (0.1 micrograms) clearly antagonized the gastric cytoprotective effects of DA or bromocriptine (both at 3.0 micrograms), when both chemicals were injected in the posterior BLA. The results indicate that DA-ergic mechanisms in the posterior BLA are important for the regulation of gastric mucosal integrity during cold restraint stress.

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The authors report the results of a retrospective study conducted in an effort to define the results and risks of transsphenoidal surgery for patients whose prior therapy had failed. In a series of 1210 patients undergoing transsphenoidal surgery during a 10-year period, 158 had received prior therapy: 127 for pituitary adenoma, 20 for craniopharyngioma, and 11 for other lesions. Prior therapy was considered "direct" when it consisted of craniotomy or transsphenoidal surgery (either open or stereotaxic), and "indirect" when it consisted of radiation therapy, adrenalectomy, or bromocriptine therapy. The current transsphenoidal operation was performed for persistent hyperfunctioning endocrinopathy in 63 patients, for visual loss in 72 patients, and for cerebrospinal fluid (CSF) rhinorrhea in 21 patients. Success rates were as follows: normalization of endocrinopathy was achieved in 35% of cases; improvement or stabilization of vision in 59%; and successful repair of CSF rhinorrhea in 74%. The risks associated with repeat transsphenoidal surgery are significantly greater than the same procedure in a previously untreated patient.

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The mean response rate to the questionnaire was 43% and main characteristics of respondents in this sample were very close to those found at the national level. The use of bromocriptine (89%) was the most frequently proposed. Dihydroergocryptine and cabergoline were mentioned as first or second alternatives in 39 and 24% of cases, respectively. Lisuride, homeopathy and phytotherapy were very rarely mentioned. The analysis of social security reimbursement data in the Rhône-Alpes region between 2008 and 2009 evidenced an increase in the rate of dihydroergocryptine prescriptions (from 37 to 46%), which were more frequent in women also treated with cardiovascular or psychotropic drugs, while that of bromocriptine decreased.

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Studies on nonseasonally breeding males have demonstrated that high titers of testosterone (T) stimulate reproduction, whereas high titers of prolactin (PRL) inhibit it. Recent evidence, however, suggests that for seasonally breeding males high titers of both PRL and T stimulate behaviors that support reproduction and mating. Thus, we hypothesized that high titers of both PRL and T are necessary and sufficient for male meadow voles to show a preference for the odor of long-photoperiod (LP) females. We tested this hypothesis by treating castrated LP males with bromocriptine and/or T, and by treating castrated short-photoperiod (SP) males with PRL and/or T. The data showed that high titers of both PRL and T are necessary for LP male meadow voles to maintain a preference for the odor of LP female meadow voles, but high titers of both hormones are not sufficient to induce SP males to show such a preference. Only SP males with high T and low PRL titers showed preferences for LP female odors. Interestingly. SP males with high PRL and high T titers preferred the odor of LP males, and SP males with high PRL and low T titers preferred the odors of SP females. The apparent contradictory effects of PRL and T in SP males suggest that the hormonal control of seasonal differences of male odor preferences may be more complex than previously believed.

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To establish a baseline pattern of care across academic and community settings, it is important to examine the contemporary treatment of acromegaly. We characterized medical treatment patterns for acromegaly in the US to develop a basis for tracking concordance with guidelines.

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The authors present two cases of khat addiction that were successfully treated with bromocriptine. Khat is a bush cultivated in the Mid East because of its highly stimulant effects. Its leaves contain a variety of sympathomimetics. While khat is rarely found in the U.S., American soldiers stationed in the Arabian peninsula may be exposed to it. Because of an alcohol interdiction during the current Persian Gulf crisis, these troops may be tempted to use this plant as an alternative recreational drug.

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A series of experiments were conducted to determine whether and under what conditions central prolactin (PRL) administration would stimulate the onset of maternal behavior in female rats and to identify possible neural sites of PRL action. In each experiment ovariectomized, nulliparous rats whose endogenous PRL levels were suppressed with bromocriptine were tested for maternal behavior toward foster young. In experiments 1, 2, and 4, females were also exposed to pregnancy-like levels of progesterone (days 1-11) followed by estradiol (days 11-17). In experiment 1 infusions (days 11-13) of four doses of ovine PRL (400 ng, 2 micrograms, 10 micrograms, or 50 micrograms, but not 80 ng) into the lateral ventricle resulted in a rapid onset of maternal behavior (behavioral testing, days 12-17). The stimulatory action of these doses of PRL appears to be central, since subcutaneous injections of 50 micrograms of ovine PRL failed to affect maternal responsiveness (experiment 2). Experiment 3 indicated that the stimulatory effect of intracerebroventricularly administered PRL is steroid dependent. Infusions of either 10 micrograms of ovine PRL or 10 micrograms of rat PRL failed to induce maternal behavior in nonsteroid-treated animals. In the final experiment (no. 4) bilateral infusions of 40 ng of ovine PRL into the medial preoptic area of steroid-treated rats resulted in a pronounced stimulation of maternal behavior. These findings demonstrate a central site of PRL action in the stimulation of maternal responsiveness and point to the medial preoptic area as a key neural site for PRL regulation of maternal behavior.

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Two reviewers applied the eligibility criteria and assessed trial quality independently.

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The effectiveness of CV 205-502 was identical to bromocriptine: its tolerability appeared to be better, especially in the initial phase of treatment. At baseline, the mean scores of the SCL-90 were significantly elevated over the reference values. Sixteen patients had normal scores. The elevations were caused by 8 patients with scores in the range found in psychiatric disease (211 +/- 30 [SD] [CV 205-502] and 182 +/- 32 [bromocriptine]). They were depressed, anxious, and hostile. At 24 weeks, the patients treated with CV 205-502 scored better (130 +/- 23.5) in the SCL-90 than the patients treated with bromocriptine (149.5 +/- 20).

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The dopamine (DA) D(2) receptor (D2R) agonist bromocriptine (BC) decreases body fat in animal and human models and increases lean muscle mass, improves glucose intolerance and insulin resistance, and reduces triglycerides and free fatty acids. We have previously shown a negative correlation between D2R and body weight in obese individuals and in rodents, and that chronic food restriction increases D2R binding in genetically obese rats. The purpose of this study was to assess whether the antiobesity and metabolic effects of BC are related to changes in midbrain DA and D2R activity by measuring D2R and DA transporter (DAT) binding in a genetic (leptin-receptor-deficient) and environmental (diet-induced) rodent obesity model.

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Our hypothesis is that leptin release is controlled neurohormonally. Conscious, male rats bearing indwelling, external, jugular catheters were injected with the test drug or 0.9% NaCl (saline), and blood samples were drawn thereafter to measure plasma leptin. Anesthesia decreased plasma leptin concentrations within 10 min to a minimum at 120 min, followed by a rebound at 360 min. Administration (i.v.) of lipopolysaccharide (LPS) increased plasma leptin to almost twice baseline by 120 min, and it remained on a plateau for 360 min, accompanied by increased adipocyte leptin mRNA. Anesthesia largely blunted the LPS-induced leptin release at 120 min. Isoproterenol (beta-adrenergic agonist) failed to alter plasma leptin but reduced LPS-induced leptin release significantly. Propranolol (beta-receptor antagonist) produced a significant increase in plasma leptin but had no effect on the response to LPS. Phentolamine (alpha-adrenergic receptor blocker) not only increased plasma leptin (P < 0.001), but also augmented the LPS-induced increase (P < 0.001). alpha-Bromoergocryptine (dopaminergic-2 receptor agonist) decreased plasma leptin (P < 0.01) and blunted the LPS-induced rise in plasma leptin release (P < 0.001). We conclude that leptin is at least in part controlled neurally because anesthesia decreased plasma leptin and blocked its response to LPS. The findings that phentolamine and propranolol increased plasma leptin concentrations suggest that leptin release is inhibited by the sympathetic nervous system mediated principally by alpha-adrenergic receptors because phentolamine, but not propranolol, augmented the response to LPS. Because alpha-bromoergocryptine decreased basal and LPS-induced leptin release, dopaminergic neurons may inhibit basal and LPS-induced leptin release by suppression of release of prolactin from the adenohypophysis.

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Three experiments were conducted on Texel ewes to study the influence of prostaglandin F(2,alpha) (PGF(2 alpha)), prolactin (PRL), estradiol (E(2)), and gonadotrophin releasing hormone (GnRH) on postpartum reproductive activity. In Experiment 1, oral administration of indomethacin (25 to 50 mg/day/ewe) from Day 3 post partum to the first detected estrus inhibited plasma 13, 14-dihydro-15-keto, PGF(2 alpha) (PGFM) concentrations (P < 0.0001). This treatment resulted in an earlier rise in the frequency and amplitude of luteinizing hormone (LH) pulses and a resumption of estrous behavior (P < 0.05), while ovarian activity estimated by progesterone (P(4)) concentrations resumed to the same extent in treated ewes and controls. Bromocriptine treatment (2.5 mg/day/ewe) reduced plasma PRL levels (P < 0.0001) but had no effect on ovarian activity as evidenced by P(4) and resumption of estrus or on either the frequency or amplitude of the LH pulse. In Experiment 2, a single injection of GnRH agonist (42 mcg of buserelin/ewe) on Day 16 post partum resulted in an abrupt elevation of plasma LH concentrations; mean LH values were 18 to 27 times higher when compared with those of the control ewes. Two days after this treatment, ovulations occurred in 5 of the treated ewes and in 2 of the control ewes. This induced ovarian activity was not associated with estrous behavior; however, after an adequate subsequent luteal phase all the treated ewes displayed estrus, the resumption of estrus thus being earlier in treated than in control ewes (P < 0.01). In Experiment 3, E(2) supplementation from Day 16 to Day 28 post partum increased the number of LH pulses per 6 hours in suckling ewes (P < 0.05) and induced earlier resumption of estrus in dry ewes but not in suckling ewes (P < 0.01). Luteal function was detected about 5 and 8 days after the insertion of E(2) implants in 4 dry ewes and in 2 suckling ewes, respectively.

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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 and discuss the main current therapeutic possibilities.

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Schizophrenic patients show a loss of sensory gating, which is reflected in a reduced P50 suppression. Because most of the symptoms in schizophrenia can be reduced by antagonists of the dopaminergic (D2) system, the loss in sensory gating might be related to an increased dopaminergic activity. Therefore, in the present study, the effects of increased dopaminergic neurotransmisson on sensory gating in healthy volunteers were investigated. In a double-blind, balanced, placebo-controlled design, healthy male volunteers were challenged in two separate studies with either 300 mg L-dopa (precursor of dopamine) or placebo (n=16) and 1.25 mg bromocriptine (D2 agonist) or placebo (n=17). Subsequently, they were tested for their sensory gating (P50 suppression). P50 suppression values in the placebo condition were comparable to those found in literature. Although both L-dopa and bromocriptine reduced P50 amplitude, they did so in an equal ratio for both the response to the conditioning (C) and the testing (T) stimuli, therefore not resulting in a reduction of the P50 suppression ratio (T/C). In the present study, neither L-dopa nor bromocriptine reduced sensory gating in healthy volunteers. This suggests that an increased dopaminergic activity in humans is not responsible for the reduction in sensory gating as seen, for example, in schizophrenia.

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A patient was successfully treated with bromocriptine for neuroleptic-induced galactorrhea. The correlations of the weekly plasma prolactin levels with the severity of galactorrhea (p less than .005) and with the duration of treatment (p less than .001) were highly significant. Because symptomatic relief occurs an average of 6 to 8 weeks after initiation of pharmacotherapy, clinicians presently manage neuroleptic-induced galactorrhea by trial and error. The authors suggest that weekly plasma prolactin levels may provide a readily obtainable, early indicator of proper dosage and thus minimize the chance of iatrogenic illness.

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To evaluate whether dopaminergic treatment may modify endogenous opioid activity at the hypothalamic-pituitary level, the effects of naloxone infusion (1.6 mg/h for 4 h) on luteinizing hormone (LH) secretion were studied in 5 postmenopausal women either before or after chronic administration of the dopaminergic drug bromocriptine (BCT; 5 mg/day for 30 days). BCT administration did not modify mean plasma LH levels. Before treatment naloxone infusion did not induce any significant modification of LH secretion. Conversely, after chronic BCT administration naloxone induced a significant (p less than 0.05) increase in plasma LH levels. The LH response to naloxone was significantly (p less than 0.001) higher than that observed before BCT. The present data show that chronic BCT administration restores the LH response to naloxone in postmenopausal women. Therefore, these results seem to demonstrate that BCT administration can enhance opioid activity, suggesting an involvement of the endogenous opioid system in dopaminergic modulation of gonadotropin release.

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In the present study we have identified biochemically DA receptors in rat Lower Esophageal Sphincter (LES) and have identified their role in the control of the sphincter motility. Dopamine (DA) both stimulated and inhibited cyclic AMP formation in rat LES; the pharmacological characterization of these effects indicated that they were mediated by D-1 and D-2 receptors, respectively. The results obtained with LES helical strips showed that DA plays both inhibitory and stimulatory effects on the sphincter function; the pharmacological characterization with selective D-1 and D-2 agonists and antagonists strongly suggested that D-1 receptors are involved in LES contraction, while D-2 receptors mediate the relaxation of the sphincter. The same results were obtained by measuring intraluminal LES pressure in anesthetized rats. The selective D-1 agonist fenoldopam (40 micrograms/kg, i.v.) increased the LES pressure; on the other hand bromocriptine (10 micrograms/kg, i.v.), which preferentially interacts with D-2 receptors, induced a decrease of the resting LES pressure.

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Progression from early to late anoestrus is characterized by the appearance of a larger number of gonadotrophin-releasing hormone (GnRH) pulses with a higher amplitude, an increase in the sensitivity of the pituitary to GnRH, an increase in ovarian responsiveness to gonadotrophins, and an increase in basal plasma follicle-stimulating hormone (FSH) concentration. A period of increased luteinizing hormone (LH) pulsatility has been observed shortly before the onset of pro-oestrus. Apart from these changes in the hypothalamus-pituitary-ovary axis, the initiation of a new follicular phase in the bitch is also stimulated by dopaminergic influences other than the accompanying plasma prolactin decrease. Metergoline, a drug which in a low dosage lowers the plasma prolactin concentration via a serotonin-antagonistic pathway, does not shorten the anoestrus; while bromocriptine, in a dosage insufficient to cause a decrease in the plasma prolactin concentration, does prematurely induce a follicular phase. These observations indicate that it is not the decrease in the plasma prolactin concentration, but another dopamine-agonistic influence that plays a crucial role in the transition to a new follicular phase. The dopamine-agonist induced oestrus is associated with a rapid rise in the basal plasma FSH concentration, similar to what is observed during the physiological late anoestrus. Administration of GnRH, eCG and oestrogens may also be used to induce oestrus but with variable results. Oestrus can be prevented surgically or medically, for which purpose progestagens are the most important drugs. The mechanism is still unclear, although it has been demonstrated that with continuing medroxyprogesterone acetate (MPA) treatment the FSH response to GnRH stimulation decreases and changes occur in the pulsatile release of the gonadotrophins. In general, LH pulses coincide with a FSH pulse, but during MPA treatment, LH pulses were observed while there was such a small increase in FSH that it was not recognized as significant FSH pulse.

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Paroxysmal phenomena are rare but relatively typical clinical symptoms of multiple sclerosis (MS) caused by abnormal excitation in demyelinated plaques. We report the case of a 25-year-old woman with ocular convergence spasms as a new type of paroxysmal phenomenon in MS. MRI revealed the associated brainstem lesion in the region of the medial longitudinal fasciculus. Bromocriptine treatment was successful in resolving the paroxysms.

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parlodel 1 mg 2017-10-05

A complete reassessment of ovulation, pituitary reserve and function, and sella turcica anatomy was carried out in nine multiparous patients with intrasellar prolactinomas to determine whether long-term bromocriptine therapy was required and to document the natural history of the disease after two or more pregnancies. After the last buy parlodel pregnancy, bromocriptine was discontinued and pituitary function and anatomy and prolactinoma activity were reassessed with documentation of ovulation (basal body temperature graphs and menstrual history), search for fat droplet-positive galactorrhea, pituitary fossa tomography, computerized tomographic scan, triple-bolus testing, and visual fields. These data were compared with a similar workup carried out prior to the first pregnancy. Three groups of eventual outcomes were identified radiologically. Anterior pituitary gland function and reserve remained normal in all, and no neurological sequelae were noted. Four patients did not require long-term treatment. A hypothesis of autoinfarction of the adenoma is raised, since three patients were shown to have empty sellae.

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The etiology, pathophysiology, clinical presentation, and management of drug-induced hyperthermia buy parlodel (DIH) syndromes are reviewed.

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The neuroleptic malignant syndrome is characterized by hyperpyrexia, muscle rigidity, extrapyramidal motion disorder, vegetative symptoms and mental disorientation. This group of symptoms develops abruptly and may lead to serious complications. One of these complications is the acute renal failure. Permanent muscle rigidity causes the damage of muscle cells which result in myoglobinaemia, myoglobinuria and elevations in muscle related creatine phosphokinase. The authors report the case of a young man who underwent neuroleptic medication because of hebephrenia. During the medication the buy parlodel following symptoms were developed: extrapyramidal symptoms, restlessness, muscle rigidity, high fever. These symptoms eventually lead to acute renal failure caused by rhabdomyolysis (characteristic urine finding, significant elevations in serum creatine phosphokinase). With regards to the neuroleptic malignant syndrome dantrolenum and bromocriptin treatment were applied with the discontinuation of neuroleptic medication. As a part of the complex therapy a massive volumen-supplementing and alkalizing treatment was used but haemodialysis had also become necessary. During the above mentioned treatment symptoms referring to the neuroleptic malignant syndrome resolved and the acute renal failure was cured. The case report calls attention to a specific group of symptoms and the possibilities for prevention and treatment. The above case report is the first observation in Hungary.

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1. Experiments were designed to study the involvement of alpha-adrenoceptors and dopamine receptors in the hypotensive and bradycardic actions of bromocriptine in rats. 2. Intravenous administration of bromocriptine reduced blood pressure and heart rate which was inhibited by ganglionic blocking agents or by pithing. 3. The fall in blood pressure produced by bromocriptine was not modified by atropine, atenolol, prazosin, yohimbine, bilateral vagotomy or carotid ligation, but was blocked by sulpiride, domperidone and haloperidol. 4. The bradycardia produced by bromocriptine in intact rats was assumed to be mediated by the autonomic nervous system since it was partly reduced by bilateral vagotomy or atenolol, and buy parlodel entirely prevented by pithing. Furthermore, sulpiride but not yohimbine antagonized this effect. 5. In pithed rats, bromocriptine decreased both the pressor response (above 10 micrograms kg-1) and the tachycardia (above 50 micrograms kg-1) elicited by electrical stimulation of spinal cord outflow. Both effects were inhibited by sulpiride or yohimbine. 6. In pithed rats, bromocriptine did not affect the hypertension due to exogenous noradrenaline, phenylephrine, B-HT 920, nor the bradycardia evoked by stimulation of the cardiac muscarinic receptors by carbachol. 7. These results suggest that, in rats, bromocriptine produces hypotension via an action on presynaptic and/or ganglionic dopamine receptors, and causes bradycardia by activation of central dopamine receptors.

parlodel reviews 2015-01-25

We studied the influence of pregnancy on the serum prolactin levels after surgery in 35 patients with prolactinomas. Eighteen out of 22 patients with postoperative normalization of the buy parlodel prolactin level were able to achieve repeated spontaneous pregnancies and endocrine cure by surgery alone, but the other 4 had recurrent hyperprolactinemia. Thirteen patients with persistent hyperprolactinemia after surgery achieved one pregnancy with or without bromocriptine treatment, but did not achieve a second one owing to an increase in the prolactin level after delivery. None of the patients with postoperative hyperprolactinemia showed spontaneous normalization of the prolactin level or restoration of menstruation after delivery. In these 13 patients, the mean increase from the postoperative to the post-delivery prolactin level was less for the patients with bromocriptine-induced pregnancy than for those with spontaneous pregnancy. It is concluded that pregnancy did not adversely affect the serum prolactin level in the patients with a normal postoperative level.

parlodel dose 2015-10-21

The factors regulating serum leptin concentration and its relationship to the hyperphagia of lactation have been investigated in rats. Lactation results in hypoleptinaemia and loss, or at least marked attenuation, of the nocturnal rise in serum leptin. Litter removal resulted in a fall in food intake and restoration of the nocturnal rise in serum leptin. Returning the litter to the mother after a 48-h absence increased food intake and began to reinitiate milk production, but the nocturnal serum leptin levels were still increased at 48 h after litter restoration. Adjusting litter size to four, eight, ten or fourteen pups at parturition resulted in different rates of litter growth and food intake during the subsequent lactation, but had no effect on the degree of hypoleptinaemia. Reducing litter size from ten to four pups at mid-lactation resulted in a transient increase in both serum leptin and pup growth rate, while food intake fell to a level found in rats suckling four pups throughout lactation. Reducing milk production by injection of bromocriptine increased serum leptin, but did not restore the nocturnal rise in serum leptin; food intake decreased, but remained much higher than in non-lactating rats. Feeding a varied, high-energy diet resulted in a decrease in the weight of food ingested, but no change in calorie intake, and had no effect on the hypoleptinaemia. These studies suggested that the hypoleptinaemia of lactating rats is due to negative energy balance, but the loss of the nocturnal rise in serum leptin is due to the suckling stimulus. The negative energy balance of lactation does not appear to be caused by a physical constraint on food intake. While the buy parlodel hypoleptinaemia should facilitate the hyperphagia of lactation, other orexigenic signals must also be involved.

parlodel drug 2017-11-09

A large pituitary tumour was discovered in a 20 year old man who came to medical attention because of grand-mal seizures. The tumour produced biologically active LH as demonstrated by supranormal plasma LH and plasma testosterone values. Free alpha-subunit values were also elevated. In contrast, plasma FSH was in the lower normal range. Transsphenoidal operation failed to remove all tumour tissue. Detailed studies were carried out in the postoperative period. TRH and GnRH administration were associated with a rise of plasma LH and alpha-subunit, whereas buy parlodel plasma FSH was low and unresponsive. Bromocriptine treatment was ineffective. In contrast, both during and after treatment with SMS 201-995 for 6 weeks, a decrease of basal plasma LH values was observed. Furthermore, the administration of a single dose of SMS 201-995 reproducibly induced a decrease of plasma LH lasting for a period of about 6 h. The study suggests that SMS 201-995 may be useful in the treatment of patients with gonadotrope cell adenomas.

parlodel 5mg tablets 2016-06-29

At the end of the study, the prolactin reduction was significantly greater in the cabergoline group than buy parlodel in the bromocriptine group (-93 vs. -87.5 %, respectively, p < 0.05). Normalization of prolactin levels was achieved in 10 of 17 patients (59%) in the bromocriptine group, and in 14 of 17 patients (82%) in the cabergoline group (p = 0.13). Two patients (50%) with macroprolactinoma in the bromocriptine group and three patients (75%) with macroprolactinoma in the cabergoline group demonstrated a normalization of their serum prolactin levels. Adverse events were noted in 53% of bromocriptine patients and in 12% of cabergoline patients (p < 0.01).

parlodel drug study 2017-12-12

A patient with hyperprolactinemia, amenorrhea, and an enlarged sella turcica, but without galactorrhea, was treated with Bromocriptin to effect restoration of ovarian function. The subsequent pregnancy was without problems from an obstetric point of view, but visual field abnormalities developed progressively, leading to termination of the pregnancy in the 39th buy parlodel week. However, within 1 week after delivery, the field defects disappeared and the visual acuity returned to normal.

bromocriptine parlodel dosage 2015-03-06

Chronic administration of L-DOPA to MPTP-treated common marmosets induces marked dyskinesia while repeated administration of equivalent antiparkisonian doses of ropinirole and bromocriptine produces only mild involuntary movements. The occurrence of dyskinesia has been associated with an altered balance between the direct and indirect striatal output pathways. Using in situ hybridisation histochemistry, we now compare the effects of these drug treatments on striatal preproenkephalin-A (PPE-A) and adenosine A(2a) receptor mRNA expression as markers of the indirect pathway and striatal preprotachykinin (PPT) mRNA and preproenkephalin-B (PPE-B, prodynorphin) mRNA expression as markers of the direct pathway.The equivalent marked losses of specific [3H]mazindol binding in the striatum of all drug treatment groups confirmed the identical nature of the nigral cell loss produced by MPTP treatment. MPTP-induced destruction of the nigro-striatal pathway markedly increased the level of PPE-A mRNA in the caudate nucleus and putamen and decreased the levels of PPT and PPE-B mRNA relative to normal animals. Repeated treatment with L-DOPA for 30 days produced marked dyskinesia but had no effect on the MPTP-induced increase in PPE-A mRNA in the caudate nucleus and putamen. In contrast, L-DOPA treatment normalised the MPTP-induced decrease in the level of PPT and PPE-B mRNA. Repeated treatment with ropinirole produced little or no dyskinesia but markedly reversed the MPTP-induced elevation buy parlodel in PPE-A mRNA in the caudate nucleus and putamen. However, it had no effect on the decrease in PPT or PPE-B mRNA. Similarly, bromocriptine treatment which induced only mild dyskinesia attenuated the MPTP-induced elevation in PPE-A mRNA in the caudate nucleus and putamen with no effect on reduced striatal PPT or PPE-B mRNA. Neither MPTP treatment nor treatment with L-DOPA, bromocriptine or ropinirole had any effect on adenosine A(2a) receptor mRNA in the striatum. These patterns of alteration in striatal PPE-A and PPT and PPE-B mRNA produced by L-DOPA, bromocriptine and ropinirole show differential involvement of markers of the direct and indirect striatal output pathways related to improvement of locomotor activity and mirror the relative abilities of the drugs to induce dyskinesia.

parlodel dosage hyperprolactinemia 2016-08-25

The relationship between basal and stimulated plasma GH and somatomedin-C (SmC) levels in acromegalic patients was evaluated. The basal plasma SmC levels of 66 patients were significantly correlated (P less than 0.01) with mean daily plasma GH levels, but not with the percent GH increase after GH-releasing hormone or TRH or the GH decrease after acute bromocriptine administration. Bromocriptine (7.5-15 mg/day) administration for 9.2 +/- 0.9 (+/- SD) months in 20 patients significantly (P less than 0.05) decreased GH levels. SmC decreased significantly [from 9.8 +/- 1.9 to 5.1 +/- 0.7 U/ml (mean +/- SE)] only in the 10 patients who had the more marked GH inhibition. The administration of a somatostatin analog, SMS 201-995 (100 micrograms twice daily), to 12 patients for 16 weeks significantly decreased plasma GH and SmC levels beginning on the second day of therapy; normal SmC buy parlodel levels were achieved in 5 of 12 patients. Pituitary adenomectomy resulted in normal GH and SmC levels in 10 of 12 and 8 of 12 patients, respectively. Our data indicate an overall dependency of plasma SmC levels on plasma GH levels in acromegaly, although similar GH levels may have differing somatomedin-stimulating activities. A derangement in the feedback mechanisms controlling GH secretion is indicated by the failure of elevated SmC levels to influence the GH responsiveness to releasing hormones. In evaluating pharmacological or surgical treatments of acromegaly, a single plasma SmC value can reliably replace several plasma GH determinations.

parlodel generic name 2017-09-22

To assess the effectiveness buy parlodel of dopamine agonist bromocriptine in reducing the incidence and severity of OHSS in patients undergoing assisted reproduction and its effect on pregnancy rates.

parlodel medication 2016-11-15

Epithelial cell-rich fractions of rat mammary gland were prepared using percoll gradients after collagenase dispersion. Their insulin-binding characteristics were similar to those of crude acini but superior to unfractionated isolated cells. Optimal binding was obtained after 60 min at 20 degrees C or 16 h at 4 degree C at pH 7.8 Binding at 37 degrees C was lower due probably to an enhanced rate of insulin degradation. 48 h after ovariectomy of 18-day pregnant rats insulin binding to acini doubled due to an increase in the number of insulin receptors. Progesterone but not bromocriptine (which buy parlodel prevented the rise in serum prolactin which occurred after ovariectomy) prevented this increase in insulin binding. These results illustrate that the change in serum progesterone rather than prolactin increases insulin binding to the mammary cell at parturition whilst insulin binding decreases in adipose tissue at the same time (Flint et al., Mol. Cell Endocrinol, 20, 101-111, 1981) enabling coordinated changes in the metabolism of these 2 tissues to take place during the perinatal period.

parlodel drug classification 2016-12-14

Tumour mass decreased or remained stable in 18/20 patients in whom DA treatment was initiated upon buy parlodel detection of residual tumour on postoperative MRI (group I). In 13 subjects (group II), DA therapy was started when tumour remnant growth became evident during the course of routine follow-up. Tumour growth stabilized or decreased in 8/13 (61.5%) of these patients. In contrast, tumour size remained stable in only 38.3% (18/47) of the untreated subjects (P < 0.0001 for comparisons among the three groups) and increased in the remaining 29 patients. Tumour enlargement free mean survival time was 103.7 +/- 8.8 months (CI 86.3-121) for group I, 43.9 +/- 9.6 months (CI 25.2-62.8) for group II and 36.7 +/- 3.8 (CI 29.2-44.2) for the control group (P = 0.0017). Treatment vs. control hazard ratio for tumour enlargement was 0.135 for group I (P = 0.007, 95% CI 0.032-0.577) and 0.892 for group II (P = 0.817; 95% CI 0.34-2.34).

parlodel medicine 2015-03-04

The therapeutic efficacy of L-deprenyl (10 mg daily) as an adjunct to low-dose bromocriptine monotherapy (up to 25 mg daily) in patients with early Parkinson's disease (PD) was evaluated in a double-blind placebo-controlled short-term study (11 patients) and subsequently in a long-term prospective open follow-up (21 patients Triphala 2000 Mg ) until L-dopa was required, over a 4-year period. The combined regimen of bromocriptine plus L-deprenyl produced a mildly significant improvement, as shown by the majority of clinical rating scales used after 6 weeks of sustained treatment (as compared to bromocriptine alone and bromocriptine plus placebo). In the prospective long-term study, a stabilization of the clinical status was observed until 12 months of sustained treatment, whereas after that, a gradual worsening of the scores on all motor rating scales occurred. However, at 24 months, fewer than one third of the patients had required L-dopa, a proportion comparatively smaller than that reported in the literature with bromocriptine alone. This finding could be related to the persistence of initial symptomatic effect of L-deprenyl, but a slowing action on the course of the disease process exerted by the monoamine oxidase typeB (MAO-B) inhibitor cannot be ruled out.

buy parlodel online 2016-10-21

We evaluated bromocriptine monotherapy during the early stage of Parkinson's disease (Hoehn and Yahr stage I or II). Of the 120 patients registered as participants in this trial, 96 were studied. The follow-up period was 48 weeks. For the first 24 weeks they were all placed on Nexium Generic Equivalent bromocriptine with or without anticholinergic drugs; for the second 24 weeks, 75 of them were still kept on the same medication, with 21 requiring additional levodopa. Clinically, the former group showed a good response to the bromocriptine monotherapy, while the latter responded poorly to it (requiring in addition levodopa). We think that Parkinson's disease encompasses a heterogeneous group of patients of whom about 75% are well treated by bromocriptine alone at the early stages of the illness.

parlodel gel 2016-07-23

All patients <18 years, who were operated Evista Medication on at our center for GPA (tumor >40 mm in maximum diameter) were included in study. Clinical features, hormonal profile, radiology, surgical approach, results and complications were analysed.

parlodel tablet price 2016-08-14

The objectives of the treatment of hyperprolactinaemia are to suppress excessive hormone secretion and its clinical consequences, to remove tumour mass, to preserve the residual pituitary function and to prevent disease recurrence or progression. Prior to the advent of pharmacotherapy, therapy usually consisted of surgical resection and/or pituitary irradiation. In microprolactinomas, trans-sphenoidal surgical resection normalizes prolactin (PRL) levels, restores normal menses and produces the disappearance of galactorrhoea in a great majority of patients, but normalization of serum PRL levels varies from 35-70%. In macroprolactinomas, trans-sphenoidal surgery is less successful with only 32% of patients appearing to be cured initially. However, the recurrence rate is 19%, and the long-term cure rate is only 26%. In more than 80% of the patients with microprolactinoma, suppression of PRL levels and tumour shrinkage can be achieved with bromocriptine therapy given at doses of 2.5-5 mg per day. In 5-10% of the patients, the appearance of side-effects (nausea, dizziness and postural hypotension) is a limiting factor in continuing the treatment. Dopaminergic compounds cause notable tumour shrinkage in most macroprolactinomas. Treatment with cabergoline, a selective and long-lasting dopamine 2-receptor agonist at weekly Levitra Online Purchase doses of 0.5-2 mg has been shown to be effective both in normalizing PRL levels and in inducing tumour shrinkage. Pharmacotherapy with dopamine (DA) agonists is an appropriate first-line treatment for both micro- and macroprolactinomas. Surgery should be recommended for those patients who are severely intolerant of or resistant to DA agonists.

parlodel dosing 2017-03-12

Bromocriptine was used for Parkinson's disease in 15 patients for 20 weeks. Immunoreactive plasma lutrophin (LH), follitrophin (FSH), prolactin, and somatotrophin (GH, growth hormone) concentrations were analysed before and during the treatment. Plasma prolactin levels were very markedly reduced during treatment. Plasma lutrophin levels were increased significantly in female patients, but not in male patients. No changes were noticed in follitrophin levels, but plasma somatotrophin levels were reduced during treatment. No correlations were found between the degree of clinical response and changes in plasma gonadotrophin and somatotrophin. This suggests that the effects of bromocriptine on extrapyramidal and neuroendocrine dopaminergic neurones Pamelor Dose Maxima are unrelated. We suggest careful and frequent controls of neuroendocrine secretion patterns in patients with Parkinson's disease who are treated with high doses of dopamine receptor stimulators, since the response of some pituitary hormones to bromocriptine are very marked.

parlodel maximum dose 2015-09-28

The therapeutic efficacy of sustained dopaminergic stimulation in Cushing's disease (CD), was investigated performing a three-month trial with monthly 50-100 mg injections of a bromocriptine depot preparation (Parlodel LAR Motilium 10mg Dosage , Sandoz) in six patients with CD. Dopaminergic treatment did not consistently influence pituitary-adrenal activity, as judged by plasma ACTH, cortisol and urinary free cortisol levels as well as by clinical findings. Interestingly, treatment with bromocriptine was associated with reappearance of menses in the three patients who were amenorrheic. In the five patients submitted to inferior petrosal sinus sampling, a parallelism between ACTH and PRL concentrations could be observed with a PRL rise, ipsilateral to that of ACTH, ensuing in three patients after administration of corticotropin-releasing hormone. In one patient a 55% reduction in the size of the pituitary adenoma was demonstrated by MRI carried out at the end of treatment. Our findings lead to the following conclusions: a) administration of depot injections of bromocriptine to patients with CD appears unable to correct hypercortisolism, although it can induce restoration of menses in amenorrheic patients; b) enhanced PRL concentrations at the pituitary level are probably involved in the amenorrhea often accompanying Cushing's disease.

parlodel 5 mg 2017-12-24

Chronic treatment with the dopamine (DA) agonist B-HT 920 (0.25-1 mg/kg) or bromocriptine (1 mg/kg) followed by morphine (10 mg/kg) on days 1-9 prevented the development of tolerance to the antinociceptive effect of morphine as measured by the tail-flick test in mice, but failed to suppress the development of morphine dependence as assessed by naloxone (2 mg/kg)-precipitated withdrawal jumps on day 10 of testing. Repeated administration of SKF 38393 (5 mg/kg) followed by morphine for 9 days significantly reduced naloxone-precipitated jumps on day 10 but failed to produce any significant change in tail-flick latency from the saline-pretreated group of mice on days 9 and 10 of testing. Repeated administration of B-HT 920 or bromocriptine enhanced the ability of MK-801 to attenuate the development of morphine tolerance and dependence while SKF 38393 failed to Coumadin Drug do so. The above data suggest a preferential role of D2 DA receptors in morphine tolerance and D1 receptors in the development of morphine dependence. D2 DA receptor stimulation may also play an important role in enhancing the effectiveness of MK-801 in the treatment of opiate tolerance and dependence.

parlodel tab 2016-12-27

Contradictory data on behavioral changes in MPTP-treated C57BL/6 mice have been reported, even though the toxin-treated mice Plavix Tablet 75mg have been widely used for non-clinical studies as an in vivo model of Parkinson's disease (PD). We found that the duration of immobility in the tail suspension test (TST) was significantly increased in MPTP-treated C57BL/6 mice as compared with control mice without a significant change in the locomotor activity (LA). Dopamine (DA) contents and protein levels of tyrosine hydroxylase and dopamine transporter in the striatum were profoundly decreased in the toxin-treated mice. These behavioral and neurobiochemical changes were almost completely inhibited by a pretreatment with deprenyl, a monoamine oxidase-B inhibitor. The stimulation of dopaminergic neurotransmission induced by L-dopa or a dopamine D2 receptor agonist ameliorated the increase in immobility time. Threshold level of striatal DA that produced the increase in immobility time in MPTP-treated mice was estimated to be between 11 and 27% of control level. We concluded that the increase in immobility time in the TST was induced by the nigrostriatal dopaminergic degeneration and was thought to be a consequence of motor dysfunction in this mouse model of PD.

parlodel cost 2016-10-03

A woman with secondary amenorrhea was Seroquel 4 Mg found to have hyperprolactinemia without clinical galactorrhea. Radiological findings of an enlarged sella turcica with displacement of the pituitary stalk were considered consistent with a prolactin macroadenoma. Treatment with bromocriptine corrected the amenorrhea and hyperprolactinemia, and the patient inadvertently became pregnant. However, no complications to the mother or fetus occurred during pregnancy or postpartum. On transsphenoidal surgery three months postpartum, the unexpected presence of a large Rathke's pouch cyst with a microadenomatous or nodular hyperplasia type of prolactin-secreting tumor was observed to account for the preoperative clinical and radiological findings.

parlodel drug uses 2016-03-17

Case report Arcoxia 60mg Dosage .

parlodel 10 mg 2015-09-11

Isolated mammary nuclei were incubated in the presence of HgCTP and the neosynthesized RNA was isolated with a SH-Sepharose column. The concentration of beta-casein mRNA and 28-S ribosomal RNA in the neosynthesized RNA fractions was evaluated using [3H]DNA probes complementary to beta-casein mRNA and 28-S rRNA respectively. In the unstimulated pseudopregnant rabbit, the transcription of both genes was easily detectable. Injections of prolactin progressively enhanced the transcription rate of both genes and preferentially the beta-casein gene. A comparison between the transcription rates and the accumulation of the corresponding gene products in the cell revealed that there is a good correlation between these two parameters for the 28-S rRNA gene. By contrast, the acceleration of beta-casein gene transcription by prolactin is unable to account for the simultaneous accumulation of beta-casein mRNA, indicating that prolactin is a potent stabilizer of casein mRNA. Injections of CB154 into lactating rabbits (a drug which suppresses the secretion of prolactin by hypophysis), induced a rapid drop of beta-casein Aldactone Medicine mRNA concentration and a slow decline of beta-casein gene transcription. Simultaneously the drug was responsible for a marked and rapid decrease of 28-S rRNA gene transcription, while the concentration of the rRNA remained elevated. During weaning the transcription of the beta-casein gene and, to a lower degree, the transcripton of the 28-S rRNA gene proceeded more slowly and this phenomenon was accompanied by a progressive decline of the RNA concentrations.