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Overview Of Cabergoline Tablets

cabergoline 0.5 mg tablets
Cabergoline tablets is a synthetic ergoline-derived dopamine agonist that is indicated for the treatment of hyperprolactinemic disorders, either idiopathic or because of pituitary adenomas. Until the availability of cabergoline in 1996, bromocriptine was the only agent approved by the FDA for the treatment of hyperprolactinemias. Results from comparative studies of the two medications indicate that cabergoline is more effective than bromocriptine in suppressing prolactin secretion and it has a more favorable tolerability profile. In addition, the unique dosing strategy of cabergoline is a potential advantage of the drug. Whereas bromocriptine requires multiple daily dosages for effectiveness, cabergoline has a long half-life and is administered once to twice weekly for hyperprolactinemia. Although there is evidence for the efficacy of cabergoline tablets in the treatment of restless legs syndrome, the drug is rarely used in clinical practice because of the risk of cardiac valvulopathy and the availability of safer alternatives.
Cabergoline tablets is a centrally-acting synthetic ergot alkaloid. Cabergoline tablets causes a dose-dependent suppression of prolactin levels via dopamine agonist activity at dopamine-2 (D2) receptors in the anterior pituitary. Stimulation of D2 receptors in this region of the brain inhibits prolactin secretion by lactotrophs. Cabergoline tablets are 7-times more selective for D2 receptors than bromocriptine. The relative selectivity of cabergoline may account for its favorable tolerability profile compared to other dopamine agonists such as bromocriptine. There is minimal affinity for adrenergic, serotonin, or histamine receptors. Cabergoline has little or no effect on the secretion of pituitary hormones such as cortisol, GH, FSH, LH, ACTH, or TSH. Symptoms that may be corrected by the normalization of prolactin levels include loss of libido, amenorrhea, infertility, galactorrhea, gynecomastia, and impotence.
Cabergoline tablets are administered orally. Cabergoline is moderately bound (40% to 42%) to human plasma proteins in a concentration-independent manner. In animals, based on total radioactivity, cabergoline (and/or its metabolites) has shown extensive tissue distribution. A considerable amount of the drug may be found in the pituitary as compared with the plasma. Radioactivity in the pituitary exceeded that in plasma by more than 100-fold and was eliminated with a half-life of approximately 60 hours. This finding is consistent with the long-lasting prolactin-lowering effect of the drug. Significant radioactivity (parent plus metabolites) detected in the milk of lactating rats suggests a potential for exposure to nursing infants. A significant fraction of the administered oral dose undergoes a first-pass effect. In both animals and humans, cabergoline is extensively metabolized, predominately via hydrolysis and cytochrome P450 mediated metabolism appears to be minimal. Hydrolysis of the acylurea or urea moiety abolishes the prolactin-lowering effect of cabergoline. None of the major metabolites identified contribute to the therapeutic effect of the drug. The average elimination half-life is 63 to 69 hours. Cabergoline and its metabolites are eliminated primarily in the feces. After the administration of radioactive cabergoline to five healthy volunteers, approximately 60% of the dose was excreted in the feces, and approximately 22% of the dose was excreted in the urine within 20 days. Less than 4% of the dose was excreted unchanged in the urine. Nonrenal and renal clearances for cabergoline are about 3.2 L/minute and 0.08 L/minute, respectively.
Affected cytochrome P450 (CYP450) isoenzymes and drug transporters: None CYP450 metabolism of cabergoline is minimal and cabergoline does not cause enzyme induction and/or inhibition in the rat.

Route-Specific Pharmacokinetics

Oral Route: After oral administration, peak plasma concentrations occur in 1 to 3 hours. The absolute bioavailability of cabergoline is unknown, and the rate and extent of absorption are not affected by food. A significant fraction of the administered oral dose undergoes a first-pass effect. After a once-weekly dosing schedule, steady-state concentrations are expected to be 2- to 3-fold higher than after a single dose. Higher doses produce prolactin suppression in a greater proportion of patients. Also, higher doses are associated with an earlier onset and longer duration of prolactin inhibition. In 12 healthy volunteers, complete prolactin inhibition was obtained in 50% of subjects after a 0.5 mg dose, in 92% after a 1 mg dose, and in 100% after a 1.5 mg dose. Single or multiple doses up to 2 mg in healthy patients had no apparent effect on other anterior pituitary hormones such as growth hormone (GH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), adrenocorticotropin hormone (ACTH), or cortisol. Among 51 hyperprolactinemic patients who received a single 0.6 mg dose, the duration of effect was 14 days, and the time to maximal effect was 48 hours. In contrast, after a single bromocriptine 2.5 mg dose, the duration of effect was 24 hours, and the time to maximal effect was 6 hours. The prolonged prolactin-lowering effect of cabergoline may be related to its slow elimination and long half-life.

Special Populations

Hepatic Impairment: Caution is advised in patients with hepatic impairment. The area under the plasma concentration curve (exposure, or AUC) and peak plasma concentrations (Cmax) of cabergoline are increased in the presence of severe hepatic impairment. Among patients with a Child-Pugh score greater than 10 (e.g., Child-Pugh class C), substantial increases in the mean cabergoline Cmax and AUC were observed. No effect on the mean cabergoline Cmax or AUC was observed in patients with mild to moderate hepatic dysfunction (i.e., Child-Pugh score of 10 or less, n = 12).

Renal Impairment: The pharmacokinetic parameters of cabergoline were not altered in patients with moderate to severe renal insufficiency (n = 12), as assessed by creatinine clearance (CrCl).

Geriatric: The effect of age on the pharmacokinetics of cabergoline tablets has not been studied.
For the treatment of hyperprolactinemia, either idiopathic or due to a pituitary adenoma:
Oral dosage
Adults: Initially, cabergoline tablets 0.25 mg PO twice per week. Perform a cardiovascular evaluation and consider echocardiography to assess for valvular disease before initiating treatment. May titrate by 0.25 mg/dose no more than every 4 weeks up to 1 mg PO twice per week, if needed. If the patient does not respond adequately and no additional benefit is observed with higher doses, use the lowest dose that achieved maximal response and consider other therapeutic approaches. Once weekly administration has also been found effective at dosages of 0.5 to 3 mg/week PO. Prolactin levels normalized in 73% of patients, and tumor size decreased by a mean of 31% (range: 5% to 95%). CONTINUED TREATMENT: Efficacy beyond 24 months of treatment has not been established. Periodic assessment of cardiac status and consideration of echocardiography are needed for patients who receive long-term treatment. Discontinuation may be considered after 6 months of acceptable serum prolactin concentrations. Assess the need for re-initiation of cabergoline treatment by periodic prolactin determinations.
Cabergoline is contraindicated in patients with a known ergot derivative or ergot alkaloid hypersensitivity because of the possibility of an allergic reaction.
Cabergoline is contraindicated in patients with a history of valvular heart disease, as suggested by anatomical evidence of valvulopathy of any valve, determined by pre-treatment evaluation including echocardiographic demonstration of valve leaflet thickening, valve restriction, or mixed valve restriction stenosis. Postmarketing cases of cardiac valvulopathy have been reported in patients receiving cabergoline. These cases have generally occurred during the use of high doses of the drug (i.e., more than 2mg/day). Cases of cardiac valvulopathy have also been reported in patients receiving lower doses of cabergoline for the treatment of hyperprolactinemic disorders. Cautious use of cabergoline is recommended in patients who have been exposed to other medications associated with valvulopathy. All patients should undergo a cardiovascular evaluation, including an echocardiogram, before cabergoline initiation to assess for valvular disease. If valvular disease is present, cabergoline treatment should not be initiated. Clinical and diagnostic monitoring (e.g., chest x-ray, CT scan, cardiac echocardiogram) should be conducted periodically in all patients receiving cabergoline to evaluate the risk of cardiac valvulopathy. Echocardiographic monitoring should be conducted every 6 to 12 months or as needed by the presence of edema, new cardiac murmur, dyspnea, congestive heart failure, or other signs and symptoms of valvulopathy. Cabergoline should be discontinued if an echocardiogram demonstrates new valvular regurgitation, valvular restriction, or valve leaflet thickening.
Cabergoline is contraindicated for use by patients with a history of pulmonary, pericardial, cardiac valvular or retroperitoneal fibrotic disorders. Cabergoline should not be used in patients with a history of or current signs/clinical symptoms of respiratory, cardiac, or other disorders linked to fibrotic tissue such as pulmonary fibrosis, retroperitoneal fibrosis, or constrictive pericarditis. One case of constrictive pericarditis with subsequent pleuropulmonary inflammatory-fibrotic syndrome has occurred with cabergoline administration. Similar to other ergot derivatives, cabergoline can cause fibrotic changes, inflammatory fibrosis, pleural effusion, and valvulopathy. Therefore, patients receiving cabergoline should be monitored for the potential development of fibrotic disorders. Clinical and diagnostic monitoring (e.g., erythrocyte sedimentation rate, chest x-ray, serum creatinine) should be considered at baseline and as needed during treatment. Potential signs and symptoms of fibrotic disorders, including dyspnea, chronic cough, chest pain, renal insufficiency, ureteral/abdominal vascular obstruction, abdominal masses or tenderness, and cardiac failure, should be promptly evaluated. Discontinuation of cabergoline may result in improvement in the symptoms of pleural effusion and pulmonary fibrosis.
Like other ergot derivatives, cabergoline is contraindicated in patients with uncontrolled hypertension. Ergot-derived dopamine agonists have been associated with hypertension, strokes, and seizures. Patients should be advised to immediately report new or worsening hypertension, severe headaches, or other adverse CNS effects.
Cabergoline has been associated with orthostatic hypotension. Initiating treatment with dosages greater than 1 mg are most likely to produce this effect. Cabergoline should be used cautiously in those with a history of hypotension or those receiving medications known to cause hypotension.
Since cabergoline is extensively metabolized by the liver, caution should be used, and careful monitoring implemented, when administering cabergoline to patients with hepatic disease. No effects on the kinetics of cabergoline have been observed in patients with mild to moderate hepatic impairment, but patients with significant impairment had significantly increased exposure to the drug.
Some patients receiving dopamine agonists, including cabergoline, have reported impulse control symptoms/compulsive behaviors, including pathological gambling, increased libido, and hypersexuality. Generally, these impulse control symptoms are reversible after the dose is reduced or the drug is discontinued. Practitioners should inquire periodically about new or worsening impulsivity in patients receiving cabergoline. Likewise, patients should be instructed to report such changes while receiving cabergoline. Dose reduction or discontinuation should be considered in those who experience these effects.
Although the available data suggest a low fetal risk in early pregnancy, the risk to the developing fetus during chronic cabergoline exposure is unknown. Therefore, cabergoline should be used during pregnancy only if clearly needed. Dopamine agonists, like cabergoline, should generally not be used in patients with pregnancy-induced hypertension (e.g., preeclampsia, eclampsia, or postpartum hypertension), unless the potential benefit is judged to outweigh the possible risk. There is an association of use of these drugs with hypertension, seizures, myocardial infarction, and stroke in postpartum patients.
In one review of over 200 pregnancies in cabergoline-exposed women, no increased miscarriage rates, congenital malformations, abnormal distribution of birthweights, or disturbances in postnatal development were noted in comparison to the expected population rate. The range of embryo-fetal exposure to cabergoline was between 1 and 144 days.
Among 56 women receiving cabergoline for amenorrhea secondary to hyperprolactinemia, the following outcomes were reported in 17 subsequent pregnancies: 1 spontaneous abortion, 6 pending outcomes, and 10 term infants with normal physical and mental development.
In a separate group of women receiving cabergoline for hyperprolactinemia, the following outcomes were reported in 61 pregnancies: 5 elective abortions (1 suspected malformation), 6 spontaneous abortions, 1 hydatidiform mole, and 49 live births (1 minor defect and 1 trisomy).
In one study enrolling 47 hyperprolactinemic females, 9 became pregnant against medical advice. Treatment with cabergoline was interrupted when pregnancy was diagnosed. The pregnancy outcomes included 1 voluntary termination, 1 spontaneous termination, and 7 healthy term infants showing normal development during 8 years of continued follow-up. One case describes a patient with two separate pregnancies and the use of levodopa and cabergoline for Parkinson’s disease throughout the pregnancies. There were no fetal complications; however, C-section was required in the second birth due to placental abruption.
Instruct patients to notify their physician if they suspect they are pregnant, become pregnant, or intend to become pregnant during therapy. Cabergoline treatment in a patient with infertility due to hyperprolactinemia may restore fertility. Conduct pregnancy testing if there is any suspicion of pregnancy.
A decision should be made whether to discontinue breast-feeding or to discontinue the drug, taking into account the importance of the drug to the mother. Cabergoline interferes with lactation due to a central prolactin-lowering effect. Cabergoline is also not indicated for postpartum lactation inhibition because the use of other dopamine agonists (e.g., bromocriptine) for this purpose has resulted in hypertension, stroke, and seizures.
Clinical studies of cabergoline did not include a sufficient number of patients 65 years and older to determine whether they respond differently than younger adults. Other reported clinical experience has not identified differences in responses between geriatric and younger adult patients. However, cabergoline dosing and titration should be more cautious in geriatric patients, starting at the lower end of the dose range to account for differences in renal, hepatic, or cardiac systems as well as concomitant disease states and medications.
The safety and efficacy of cabergoline in pediatric patients, particularly children and infants, have not been established.
Although the available data suggest a low fetal risk in early pregnancy, the risk to the developing fetus during chronic cabergoline exposure is unknown. Therefore, cabergoline should be used during pregnancy only if clearly needed. Dopamine agonists, like cabergoline tablets, should generally not be used in patients with pregnancy-induced hypertension (e.g., preeclampsia, eclampsia, or postpartum hypertension), unless the potential benefit is judged to outweigh the possible risk. There is an association of use of these drugs with hypertension, seizures, myocardial infarction, and stroke in postpartum patients. In one review of over 200 pregnancies in cabergoline-exposed women, no increased miscarriage rates, congenital malformations, abnormal distribution of birthweights, or disturbances in postnatal development were noted in comparison to the expected population rate. The range of embryo-fetal exposure to cabergoline was between 1 and 144 days. Among 56 women receiving cabergoline for amenorrhea secondary to hyperprolactinemia, the following outcomes were reported in 17 subsequent pregnancies: 1 spontaneous abortion, 6 pending outcomes, and 10 term infants with normal physical and mental development. In a separate group of women receiving cabergoline tablets for hyperprolactinemia, the following outcomes were reported in 61 pregnancies: 5 elective abortions (1 suspected malformation), 6 spontaneous abortions, 1 hydatidiform mole, and 49 live births (1 minor defect and 1 trisomy). In one study enrolling 47 hyperprolactinemic females, 9 became pregnant against medical advice. Treatment with cabergoline was interrupted when pregnancy was diagnosed. The pregnancy outcomes included 1 voluntary termination, 1 spontaneous termination, and 7 healthy term infants showing normal development during 8 years of continued follow-up. One case describes a patient with two separate pregnancies and the use of levodopa and cabergoline for Parkinson’s disease throughout the pregnancies. There were no fetal complications; however, C-section was required in the second birth due to placental abruption. Instruct patients to notify their physician if they suspect they are pregnant, become pregnant, or intend to become pregnant during therapy. Cabergoline treatment in a patient with infertility due to hyperprolactinemia may restore fertility. Conduct pregnancy testing if there is any suspicion of pregnancy.
A decision should be made whether to discontinue breast-feeding or to discontinue the drug, taking into account the importance of the drug to the mother. Cabergoline interferes with lactation due to a central prolactin-lowering effect. Cabergoline is also not indicated for postpartum lactation inhibition because the use of other dopamine agonists (e.g., bromocriptine) for this purpose has resulted in hypertension, stroke, and seizures.
During a placebo-controlled, fixed-dose study of cabergoline 0.125 mg to 1 mg PO twice weekly for hyperprolactinemic disorders, the following gastrointestinal effects were reported more frequently in the cabergoline groups than the placebo groups: nausea (27%), constipation (10%), dyspepsia (2%), and vomiting (2%). Nausea was considered a possible dose-related effect. In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, the following GI effects were reported in the cabergoline group versus the bromocriptine group: nausea (29% vs. 43%), constipation (7% vs. 9%), abdominal pain (5% vs. 8%), dyspepsia (5% vs. 7%), vomiting (4% vs. 7%), xerostomia (2% vs. 1%), diarrhea (2% vs. 3%), flatulence (2% vs. 1%), throat irritation (1% vs. 0%), anorexia (1% vs. 1%), and dental pain (toothache 1% vs. 0%). Nausea and vomiting were among the most common causes of treatment discontinuation in both groups. In clinical studies overall, xerostomia, flatulence, diarrhea, weight gain, weight loss, and anorexia occurred at an incidence of less than 1%. Gastric or duodenal peptic ulcer was reported rarely in Parkinson’s disease patients who received cabergoline doses up to 11.5 mg daily.

During a placebo-controlled, fixed-dose study of cabergoline 0.125 mg to 1 mg PO twice weekly for hyperprolactinemic disorders, the following centrally-mediated effects were reported more frequently in the cabergoline groups than the placebo groups: headache (26%), dizziness (15%), paresthesias (1%), and vertigo (1%). In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, the following CNS effects were reported in the cabergoline group versus the bromocriptine group: headache (26% vs. 27%), dizziness (17% vs. 18%), vertigo (4% vs. 4%), paresthesias (2% vs. 3%), drowsiness (2% vs. 2%), and insomnia (1% vs. 1%). Headache was among the most common causes of treatment discontinuation in the cabergoline group while headache and dizziness/vertigo were among the common causes of treatment discontinuation in the bromocriptine group. In clinical studies overall, drowsiness, paresthesias, and insomnia occurred at an incidence of less than 1%.

During a placebo-controlled, fixed-dose study of cabergoline 0.125 mg to 1 mg PO twice weekly for hyperprolactinemic disorders, the following reproductive effects were reported more frequently in the cabergoline groups than the placebo groups: mastalgia (1%) and dysmenorrhea (1%). In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, the following reproductive effects were reported in the cabergoline group versus the bromocriptine group: mastalgia (2% vs. 3%) and dysmenorrhea (1% vs. 0.4%). In clinical studies overall, dysmenorrhea occurred at an incidence of less than 1%.

During a placebo-controlled, fixed-dose study of cabergoline 0.125 mg to 1 mg PO twice weekly for hyperprolactinemic disorders, fatigue (7%) was reported more frequently in the cabergoline groups than the placebo groups. In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, the following general effects were reported in the cabergoline group versus the bromocriptine group: asthenia (6% vs. 6%), fatigue (5% vs. 8%), influenza-like symptoms (1% vs. 0%), malaise (1% vs. 0%), periorbital edema (1% vs. 1%), and hot flashes (3% vs. 1%). In clinical studies overall, facial edema, influenza-like symptoms, and malaise occurred at an incidence of less than 1%.

Although cabergoline has only minimal affinity for adrenergic receptors, orthostatic hypotension has been a frequently reported side effect in some studies. Most instances of hypotension are asymptomatic and do not require discontinuation of the drug. Caution is recommended if cabergoline is used concomitantly with drugs that may lower blood pressure. Initial doses higher than 1 mg may produce orthostatic hypotension. Among 168 patients who received cabergoline 0.125 mg to 1 mg PO twice weekly, 4% had orthostatic hypotension vs. 0% with placebo. In an 8-week comparative trial of cabergoline to bromocriptine, the following cardiovascular effects were reported in the cabergoline group versus the bromocriptine group: hypotension (1% vs. 2%), palpitations (1% vs. 2%), dependent edema (1% vs. 0.4%), syncope (1% vs. 1%), and peripheral edema (1% vs. 0.4%). In clinical studies overall, hypotension, syncope, and palpitations occurred at an incidence of less than 1%. Peripheral edema was a common event among patients with Parkinson’s disease who received doses up to 11.5 mg PO daily; cardiac failure occurred rarely.

Similar to other ergot derivatives, cabergoline has been associated with pleuropulmonary changes, pleural effusion, and pulmonary fibrosis. Pleural effusion and pulmonary fibrosis occurred rarely among patients with Parkinson’s disease who received doses up to 11.5 mg PO daily. One case of constrictive pericarditis with subsequent pleuropulmonary inflammatory-fibrotic syndrome occurred in a patient with Parkinson’s disease receiving cabergoline. Pleural, pericardial, and retroperitoneal fibrosis have been reported during postmarketing use. An elevated erythrocyte sedimentation rate (ESR) has been associated with pleural effusion/fibrosis. A chest X-ray is recommended for unexplained clinically relevant ESR elevations. Valvular and pericardial fibrosis have often manifested as cardiac failure; therefore, valvular fibrosis and constrictive pericarditis should be excluded if such symptoms occur. Renal insufficiency or ureteral/abdominal vascular obstruction, loin/flank pain, lower limb edema, or abdominal mass/tenderness may indicate retroperitoneal fibrosis. Clinical and diagnostic monitoring (e.g., ESR, chest X-ray, serum creatinine) should be considered at baseline and as necessary during treatment. After a diagnosis of pleural effusion or pulmonary fibrosis, discontinuation of cabergoline may result in symptom improvement. Instruct patients to report shortness of breath, persistent cough, difficulty breathing when lying down, chest pain, or extremity swelling.

Cardiac valvulopathy may occur with cabergoline treatment, especially with chronic cabergoline doses of at least 2 mg/day, and rarely with short-term treatment (less than 6 months) or lower doses for hyperprolactinemia. All patients should undergo a cardiovascular evaluation, including an echocardiogram, to assess for a valvular disease before cabergoline initiation in addition to periodic evaluation for cardiac valvulopathy (e.g., chest x-ray, CT scan, echocardiogram). Echocardiographic monitoring should be conducted every 6 to 12 months. Patients who develop signs or symptoms of cardiac disease such as edema or fluid retention, new cardiac murmur, dyspnea, congestive heart failure, or other signs and symptoms of valvulopathy should also be evaluated. Valvular fibrosis has often manifested as heart failure; therefore, valvular fibrosis and constrictive pericarditis should be excluded if such symptoms occur. Clinical and diagnostic monitoring (e.g., chest X-ray, echocardiograms) should be considered at baseline and as necessary during treatment. Instruct patients to report shortness of breath, persistent cough, difficulty breathing when lying down, chest pain, fatigue on exertion, or extremity swelling. Cabergoline should be discontinued if an echocardiogram demonstrates new valvular regurgitation, valvular restriction, or valve leaflet thickening.2 The risk for valvular heart disease was assessed in a placebo-controlled prevalence study of patients taking dopamine agonists for Parkinson’s disease (n = 155) and controls without the disease (n = 90). Of the patients taking dopamine agonists, 49 were receiving cabergoline. Echocardiography was performed to assess the severity of regurgitation of the mitral, aortic, and tricuspid valves and degree of deformity of the mitral valve apparatus. Moderate to severe regurgitation (grade 3 to 4) occurred significantly more frequently in the ergot dopamine agonist group (pergolide 23.4%, cabergoline 28.6%) than the non-ergot dopamine agonist group (pramipexole 0%, ropinirole 0%), or the control group (5.6%). In a separate population-based cohort study of patients receiving various antiparkinsonian medications (n = 11,417), the risk of newly diagnosed cardiac valve regurgitation (CVR) was greater with cabergoline and pergolide than other dopamine agonists. In a multi-country, retrospective study assessing the association between new use of dopamine agonists for Parkinson’s disease or hyperprolactinemia (n = 27,812) and CVR, other types of fibrosis, and other cardiopulmonary events, Parkinson’s patients receiving cabergoline had an increased risk for CVR compared to patients receiving non-ergot-derived dopamine agonists and levodopa. Conversely, patients with hyperprolactinemia receiving cabergoline or other dopamine agonists did not have an increased risk of CVR compared to patients not receiving dopamine agonists.

During a placebo-controlled, fixed-dose study of cabergoline 0.125 mg to 1 mg PO twice weekly for hyperprolactinemic disorders, nervousness (2%) was reported more frequently in the cabergoline groups than the placebo groups. In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, the following CNS effects were reported in the cabergoline group versus the bromocriptine group: depression (3% vs. 2%), anxiety (1% vs. 1%), impaired concentration (1% vs. 0.4%), and nervousness (1% vs. 2%). In clinical studies overall, nervousness, anxiety, and libido increase occurred at an incidence of less than 1%. Commonly observed adverse effects among patients with Parkinson’s disease who received cabergoline doses up to 11.5 mg PO daily were confusion, dyskinesia, and hallucinations. Aggression, psychotic disorder (psychosis), and impulse control symptoms (i.e., hypersexuality, libido increase, pathological gambling) have been reported during the use of cabergoline and other dopamine agonists.

During a placebo-controlled, fixed-dose study of cabergoline 0.125 mg to 1 mg PO twice weekly for hyperprolactinemic disorders, visual impairment (1%) was reported more frequently in the cabergoline groups than the placebo groups. In an 8-week comparative trial of cabergoline to bromocriptine, visual impairment was reported in both the cabergoline and bromocriptine groups at an incidence of 1%. In clinical studies overall, abnormal vision occurred at an incidence of less than 1%.

In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, the following dermatologic effects were reported in the cabergoline group versus the bromocriptine group: acne vulgaris (1% vs. 0%) and pruritus (1% vs. 0.4%). In clinical studies overall, acne and pruritus occurred at an incidence of less than 1%. Alopecia has been reported; however, the frequency is unknown.

In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, the following musculoskeletal effects were reported in the cabergoline group versus the bromocriptine group: musculoskeletal pain (2% vs. 3%) and arthralgia (1% vs. 0%).

In an 8-week comparative trial of cabergoline to bromocriptine for hyperprolactinemic disorders, rhinitis was reported in 1% of patients in the cabergoline group versus 4% of patients in the bromocriptine group. In clinical studies overall, nasal congestion and epistaxis occurred at an incidence of less than 1%.
Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.
You can buy cabergoline pills online from MediLab’s compounding pharmacy in the following Florida regions:

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  • Webster J, Piscitelli G, Polli A, et al. A comparison of cabergoline and bromocriptine in the treatment of hyperprolactinemic amenorrhea. N Engl J Med 1994;331:904-909.
  • Dostinex (cabergoline) package insert. Kalamazoo, MI: Pharmacia and Upjohn Company; 2019 Dec.
  • Aurora RN, Kristo DA, Bista SR, et al. The treatment of restless legs syndrome and periodic limb movement disorder in adults-an update for 2012: practice parameters with an evidence-based systematic review and meta-analyses: an American Academy
  • Iller BM, Molitch ME, Vance ML, et al. Treatment of prolactin-secreting macroadenomas with the once-weekly dopamine agonist cabergoline. J Clin Endocrin Metabol 1996;81:2338-2343.
  • Dostinex (cabergoline) package insert. Kalamazoo, MI: Pharmacia and Upjohn Company; 2019 Dec