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Dostinex?

monkeyballs

New member
It's as expensive as Balls, but it does to prolactin what ron jeremy does to poons.

Any of yall have expereince with it? Huck feels that it's vastly superior to Bromo, and much safer to boot. Thinking of getting my hands on some, since it's about as easy as penicillian to get covered by insurance because it's commonly used to treat parkinsons.
 
If you can get cabergoline then you should be able to get pergolide mesilate, which seems superior to cabergoline from the abstracts I've seen.
 
Got it...it's called permax and from what I can tell it's actually cheaper than dostinex.
Here is the extract.
Bromo is a thing of the past.


The P-I-E-N-O Parkinsn's List Drug Database

pergolide / PermaxTM

ANTIPARKINSON:

Dopamine agonist

Description: Pergolide is an oral, semisynthetic ergot alkaloid derivative used in the management of Parkinson's disease. Pergolide is similar in action to other drugs in this class such as bromocriptine and lisuride. Pergolide has 10 to 1000 times the potency of bromocriptine on a milligram basis and may be effective in patients who have become tolerant to bromocriptine. Pergolide was approved by the FDA in December 1988.

Mechanism of Action: As a potent dopaminergic agonist, pergolide directly stimulates postsynaptic dopamine receptors in the nigrostriatal system. Like apomorphine and lisuride, the dopamine-agonist properties of pergolide are not associated with presynaptic dopamine synthesis or stores; pergolide is an agonist at postsynaptic receptors. Pergolide is one of the most potent dopaminergic agonists. Unlike bromocriptine, pergolide stimulates both DA and DA receptors. Pergolide also causes less nausea and orthostatic hypotension than does bromocriptine and may be effective in patients who have become tolerant to bromocriptine.
Pergolide inhibits the secretion of prolactin in humans and causes transient increases in serum growth hormone and decreases in luteinizing hormone. The effects on prolactin secretion persist much longer than antiparkinsonian action.

Pharmacokinetics: Pergolide is administered orally and is well absorbed. It is approximately 90% bound to plasma proteins. The drug undergoes metabolism to 10 metabolites, some of which are pharmacologically active. Elimination of the drug is primarily renal. The elimination half-life has been reported as 27 hours.

CONTRAINDICATIONS/PRECAUTIONS: Pergolide is contraindicated in patients who are known to have ergot alkaloid hypersensitivity.

Pergolide can cause symptomatic orthostatic hypotension or sustained hypotension, especially during initial administration. Tolerance to these effects will develop if doses are titrated gradually. Patients should be warned of this risk. Initial doses should be small, gradually increasing over a 3-to 4-week period.

Hallucinations have occurred in patients receiving pergolide, requiring discontinuation of therapy in some patients. Patients should be warned of this adverse reaction.

Pergolide is classified as pregnancy category B. No adequate studies have examined the effects of pergolide on the human fetus. Animal reproduction studies have shown no adverse fetal effects.

DRUG INTERACTIONS: Pergolide is a potent dopamine-receptor agonist. Dopamine-receptor antagonists, including the neuroleptics (phenothiazines, haloperidol, and thiothixene), or metoclopramide should not be administered concurrently because they can antagonize the effects of pergolide.

ADVERSE REACTIONS: Pergolide is administered as adjunctive therapy to levodopa/carbidopa. The adverse effect profile reported from clinical trials reflect either combined therapy with pergolide/levodopa/carbidopa or placebo/levodopa/carbidopa.

Adverse CNS effects associated with pergolide administration occur frequently. Those seen more often in pergolide-treated patients as opposed to those treated with placebo are dyskinesias (involuntary movements of the head, face, tongue, upper arms and body), dystonia, hallucinations, drowsiness, anxiety and insomnia. Less frequent CNS reactions include akathisia, confusion, dizziness, psychosis, and personality changes. Sudden withdrawal of pergolide therapy can precipitate CNS adverse effects such as hallucinations and confusion in patients remaining on levodopa/carbidopa. For these patients a gradual decrease in dosage is recommended.

In clinical trials symptomatic orthostatic hypotension and/or sustained hypotension occurred in more than 10% of patients, compared to 7% taking placebo (both taken in conjunction with levodopa/carbidopa). Careful dosage titration can improve this profile, and tolerance can develop with continued therapy. Patients need to be aware of the risk of syncope and the need for gradual dosage increase. Other cardiovascular adverse events include occasional hypertension, palpitations and the possibility of myocardial infarction. Vasodilatation may occur. There have been rare cases of CNS hemorrhage. Diplopia and headache may be symptomatic of cerebrovascular hemorrhage.

Gastrointestinal complaints with pergolide were frequently reported in clinical trials, usually at a rate about twice that for placebo. They include abdominal pain, constipation, diarrhea, dyspepsia, anorexia, nausea/vomiting and less frequently xerostomia.

For the body as a whole, pain has been reported at a variety of sites while taking pergolide. These include chest, neck and back pain. A flu-like syndrome occurs infrequently with fever and chills. Rhinitis was reported by 12% of patients taking pergolide as opposed to 5% taking placebo. Dyspnea occurred in 4.8% vs 1.1% on placebo.

Other less frequent adverse reactions with pergolide include myalgia, weakness, weight gain or weight loss.Pergolide inhibits the secretion of prolactin in humans and causes transient increases in serum growth hormone and decreases in luteinizing hormone
 
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