Hyperprolactinemia bromocriptine

For the management of hyperprolactinemia, bromocriptine therapy is typically initiated at a dose of 1.25 to 2.5 mg once daily at bedtime to minimize adverse effects. The dose can be gradually increased by 1.25-mg increments every week to obtain desirable serum prolactin concentrations. Usual therapeutic doses of bromocriptine range from 2.5 to 15 mg per day, although some patients may require doses as high as 40 mg per day. Bromocriptine is usually administered in two or three divided doses, but once-daily dosing has also been shown to be effective. ... 

If hyperprolactinemia is identified as the cause of amenorrhea, the use of bromocriptine, a dopamine agonist, results in a reduction in prolactin concentrations and the resumption of menses. 

The answer is b. (Hardman, pp 282—283J Central dopamine receptors are divided into Dt and D2 receptors. Antipsychotic activity is better correlated to blockade of D2 receptors. Haloperidol, a potent antipsychotic, selectively antagonizes at Dz receptors. Phenothiazine derivatives, such as chlorpromazine, fluphenazine, and promethazine, are not selective for D2 receptors. Bromocriptine, a selective D2 agonist, is useful in the treatment of parkinsonism and hyperprolactinemia. It produces fewer adverse reactions than do nonselective dopamine receptor agonists... 

It became known to suppress prolactine secretion, and it is therefore a useful tool in the treatment of prolactine dependent disorders, such as galactorrhea associated with hyperprolactinemia and postpartum, as well as certain kinds of sterility (3 - 9). In more elevated doses, the drug is a potent antiparkinsonicum. In addition, there is recent evidence of bromocriptine playing an important role in the trace heavy metals balance of the brain (10). 

Bromocriptine (Parl el) [Antiparkinsonian Agent/Dopamine Receptor Agonist] Uses Parkin on Dz, hyperprolactinemia, acromegaly, pituitary tumors Action Direct-acting on the striatal dopamine receptors X prolactin secretion Dose Initial, 1.25 mg PO bid titrate to effect, w/ food Caution [B, ] Contra Severe ischemic heart Dz or PVD Disp Tabs, caps SE X BP, Raynaud phenomenon (vasospastic disorder resulting in discoloration of the fmgers/toes), dizziness, N, hallucinations Interactions T Effects W/ erythromycin, fluvoxamine, nefazodone, sympathomimetics, antihypertensives X effects W/ phenothiazines, antipsychotics EMS Monitor BP may cause intolerance to EtOH OD May cause NA, severe hypotension give IV fluids symptomatic and supportive... 

Dopamine agonists suppress prolactin release very effectively in patients with hyperprolactinemia. GH release is reduced in patients with acromegaly, although not as effectively. Cabergoline and bromocriptine are also used in Parkinson s disease to improve motor function and reduce levodopa requirements (see Chapter 28). Newer, nonergot D2 agonists... 

A dopamine agonist alone or in combination with pituitary surgery, radiation therapy, or octreotide administration can be used to treat acromegaly. The doses required are higher than those used to treat hyperprolactinemia. For example, patients with acromegaly require 20-30 mg/d of bromocriptine and seldom respond adequately to bromocriptine alone unless the pituitary tumor secretes prolactin as well as GH. 

Bromocriptine Activates dopamine D2 receptors Suppresses pituitary secretion of prolactin dopaminergic effects on CNS motor control and behavior Treatment of hyperprolactinemia and Parkinson s disease (see Chapter 28) Administered orally or vaginally Toxicity Gastrointestinal disturbances, orthostatic hypotension, headache, psychiatric disturbances, vasospasm and pulmonary infiltrates in high doses... 

Five women with psychoses treated with amisulpride developed hyperprolactinemia and were treated with bromocriptine 1CM-0 mg/day (84). Prolactin concentrations were markedly reduced in only three of the five menses recurred in one of four patients with amenorrhea lactation decreased in one of three patients with galactorrhea,... 

Five patients (four women and one man, aged 30-45 years), who were evaluated for risperidone-induced hyperprolactinemia, had significant hyperprolactinemia, with prolactin concentrations of 66-209 pig/1 (1017). All but one had manifestations of hypogonadism, and in these four patients, risperidone was continued and a dopamine receptor agonist (bromocriptine or cabergoline) was added in three patients this reduced the prolactin concentration and alleviated the hypogonadism. 

Bliesener N, Yokusoglu H, Quednow B, Klingmiiller D, Kuhn K. Usefulness of bromocriptine in the treatment of amisulpride-induced hyperprolactinemia. Pharmacopsychiatry 2004 37 189-91. 

Tollin SR. Use of the dopamine agonists bromocriptine and cabergoline in the management of risperidone-induced hyperprolactinemia in patients with psychotic disorders. J Endocrinol Invest 2000 23(ll) 765-70. 

A vaginal suppository based on bromocriptine was employed for the therapy of hyperprolactinemia [32]. The rationale of the local vaginal delivery of bromocriptine lies in the noteworthy side effects consequent to oral therapy gastrointestinal disorders, extensive hepatic degradation, and hypotension. The pessary based on bromocriptine proved to be effective in lowering serum prolactin to normal levels after 20 days of local therapy the treatment was well tolerated by the majority of the patients and a minimal vaginal irritation was observed. 

Bromocriptine is a D2 agonist its structure is shown in Table 16-4. This drug has been widely used to treat Parkinson s disease and has also been used to treat certain endocrinologic disorders, especially hyperprolactinemia (see Chapter 37 Hypothalamic Pituitary Hormones), but in lower doses than for parkinsonism. Bromocriptine is absorbed to a variable extent from the gastrointestinal tract peak plasma levels are reached within 1-2 hours after an oral dose. It is excreted in the bile and feces. The usual daily dose of bromocriptine in the treatment of parkinsonism is between 7.5 and 30 mg, depending on response and tolerance. In order to minimize adverse effects, the dose is built up slowly over 2 or 3 months from a starting level of 1.25 mg twice daily after meals the daily dose is then increased by 2.5 mg every 2 weeks depending on the response or the development of adverse reactions. 

Arita J, Kimura F (1986) Characterization of in vitro dopamine synthesis in the median eminence of rats with haloperidol-induced hyperprolactinemia and bromocriptine-induced hypoprolactinemia. Endocrinology 779 1666-1672. 

Bromocriptine Therapy of hyperprolactinemia Oral tablet and vaginal suppository Proved to be effective and safe, without the adverse effects of oral administration vaginal suppository obtained higher reduction in serum prolactin 330... 

Dopamine inhibits prolactin synthesis. Drugs that inhibit dopamine synthesis or activity (e.g. antihypertensives, antidepressants, estrogen, phenothiazines, opiates), are the most common cause of hyperprolactinemia. Prolactin-secreting pituitary tumors sometimes are treated with bromocriptine, a dopamine agonist. 

Mesulergine is an 8-alpha-aminoergoline derivative that acts as a dopamine receptor agonist. In a blind, crossover study in six patients with hyperprolactinemia, mesulergine 0.5 mg caused fewer adverse effects than bromocriptine 2.5 mg, while the prolactin release-inhibitory effect of the two was of the same order (1). 

The dopaminergic activities of some newer ergolines (1 ) and ergolenes (1 ) have been studied. Compound (CH 29-717) is potent (10 x 15a) in suppression of hyperprolactinemia in rats. ° In behavioral and biochemical models 14c (CM 29-712) is generally bromocriptine-like in its DA agonist effects. pjjg ergolene 15b (CF 25-397) induces... 

Cabergoline is a selective D2 ergot agonist with a long half-life (70 hours) that is as effective as bromocriptine but dosed up to 4 mg once a day. It is available in the United States only as a 0.5-mg tablet (Dostinex, Pharmacia) for the treatment of hyperprolactinemia. A transdermal delivery form of the potent dopaminergic agonist... 

Bromocriptine was the first D2-receptor agonist to be used in the treatment of hyperprolactinemia and has been the mainstay of therapy for over 20 years. It inhibits the release of prolactin by directly stimulating postsynaptic dopamine receptors in the hypothalamus. Hypothalamic release of dopamine (prolactin-inhibitory hormone) inhibits the release of prolactin. Decreases in serum prolactin concentrations occur within 2 hours of oral administration with maximal suppression occurring after 8 hours, and suppressive effects persisting for up to 24 hours. Medical therapy with bromocriptine normalizes prolactin serum concentrations, restores gonadotropin production, and shrinks tumor size in approximately 90% of patients with prolactinomas. ... 

Carranza-Lira S, Gonzalez-Sanchez JL, Martinez-Chequer JC. Vaginal bromocriptine administration in patients with hyperprolactinemia. Int J Gynaecol Obstet 1999 65 77-78. 

DiSarno A, Landi ML, Cappabianca P, et al. Resistance to CabergoUne as compared with bromocriptine in hyperprolactinemia prevalence, clinical definition, and therapeutic strategy. J CUn Endocrinol Metab 2001 86 5256-5261. 

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