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Cabergoline

A Review of its Pharmacological Properties and Therapeutic Potential in the Treatment of Hyperprolactinaemia and Inhibition of Lactation

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Summary

Synopsis

Cabergoline is a synthetic ergoline which shows high specificity and affinity for the dopamine D2 receptor. It is a potent and very long-acting inhibitor of prolactin secretion. Prolactin-lowering effects occur rapidly and, after a single dose, were evident at the end of follow up (21 days) in puerperal women, and up to 14 days in patients with hyperprolactinaemia.

In the only comparative study to date, cabergoline 0.5 to 1.0mg twice weekly was more effective than bromocriptine 2.5 to 5.0mg twice daily in the treatment of hyperprolactinaemic amenorrhoea, restoring ovulatory cycles in 72% of women and normalising plasma prolactin levels in 83%, compared with 52 and 58%, respectively, for bromocriptine. In the prevention of puerperal lactation, a single dose of cabergoline 1.0mg was as effective as bromocriptine 2.5mg twice daily for 14 days. A significantly lower incidence of rebound lactation in the third postpartum week was seen with cabergoline. Unpublished data suggest cabergoline 0.25mg twice daily for 2 days is effective in suppressing established puerperal lactation in about 85% of women.

Nausea, vomiting, headache and dizziness are characteristic adverse events of the dopaminergic ergot derivatives. Cabergoline appears to be better tolerated than bromocriptine in both patients with hyperprolactinaemia and postpartum women. Most patients intolerant of other ergot derivatives can tolerate cabergoline. Bromocriptine use in the puerperium has been associated with an increased risk of serious thromboembolic events. However, there are no such reports with cabergoline and whether these events will become associated with other dopaminergic agents is unknown.

The teratogenic potential of cabergoline has not been extensively investigated in humans. Ten congenital abnormalities have been reported in 199 cabergolineassociated pregnancies. Although there is no pattern to these abnormalities, the limited experience with cabergoline in pregnancy means the drug cannot be considered as a first-line therapy for the treatment of infertility associated with hyperprolactinaemia.

At this stage of its development, cabergoline will prove useful in patients with hyperprolactinaemia who have failed treatment with, or are intolerant of, other dopamine agonists such as bromocriptine. If drug treatment is required for the prevention or suppression of puerperal lactation, cabergoline offers significant advantages over bromocriptine and should become the drug treatment of first choice for this indication.

Overview of Hyperprolactinaemia and Lactation Inhibition

Prolactin hypersecretion is the most common endocrine disorder of the hypothalamic-pituitary axis. Hyperprolactinaemia [plasma prolactin level >20 μg/L (>424 mU/L)] may lead to hypogonadism, menstrual cycle disturbances, and/or galactorrhoea. Large prolactinomas can also result in headaches and visual field defects.

Prolactin stimulates postpartum milk production. Although other hormones are involved, galactopoiesis cannot occur without prolactin. Inhibition of puerperal lactation may be desirable because of medical conditions, in either mother or infant, or through personal choice of the mother.

Dopamine is believed to be the major prolactin inhibiting factor and ergot derivatives which show dopaminergic properties have been used as hypoprolactinaemic agents since the 1970s.

Pharmacological Properties

Cabergoline has a high selectivity and affinity for the dopamine D2 receptor. Agonist activity at this receptor on the lactotroph results in inhibition of prolactin secretion.

Cabergoline has profound prolactin-lowering effects in animals, healthy volunteers, patients with hyperprolactinaemia and puerperal women. These effects are dose-dependent in humans within the range 0.2 to 1.0mg, both in terms of magnitude and duration of effect. Single doses of cabergoline produce a prolactin-lowering effect, usually within 3 hours of drug administration, which may persist for at least 21 days in puerperal women. Higher doses produce a more rapid decline in plasma prolactin levels and the rate of reduction may determine the effectiveness of cabergoline in the inhibition of puerperal lactation.

The effects of cabergoline are also dose-dependent following multiple dosing (0.25 to 2.0mg weekly) in women with hyperprolactinaemia. Maximal inhibition of prolactin secretion occurs between 4 and 8 weeks after commencing therapy. The effects on prolactin persist for some time after drug withdrawal, with normoprolactinaemia evident for up to 2 years after discontinuation of cabergoline in some patients.

In patients with hyperprolactinaemia or puerperal women, cabergoline does not appear to affect endocrine function other than prolactin, although expected increases in estrogen or testosterone levels are seen in hyperprolactinaemic female and male patients, respectively, treated with the drug. Possible antitumour activity has been suggested in animal models and reduction of prolactinoma size in humans has also been documented.

Cabergoline was widely distributed to well-perfused organs, including the pituitary, in animal studies. Plasma protein binding is estimated at 41 to 42% in humans. Cabergoline undergoes extensive metabolism after oral administration, and a number of metabolites have been identified. These do not appear to contribute to the pharmacological activity of the drug. The main route of elimination of cabergoline is the faeces, with up to 72% of the radioactivity present in an orally administered radiolabelled dose being excreted by this route. Urinary excretion of unchanged drug accounts for less than 14% of an oral dose.

Therapeutic Potential

In the treatment of hyperprolactinaemic disorders, cabergoline is more effective than placebo in restoring normoprolactinaemia and regular menstrual function. Cabergoline shows a clear dose-response relationship within the range 0.125 to 1.0mg twice weekly, although higher dosages are associated with a higher frequency of adverse events.

In the treatment of women with hyperprolactinaemic amenorrhoea, cabergoline 0.5 to 1.0mg twice weekly (n = 223) was significantly more effective than bromocriptine 2.5 to 5.0mg twice daily (n = 236) in restoring ovulation and menses (72 vs 52% of women) and normalising prolactin levels (83 vs 58%). Galactorrhoea, which was present in some women at study entry, was alleviated in 90 and 78% of women, respectively.

Long term efficacy studies have demonstrated the continued therapeutic effects of cabergoline after drug withdrawal. Menses were restored and maintained in about 90% of previously oligo- or amenorrhoeic women and in some instances this continued for 6 months to 2 years after drug withdrawal, even though hyperprolactinaemia recurred in the majority of patients. Preliminary data suggest that cabergoline restores sexual function in men with hyperprolactinaemia-induced impotence and reduces both macro- and microprolactinoma size.

Cabergoline is effective in the prevention and suppression of puerperal lactation following both normal and caesarean deliveries. A single dose of cabergoline 1.0mg was at least as effective as bromocriptine 2.5mg twice daily for 14 days in the prevention of lactation but with a lower rate (5 vs 24%) of rebound lactation in the third post partum week. Although there are no published studies on the use of cabergoline for the suppression of established puerperal lactation, a dose schedule of 0.25mg twice daily for 2 days has been suggested as the most appropriate for this indication.

Tolerability

Major congenital abnormalities have been reported in 3 of 199 (1.5%) evaluable cabergoline-associated pregnancies, with minor abnormalities occurring in a further 7 (3.5%). There was no pattern to these abnormalities and the incidence is consistent with those seen in both the general population and in bromocriptine-associated pregnancies. Although the number of drug exposures in utero is still relatively small, the incidence of spontaneous abortion (11.6%) does not appear to be any greater than that observed in the general population (11%).

The adverse events noted with cabergoline are characteristic of the dopaminergic ergot derivatives. The most commonly reported include nausea/vomiting (≤35%), headache/migraine (≤30%) and dizziness/vertigo (≤25%). Measurable falls in blood pressure occur in up to 50% of patients taking cabergoline but are rarely symptomatic. Overall, cabergoline appears to have a more favourable tolerability profile than bromocriptine, with adverse events occurring in up to 68% of patients with hyperprolactinaemia and 16% of puerperal women. The corresponding figures for bromocriptine are 78 and 25%, respectively.

Cabergoline appears to be well tolerated by most patients intolerant of other dopaminergic ergot derivatives, including bromocriptine.

Dosage and Administration

The recommended dosage of cabergoline in patients with hyperprolactinaemic disorders is 0.5 to 1.0mg twice weekly. An initial dosage of 0.25mg twice weekly is suggested, increasing in increments of 0.5 mg/week until a therapeutic response is seen. The majority of patients find that a twice weekly dosage schedule optimises tolerability.

In the prevention of puerperal lactation, a single dose of cabergoline 1.0mg is recommended. The drug should be taken as soon as possible, and preferably within the first 24 hours after parturition, to maximise response. A dose of 0.25mg twice daily for 2 days is suggested for the suppression of established puerperal lactation. This regimen has been found to be effective while maximising tolerability.

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  1. Adis International Limited, 41 Centorian Drive, Private Bag 65901, Mairangi Bay, Auckland 10, New Zealand

    Christopher P. Rains, Harriet M. Bryson & Andrew Fitton

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Various sections of the manuscript reviewed by: J.S. Bevan, Department of Endocrinology, Aberdeen Royal Infirmary, Aberdeen, Scotland; B.M.K. Billet, Neuroendocrine Unit, Massachusetts General Hospital, Boston, Massachusetts, USA; A. Caballero-Gordo, Departmento de Obstetricia y Ginecologia, Hospital Gregorio Marañón, Doctor Esquerdo, Madrid, Spain; P.G. Crosignani, Clinica Ostetrica e Ginecologica, Facoltà di Medicina, Université degli Studi di Milano, Milan, Italy; C. Ferrari, Endocrine Unit, Fatebenefratelli Hospital, Milan, Italy; A. Grossman, Department of Endocrinology, St Bartholomew’s Hospital, London, England; A. Levy, University of Bristol, Department of Medicine, Bristol Royal Infirmary, Bristol, England; P.A. Marken, Division of Pharmacy Practice, School of Pharmacy, University of Missouri-Kansas City, Kansas City, Missouri, USA; A.E. Pontiroli, Università degli Studi di Milano, Istituto Scientifico San Raffaele, Milan, Italy; S.M. Shalet, Department of Clinical Endocrinology, Christie Hospital NHS Trust, Manchester, England; G. Weir, Section of Islet Transplantation and Cell Biology, Joslin Diabetes Center, Boston, Massachusetts, USA; J. Webster, Department of Medicine, University of Wales College of Medicine, Cardiff, Wales.

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Rains, C.P., Bryson, H.M. & Fitton, A. Cabergoline. Drugs 49, 255–279 (1995). https://doi.org/10.2165/00003495-199549020-00009

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