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Annales d’Endocrinologie 68 (2007) 113–117

Original article

Drug treatment of hyperprolactinemia


Traitement médical de l’hyperprolactinemie
P. Chanson*, F. Borson-Chazot, O. Chabre, B. Estour
Service d’endocrinologie et des maladies de la reproduction, hôpital de Bicêtre, 78, rue du Général-Leclerc, 94275 Le Kremlin-Bicêtre, France
Available online 29 May 2007

Résumé
Le traitement médical de l’hyperprolactinémie fait appel aux agonistes dopaminergiques (DA) : bromocriptine, lisuride, quinagolide, caber-
goline. Dans plus de 80 % des cas, une prolactinémie normale et des cycles ovulatoires sont obtenus sous DA. En cas de résistance, il faut
changer de DA. La tolérance est parfois médiocre, en particulier avec la bromocriptine qui semble moins bien tolérée que le quinagolide et
surtout la cabergoline. En cas d’intolérance à un DA, il ne faut pas hésiter à changer d’agoniste. Sous DA, en cas de macroprolactinome, la
surveillance IRM sera faite après trois mois de traitement pour vérifier la diminution tumorale puis après un an, puis tous les ans pendant cinq ans
et une fois tous les cinq ans lorsque le volume de l’adénome est stable. En cas de microprolactinome, un contrôle est inutile sous traitement. Une
IRM peut être faite après un an puis cinq ans. Une fois la normalisation de la prolactine obtenue, on peut essayer d’arrêter le traitement. En effet,
lorsque le traitement, en particulier par cabergoline, a été prolongé, la réascension de la prolactinémie et le retour des symptômes de l’hyper-
prolactinémie ne sont observés que dans 20 à 30 % des cas environ, surtout s’il existe un résidu adénomateux après traitement prolongé. Il faudra
néanmoins poursuivre la surveillance de la prolactinémie, voire de l’IRM, après l’arrêt du DA car il faut parfois plusieurs mois ou années pour
que la prolactinémie remonte. Une autre solution consiste, lorsqu’une prolactinémie normale a été obtenue sous DA, de diminuer par paliers la
posologie du DA ou sa fréquence d’administration jusqu’à la moindre dose efficace permettant le maintien d’une prolactinémie normale et d’un
volume adénomateux stable. En cas d’hyperprolactinémie médicamenteuse, s’il est impossible d’interrompre le médicament responsable, il est
souvent inutile, voire dangereux de donner un DA. Il faut donc vérifier l’absence d’adénome hypophysaire et, si nécessaire, donner un traitement
par stéroïde sexuel de façon à assurer une imprégnation en stéroïde sexuel satisfaisante et éviter une ostéoporose. En cas de macroprolactinome,
le traitement de première intention est le traitement médicamenteux par les DA. Actuellement, il n’existe pas d’argument pour penser qu’un
traitement préalable par les DA avant la chirurgie modifie les résultats du geste chirurgical. En cas de microprolactinome, le traitement médica-
menteux par les DA constitue une bonne option thérapeutique en première intention mais la chirurgie est aussi possible. On peut interrompre le
traitement DA après la ménopause en cas de microprolactinome.
© 2007 Elsevier Masson SAS. All rights reserved.
Abstract
Medical treatment of hyperprolactinemia is based upon use of dopamine agonists (DA): bromocriptine, lisuride, quinagolide and cabergoline.
In over 80% of cases, these drugs induce normal prolactinemia and ovulatory cycles. In resistant cases, the DA should be changed. Tolerance
may occasionally be poor, particularly with bromocriptine, which appears less well-tolerated than quinagolide and than cabergoline above all. In
the event of intolerance to a given DA, another should be tried. In patients with macroprolactinoma treated with DA, MRI monitoring should be
carried out after 3 months of treatment to verify tumor size reduction, then after 1 year, yearly for the next 5 years and once every 5 years if
adenoma size is stable. In cases of microprolactinoma, control under treatment is pointless. MRI may be performed after 1 year and then after
5 years. Once normal prolactin levels have been achieved, attempts may be made to stop the treatment. When a prolonged treatment is inter-
rupted, especially with cabergoline, progressive increase in serum prolactin and return of hyperprolactinemia symptoms are seen in only around
20–30% of cases, particularly when residual adenoma exists after prolonged treatment. Nevertheless, prolactin levels should continue to be
monitored after discontinuation of DA, possibly with MRI monitoring, since prolactin levels may rise again after a number of months or
years. When normal prolactin levels have been achieved with DA, another solution consists in reducing the dose or dosing frequency of DA
in steps to the lowest effective dose consistent with maintenance of normal prolactin levels and stable adenoma size. For drug-induced hyper-
prolactinemia, where the causative medication cannot be withdrawn, it is often pointless and possibly even dangerous to administer a DA. It is

* Correspondingauthor.
E-mail address: philippe.chanson@bct.ap-hop-paris.fr (P. Chanson).

0003-4266/$ - see front matter © 2007 Elsevier Masson SAS. All rights reserved.
doi:10.1016/j.ando.2007.03.003
114 P. Chanson et al. / Annales d’Endocrinologie 68 (2007) 113–117

therefore necessary to check for absence of pituitary adenoma and where necessary, begin treatment with sex steroids so as to ensure satisfactory
impregnation with sex steroids and avoid osteoporosis. For macroprolactinoma, the first-line treatment is drug therapy with DA. At present, there
is no evidence to suggest that prior treatment with DA can modify the outcome of surgery. With microprolactinoma, DA treatment offers a good
first-line therapeutic option but surgery may also be useful. DAs for microprolactinoma may be withdrawn after menopause.
© 2007 Elsevier Masson SAS. All rights reserved.

Mots clés : Hyperprolactinémie ; Adénome ; Traitement ; Agonistes dopaminergiques

Keywords: Hyperprolactinemia; Adenoma; Treatment; Dopaminergic agonists

1. Introduction several months, but in rare cases more than 2 years), that the
vast majority of microadenomas do not progress beyond micro-
Medical treatment for hyperprolactinemia is based upon use adenomas (particularly if treated using DA) and that once
of dopamine agonists (DA): bromocriptine (Parlodel®), lisuride achieved, tumor size reductions remain stable, especially if
(Dopergine®), quinagolide (Norprolac®) and cabergoline DA therapy is continued. Neuroradiological follow-up must
(Dostinex®). thus allow for all of the above factors.
In more than 80% of cases, these drugs induce normal Thus, for macroprolactinoma an initial MRI may be per-
serum prolactin levels and ovulatory cycles [9,23,33,39]. formed after 3 months of treatment, then after 1 year of treat-
Once normal prolactin levels have been achieved (particularly ment, yearly for 5 years, and then once every 5 years where
where these are very low), the tendency is to reduce the dosage stable tumor size is achieved (provided PRL is controlled
(or the rate of administration for cabergoline) in order to obtain annually).
the lowest dose consistent with normal prolactin levels to be For microprolactinoma, most experts regard control during
maintained [39]. treatment as pointless, with very few recommending initial
In 5–10% of cases, resistance to bromocriptine requires use MRI after 1 year then 5-yearly.
of an alternative DA (with varying success rates regarding nor-
malization of serum prolactin). Many patients resistant to bro- 3. If treatment with cabergoline is better tolerated
mocriptine are sensitive to quinagolide and particularly to and more effective than the other DA, why not prescribe it
cabergoline [2,5–7,13,15,17,34,38,43,44]. Normalization of as first-line therapy?
PRL can take a number of months or years under cabergoline
in patients with “resistant” adenomas; in some patients with Everything effectively seems to point towards prescription
macroprolactinoma, dissociation of therapeutic effect may of cabergoline as first-line therapy in hyperprolactinemia.
occur, with significant reduction in tumor size despite poor However, first-line use of this drug is debated on account of
laboratory results. In such cases, the minimum aim of treatment the following two factors: treatment costs (a mean daily dose of
is to achieve normal cycles (and stabilization of tumor size), 5 mg of bromocriptine costs around €15–18 per month, a mean
irrespective of PRL. Where no DA are effective, surgery may daily dose of 75 μg of quinagolide costs around €30 per month
be contemplated; even if normal prolactin levels are not and a weekly dose of 0.5 mg of cabergoline costs €21 per
achieved (as seen especially in macroadenoma and/or invasive month) and a wish by patients to become pregnant in the
adenoma), this approach can nevertheless reduce tumor size short term, which requires crossover to bromocriptine for the
and serum prolactin levels. A DA may subsequently be reintro- sake of safety, due to lack of adequate epidemiological data
duced in the hope of achieving satisfactory therapeutic objec- concerning the absence of teratogenic effects of cabergoline.
tives starting from a lower post-surgical prolactin level.
Tolerability of DA is occasionally poor (e.g. faintness, nau- 4. Can treatment with DA be discontinued or must it be
sea, orthostatic hypotension), particularly with bromocriptine, continued for life?
which appears less well-tolerated than quinagolide, which is
itself less well-tolerated than cabergoline [5–7,13,15,17,34,38, There are no arguments suggesting any drawbacks of long-
43,44]. Where gastrointestinal intolerance occurs with a given term DA therapy (bromocriptine has been prescribed since the
DA, another should be tried, starting at a low dose and gradu- 1970s and many women have been on this treatment for more
ally up-titrating until normal prolactin levels are achieved. If than 20 years).
the doses required to ensure normal PRL are poorly tolerated, However, the current tendency is to attempt withdrawal of
the dosage may be reduced with the objective of achieving treatment in patients showing long-term (several years) normal-
normal cycles, regardless of PRL level. ization of prolactin levels, particularly in the light of our
experience with cabergoline treatment. After prolonged treat-
2. What neuroradiological follow-up is required with drug ment with bromocriptine, withdrawal results in an increase in
therapy? PRL and return of hyperprolactinemia symptoms in only
around 20–30% of patients [26,36], although after prolonged
Neuroradiological follow-up must obviously allow for spe- treatment with cabergoline, this reversal is seen in around
cific situations. Experience has nevertheless shown that two-thirds of patients [11]. Persistence of residual adenoma
changes in tumor size are generally so gradual (usually taking under treatment constitutes a risk factor for post-withdrawal
P. Chanson et al. / Annales d’Endocrinologie 68 (2007) 113–117 115

relapse [11]. It is therefore reasonable to suspend DA treatment 6. While there is some uncertainty concerning the value
from time to time (once every 2 years?) in order to check of drug therapy as first-line treatment
whether the patient still needs it. However, attention is required in microprolactinoma because of the good results obtained
where long-term treatment with cabergoline has been pre- with surgery (cure rate of 85%), there is no doubt in cases
scribed due to the extremely long half-life of the drug, since of macroprolactinoma with prolactin tumors (generally
prolactin levels can sometimes take months or even years to with prolactin levels well above 150–200 ng/ml)
increase again: extremely long-term (several years) monitoring
of PRL is therefore essential before concluding on definitive In effect, in these macroprolactinomas, surgical results are
cure of prolactinoma through drug treatment. frequently disappointing (with postoperative persistence of
Where normal prolactin levels have been achieved (and hyperprolactinemia in more than 60% of cases, since complete
where reduction in macroadenoma size is stable), another solu- tumor excision is rarely achieved) [9,21,33]. Above all, treat-
tion to determine whether attempts to withdraw treatment are ment with DA results not only in normalization of serum pro-
warranted consists in gradually reducing the dosage of DA in lactin levels but in some 70% cases, dramatic tumoral shrink-
steps (6 monthly? yearly?) in order to achieve the lowest effec- age is frequently seen (with rapid resolution of visual problems
tive dose ensuring normal PRL levels and maintenance of caused by tumoral compression of the optic chiasm) [4,9,33]. If
stable adenoma size [9,12,39]. prolactinoma is discovered in children or prepubertal adoles-
cents, in most cases, first-line drug therapy restores gonadotro-
5. What should be done about drug-induced pic function thanks to normalization of serum prolactin levels,
hyperprolactinemia symptoms? leading to satisfactory pubertal development [8,14].

The presence of hyperprolactinemia in patients on neurolep- 7. In cases of macroprolactinoma under drug treatment
tics is not necessarily synonymous with clinical signs: in most with DA, should high doses be used from the outset or do
cases, hyperprolactinemia seen in women on neuroleptics is low doses have the same effect?
without consequence [28,40] and the question of therapeutic
intervention should be considered more for secondary symp- There is as yet no data supporting the unequivocal recom-
toms of hyperprolactinemia (oligomenorrhea or amenorrhea, mendation of either approach. However, gradually increasing
vaginal dryness, sexual dysfunction or osteoporosis). dose after initiation of treatment ensures better compliance by
In the event of such symptoms, rather than prescribing a DA limiting the initial side-effects.
(which is generally ineffective), it makes more sense to with-
8. Can initial treatment with DA decrease the outcome
draw the causative medication. However, this may on occasion
of subsequent surgical treatment?
be difficult or even dangerous, particularly in psychotic
patients being treated with neuroleptics (thankfully new- After an initial sensational article describing surgical diffi-
generation or “atypical” neuroleptics appear to be associated culties following initial therapy with DA [29] resulting in a
with less hyperprolactinemia than conventional neuroleptics lower success rate for surgery, as well as studies demonstrating
[16,32,46]). fibrous remodeling of adenomas on histopathological examina-
In this case, DA may be tried, but unfortunately they are tion [30], the idea has taken root that prior treatment with DA
generally ineffective [37] and can result in risk of psychiatric should not be initiated where surgery is envisaged. In fact, a
decompensation. Routine verification should be performed by number of controlled prospective studies in which surgeons
C-T scan or MRI to rule out associated pituitary adenoma, with were unaware whether their patients had previously received
potential amplification of PRL hypersecretion, although this DA demonstrated no effect of previous medical treatment
condition may be cured by straightforward surgery (however, either on the “fibrous” nature of adenomas or on the success
prolactin levels are not necessarily a reliable indicator since rate of surgery in the event of microprolactinoma [3,19,20,25,
serum prolactin levels of up to 400 ng/ml have been seen in 45]. At most, it may be more difficult for surgeons during
patients on neuroleptics [37]). If treatment with a DA is operations to distinguish adenomas whose images have disap-
initiated, the therapeutic goal in these patients is not normal- peared from MRI scans following prior treatment with DA. In
ization of PRL at all costs but rather restoration of spontaneous the case of macroadenoma, treatment with bromocriptine, if
cycles (or induction of cycles by progestin prescribed for a given for more than 6–12 weeks, can result in development
period of 10 days each month), which indicate satisfactory of fibrosis in some patients, thereby limiting the quality of
estrogen impregnation. excision [3,19,20,25,45], but surgical treatment for macropro-
If this cannot be achieved (particularly since contraception lactinoma is very rarely adopted these days.
may be essential), it is often necessary, particularly in women
with amenorrhea due to estrogen deficiency at risk of develop- 9. Should microprolactinoma be treated after
ing early osteoporosis, to initiate estrogen–progestin replace- the menopause?
ment therapy or contraceptives (although this approach does
not resolve galactorrhea, where present) or to suggest that the Treatment with DA may be discontinued after menopause in
psychiatrist replace the patient’s current neuroleptic with an microprolactinoma for two reasons: 1) there is no evidence of
atypical neuroleptic known to be less hyperprolactinemic. harmful effects of hyperprolactinemia on the health other than
116 P. Chanson et al. / Annales d’Endocrinologie 68 (2007) 113–117

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