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
Medical treatment for hyperprolactinemia is based upon use
of dopamine agonists (DA): bromocriptine (Parlodel®), lisuride
(Dopergine®), quinagolide (Norprolac®) and cabergoline
(Dostinex®).
In more than 80% of cases, these drugs induce normal
serum prolactin levels and ovulatory cycles [9,23,33,39].
Once normal prolactin levels have been achieved (particularly
where these are very low), the tendency is to reduce the dosage
(or the rate of administration for cabergoline) in order to obtain
the lowest dose consistent with normal prolactin levels to be
maintained [39].
In 5–10% of cases, resistance to bromocriptine requires use
of an alternative DA (with varying success rates regarding nor-
malization of serum prolactin). Many patients resistant to bro-
mocriptine are sensitive to quinagolide and particularly to
cabergoline [2,5–7,13,15,17,34,38,43,44]. Normalization of
PRL can take a number of months or years under cabergoline
in patients with “resistant” adenomas; in some patients with
macroprolactinoma, dissociation of therapeutic effect may
occur, with significant reduction in tumor size despite poor
laboratory results. In such cases, the minimum aim of treatment
is to achieve normal cycles (and stabilization of tumor size),
irrespective of PRL. Where no DA are effective, surgery may
be contemplated; even if normal prolactin levels are not
achieved (as seen especially in macroadenoma and/or invasive
adenoma), this approach can nevertheless reduce tumor size
and serum prolactin levels. A DA may subsequently be reintro-
duced in the hope of achieving satisfactory therapeutic objec-
tives starting from a lower post-surgical prolactin level.
Tolerability of DA is occasionally poor (e.g. faintness, nau-
sea, orthostatic hypotension), particularly with bromocriptine,
which appears less well-tolerated than quinagolide, which is
itself less well-tolerated than cabergoline [5–7,13,15,17,34,38,
43,44]. Where gastrointestinal intolerance occurs with a given
DA, another should be tried, starting at a low dose and gradu-
ally up-titrating until normal prolactin levels are achieved. If
the doses required to ensure normal PRL are poorly tolerated,
the dosage may be reduced with the objective of achieving
normal cycles, regardless of PRL level.
2. What neuroradiological follow-up is required with drug
therapy?
Neuroradiological follow-up must obviously allow for spe-
cific situations. Experience has nevertheless shown that
changes in tumor size are generally so gradual (usually taking
several months, but in rare cases more than 2 years), that the
vast majority of microadenomas do not progress beyond micro-
adenomas (particularly if treated using DA) and that once
achieved, tumor size reductions remain stable, especially if
DA therapy is continued. Neuroradiological follow-up must
thus allow for all of the above factors.
Thus, for macroprolactinoma an initial MRI may be per-
formed after 3 months of treatment, then after 1 year of treat-
ment, yearly for 5 years, and then once every 5 years where
stable tumor size is achieved (provided PRL is controlled
annually).
For microprolactinoma, most experts regard control during
treatment as pointless, with very few recommending initial
MRI after 1 year then 5-yearly.
3. If treatment with cabergoline is better tolerated
and more effective than the other DA, why not prescribe it
as first-line therapy?
Everything effectively seems to point towards prescription
of cabergoline as first-line therapy in hyperprolactinemia.
However, first-line use of this drug is debated on account of
the following two factors: treatment costs (a mean daily dose of
5 mg of bromocriptine costs around €15–18 per month, a mean
daily dose of 75 μg of quinagolide costs around €30 per month
and a weekly dose of 0.5 mg of cabergoline costs €21 per
month) and a wish by patients to become pregnant in the
short term, which requires crossover to bromocriptine for the
sake of safety, due to lack of adequate epidemiological data
concerning the absence of teratogenic effects of cabergoline.
4. Can treatment with DA be discontinued or must it be
continued for life?
There are no arguments suggesting any drawbacks of long-
term DA therapy (bromocriptine has been prescribed since the
1970s and many women have been on this treatment for more
than 20 years).
However, the current tendency is to attempt withdrawal of
treatment in patients showing long-term (several years) normal-
ization of prolactin levels, particularly in the light of our
experience with cabergoline treatment. After prolonged treat-
ment with bromocriptine, withdrawal results in an increase in
PRL and return of hyperprolactinemia symptoms in only
around 20–30% of patients [26,36], although after prolonged
treatment with cabergoline, this reversal is seen in around
two-thirds of patients [11]. Persistence of residual adenoma
under treatment constitutes a risk factor for post-withdrawal
 P. Chanson et al. / Annales d’Endocrinologie 68 (2007) 113–117
relapse [11]. It is therefore reasonable to suspend DA treatment
from time to time (once every 2 years?) in order to check
whether the patient still needs it. However, attention is required
where long-term treatment with cabergoline has been pre-
scribed due to the extremely long half-life of the drug, since
prolactin levels can sometimes take months or even years to
increase again: extremely long-term (several years) monitoring
of PRL is therefore essential before concluding on definitive
cure of prolactinoma through drug treatment.
Where normal prolactin levels have been achieved (and
where reduction in macroadenoma size is stable), another solu-
tion to determine whether attempts to withdraw treatment are
warranted consists in gradually reducing the dosage of DA in
steps (6 monthly? yearly?) in order to achieve the lowest effec-
tive dose ensuring normal PRL levels and maintenance of
stable adenoma size [9,12,39].
5. What should be done about drug-induced
hyperprolactinemia symptoms?
The presence of hyperprolactinemia in patients on neurolep-
tics is not necessarily synonymous with clinical signs: in most
cases, hyperprolactinemia seen in women on neuroleptics is
without consequence [28,40] and the question of therapeutic
intervention should be considered more for secondary symp-
toms of hyperprolactinemia (oligomenorrhea or amenorrhea,
vaginal dryness, sexual dysfunction or osteoporosis).
In the event of such symptoms, rather than prescribing a DA
(which is generally ineffective), it makes more sense to with-
draw the causative medication. However, this may on occasion
be difficult or even dangerous, particularly in psychotic
patients being treated with neuroleptics (thankfully new-
generation or “atypical” neuroleptics appear to be associated
with less hyperprolactinemia than conventional neuroleptics
[16,32,46]).
In this case, DA may be tried, but unfortunately they are
generally ineffective [37] and can result in risk of psychiatric
decompensation. Routine verification should be performed by
C-T scan or MRI to rule out associated pituitary adenoma, with
potential amplification of PRL hypersecretion, although this
condition may be cured by straightforward surgery (however,
prolactin levels are not necessarily a reliable indicator since
serum prolactin levels of up to 400 ng/ml have been seen in
patients on neuroleptics [37]). If treatment with a DA is
initiated, the therapeutic goal in these patients is not normal-
ization of PRL at all costs but rather restoration of spontaneous
cycles (or induction of cycles by progestin prescribed for a
period of 10 days each month), which indicate satisfactory
estrogen impregnation.
If this cannot be achieved (particularly since contraception
may be essential), it is often necessary, particularly in women
with amenorrhea due to estrogen deficiency at risk of develop-
ing early osteoporosis, to initiate estrogen–progestin replace-
ment therapy or contraceptives (although this approach does
not resolve galactorrhea, where present) or to suggest that the
psychiatrist replace the patient’s current neuroleptic with an
atypical neuroleptic known to be less hyperprolactinemic.
115
6. While there is some uncertainty concerning the value
of drug therapy as first-line treatment
in microprolactinoma because of the good results obtained
with surgery (cure rate of 85%), there is no doubt in cases
of macroprolactinoma with prolactin tumors (generally
with prolactin levels well above 150–200 ng/ml)
In effect, in these macroprolactinomas, surgical results are
frequently disappointing (with postoperative persistence of
hyperprolactinemia in more than 60% of cases, since complete
tumor excision is rarely achieved) [9,21,33]. Above all, treat-
ment with DA results not only in normalization of serum pro-
lactin levels but in some 70% cases, dramatic tumoral shrink-
age is frequently seen (with rapid resolution of visual problems
caused by tumoral compression of the optic chiasm) [4,9,33]. If
prolactinoma is discovered in children or prepubertal adoles-
cents, in most cases, first-line drug therapy restores gonadotro-
pic function thanks to normalization of serum prolactin levels,
leading to satisfactory pubertal development [8,14].
7. In cases of macroprolactinoma under drug treatment
with DA, should high doses be used from the outset or do
low doses have the same effect?
There is as yet no data supporting the unequivocal recom-
mendation of either approach. However, gradually increasing
dose after initiation of treatment ensures better compliance by
limiting the initial side-effects.
8. Can initial treatment with DA decrease the outcome
of subsequent surgical treatment?
After an initial sensational article describing surgical diffi-
culties following initial therapy with DA [29] resulting in a
lower success rate for surgery, as well as studies demonstrating
fibrous remodeling of adenomas on histopathological examina-
tion [30], the idea has taken root that prior treatment with DA
should not be initiated where surgery is envisaged. In fact, a
number of controlled prospective studies in which surgeons
were unaware whether their patients had previously received
DA demonstrated no effect of previous medical treatment
either on the “fibrous” nature of adenomas or on the success
rate of surgery in the event of microprolactinoma [3,19,20,25,
45]. At most, it may be more difficult for surgeons during
operations to distinguish adenomas whose images have disap-
peared from MRI scans following prior treatment with DA. In
the case of macroadenoma, treatment with bromocriptine, if
given for more than 6–12 weeks, can result in development
of fibrosis in some patients, thereby limiting the quality of
excision [3,19,20,25,45], but surgical treatment for macropro-
lactinoma is very rarely adopted these days.
9. Should microprolactinoma be treated after
the menopause?
Treatment with DA may be discontinued after menopause in
microprolactinoma for two reasons: 1) there is no evidence of
harmful effects of hyperprolactinemia on the health other than
116 P. Chanson et al. / Annales d’Endocrinologie 68 (2007) 113–117
on gonadotropic function (and thus on ovarian function with
problems of infertility and estrogen deficiency and which are
therefore only relevant during the childbearing years). In parti-
cular, there are no convincing epidemiological arguments in
favor of an association between hyperprolactinemia and breast
cancer. The majority of studies have found either no associa-
tion, or at most a non-significant positive association, between
post-menopausal breast cancer and serum prolactin [10]. Only
one recent study reports an association with borderline signifi-
cance [41]. Post-menopausal hyperprolactinemia thus appears
not to expose patients to risk of breast cancer. 2) The second
reason is the spontaneous gradual normalization commonly
seen in PRL levels after menopause (44% of cases in one
study [27]). Hormone replacement therapy for menopause is
not contraindicated. Treatment can be resumed in the event of
troublesome galactorrhea.
10. Are there any indications for drug treatment
of macroprolactinemia?
In principle, macroprolactinemia should not be treated with
DA if it is asymptomatic (in other words, if it is discovered by
chance and the patient has no menstrual disorders or galactor-
rhea) or if the menstrual disorders are due to another cause [22,
31,42], such as polycystic ovarian disease, the high prevalence
of which among the general population is well known [1,18],
since drug treatment is effective in such cases and can even
delay investigation for other causes of gonadic or sexual dis-
orders, or lead to infertility [24].
However, authentic prolactinomas are accompanied by
authentic hyperprolactinemia as well as macroprolactinemia
[35]. In this event, treatment should naturally not be stopped
on discovery of macroprolactinemia but drugs should be given
as for all cases of hyperprolactinemia: return of normal cycles
and/or normal fertility provides practical evidence of the role
played by hyperprolactinemia in the patient’s presenting symp-
toms.
French version
A French version of this article is available at doi:
10.1016/j.ando.2007.03.004.
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