NLM CIT. ID: No Cit. ID assigned
TITLE: Hormone levels and tumour size response to quinagolide and cabergoline
in patients with prolactin-secreting and clinically non-functioning
pituitary adenomas: predictive value of pituitary scintigraphy with
123I-methoxybenzamide.
AUTHORS: Colao A; Ferone D; Lastoria S; Cerbone G; Di Sarno A
Di Somma C; Lucci R; Lombardi G
AUTHOR AFFILIATION:
Departments of Molecular & Clinical Endocrinology and Oncology,
'Federico II' University of Naples; Nuclear Medicine, National Cancer
Institute, 'Fondazione G. Pascale', Naples, Italy.
PUBLICATION TYPES:
JOURNAL ARTICLE
LANGUAGES:
ENG
ABSTRACT:
BACKGROUND: Dopamine agonists are indicated as primary therapy for
PRL-secreting pituitary adenomas, while controversial results have
been reported in nonfunctioning adenomas (NFA). OBJECTIVE: To
evaluate whether the in vivo visualization of dopamine D2 receptor
expression detected by pituitary scintigraphy using
123I-methoxybenzamide (123I-IBZM) was correlated with the response to
chronic treatment with quinagolide or cabergoline. PATIENTS: 10
patients affected with NFA (5 men and 5 women, age ranging between 25
and 50 years), and 10 with PRL-secreting naive macroadenomas (3 men
and 7 women, age ranging between 22 and 59 years), serving as
control. STUDY DESIGN: All patients underwent an acute test with
quinagolide: at 3-day intervals and in random order all patients
received the drug (0.075 mg at 0800 h), or placebo. Blood samples
were taken 15 and 5 minutes before and every 30 minutes for 6 h after
drug or placebo administration. The test was considered positive when
PRL and/or alpha-subunit levels decreased >/=50% as compared to
baseline levels. After 6 months of treatment, 10 patients were
randomised to continue the treatment with quinagolide and the
remaining 10 received cabergoline for the remaining 6 months. The
doses of quinagolide and cabergoline ranged from 0.075 to 0.6 mg/day
and from 0.5 to 3 mg/week, respectively. At study entry, a magnetic
resonance imaging (MR) study of the pituitary region and 123I-IBZM
pituitary scintigraphy were performed. MR was repeated after 12
months of treatment to evaluate tumour shrinkage: reduction of tumour
volume = 80% in prolactinomas and = 50% in NFA was considered
significant. Basal PRL levels were 9495.0 +/- 1131.6 mU/l in
prolactinomas and 602.4 +/- 50.5 mU/l in NFA. RESULTS: The
scintigraphy was negative in 6 out of 10 patients with NFA. Moderate
uptake was observed in 3 patients with prolactinoma and 2 patients
with NFA whereas intense uptake was observed in the remaining 7
patients with prolactinoma and 2 patients with NFA. Among the 8
patients with NFA and high circulating alpha-subunit levels, the
acute test was negative in 5 while it was positive in the remaining 3
patients. The acute test was positive in all 10 patients with
prolactinoma. After 12 months of treatment with quinagolide and
cabergoline, circulating PRL levels were decreased in all 10 patients
with prolactinoma (571.8 +/- 255.9 mU/l), being normalized in 7
patients. Suppression of PRL levels was found in all 10 patients with
NFA (89.5 +/- 2.3 mU/l). A significant reduction of alpha-subunit
levels was obtained in 9 out of 10 patients with NFA: in 4 out of 8
patients alpha-subunit levels were normalized. Significant adenoma
shrinkage was recorded in 4 patients with prolactinoma among the 7
with intense pituitary uptake of 123I-IBZM. Significant adenoma
shrinkage was recorded only in the 2 out of 10 patients with NFA with
intense pituitary uptake of 123I-IBZM. A significant positive
correlation was found between the degree of uptake (considered as
score) and the response to quinagolide or cabergoline treatment
(considered as percent hormone suppression) either in patients
affected with PRL-secreting adenoma (r = 0.856, P < 0.005) or in
those affected with NFA (r = 0.787, P < 0.05). CONCLUSIONS: An
intense 123I-IBZM uptake in patients with non-functioning adenomas
was predictive of a good response to a chronic treatment with
quinagolide and cabergoline. This result suggests that a pituitary
123I-IBZM scintigraphy could be considered in selected patients with
non-functioning adenomas before starting medical treatment with
dopamine agonists.
NLM PUBMED CIT. ID:
10762286
SOURCE: Clin Endocrinol (Oxf) 2000 Apr;52(4):437-445
[Record as supplied by publisher]
UI - 99439104
AU - Abe T; Ludecke DK
TI - Mucocele-like formation leading to neurological symptoms in
prolactin-secreting pituitary adenomas under dopamine agonist therapy.
SO - Surg Neurol 1999 Sep;52(3):274-9
AD - Department of Neurosurgery, Showa University School of Medicine,
Tokyo, Japan.
BACKGROUND: Mucocele-like formation associated with pituitary adenomas,
to the best of our knowledge, has been paid little attention. We report
three adult male patients with a mucocele-like formation that developed
behind the tumor and led to neurological symptoms in prolactin-secreting
pituitary adenomas (prolactinomas) under dopamine agonist therapy.
CLINICAL PRESENTATION: Three adult male patients with prolactinomas
developed hyperprolactinemia and new neurological symptoms during
dopamine agonist treatment. In each case, the pathogenesis of these
symptoms was due in part to a mass enlargement with development of a
mucocele-like formation behind a prolactinoma. In our patients, a
prolactinoma with a suprasellar extension originally filled the sphenoid
sinus. When dopamine agonist therapy became ineffective, new symptoms,
such as progressive visual impairment other than typical hemianopsia or
headache, developed and mass enlargement was found on MRI. MRI
demonstrated two different components: an enhancing prolactinoma and a
nonenhancing mucocele-like formation behind the tumor. Two patients had
compression of the optic nerves by a mass. Transnasal removal of
mucoceles and adenomas led to resolution of the neurological symptoms.
CONCLUSION: Early suspicion of a mucocele-like formation under dopamine
agonist therapy for prolactinomas is important in order to avoid a delay
in surgery, because a change in medical treatment will be ineffective.
UI - 97035518
AU - Chanson P
TI - [Medical treatment of pituitary adenoma]
SO - Rev Prat 1996;46(12):1509-13
AD - Service d'endocrinologie Centre hospitalier universitaire de Bicetre.
AB - Dopamine agonists are able to restore ovulatory cycles in 80-90% of
hyperprolactinemic patients and to reduce tumoral volume (often
dramatically) in 80% of macroprolactinomas. Their side-effects will
be reduced with the use of parenteral forms or new agonists currently
in preparation. Somatostatin analogues administered either subcutane-
ously by three daily injections (octreotide) or intramusculary with a
long-acting formulation every 10-15 days (lanreotide) are able to
"normalize" GH levels in 70% of acromegalic patients and to shrink
tumor in half of the patients. Side effects are generally minor but
an increased incidence of gallstones has been reported. These
somatostatin analogs are also very effective in the treatment of
TSH-secreting adenomas. Medical treatment of other pituitary adenomas
is much more disappointing.
UI - 96338538
AU - Ciccarelli E; Camanni F
TI - Diagnosis and drug therapy of prolactinoma.
SO - Drugs 1996;51(6):954-65
AD - Division of Endocrinology, University of Turin, Italy.
AB - A prolactin-secreting pituitary tumour is the most frequent cause of
hyperprolactinaemia that commonly occurs in clinical practice.
Prolactinomas occur more frequently in women than in men and may
differ in size, invasive growth and secretory activity. At presentat-
ion, macroadenomas are more frequently diagnosed in men. Specific
immunohistochemical stains are necessary to prove the presence of
prolactin in the tumour cells. The main investigations in the
diagnosis of a prolactin-secreting adenoma are hormonal and
radiological. As prolactin is a pulsatile hormone, it is a general
rule to obtain several blood samples by taking a single sample on 3
separate days or 3 sequential samples (every 30 minutes) in restful
conditions. Prolactin levels of 100 to 200 micrograms/L are commonly
considered diagnostic for the presence of a prolactinoma; however,
prolactinoma cannot be excluded in the presence of lower levels, and
prolactin levels > 100 micrograms/L are present in some patients with
idiopathic hyperprolactinaemia. Several dynamic function tests have
been proposed to differentiate idiopathic from tumorous hyperprolact-
inaemia. Although they could be used for group discrimination, these
tests cannot be used for individual patients. To differentiate
between a prolactinoma and a pseudoprolactinoma, thyrotrophin
response to a dopamine receptor antagonist may be used, as only
prolactinomas may have an increased response. A short course of
dopaminergic drugs may also be of some help, as in macroprolactinomas
only a shrinkage may be observed. After hyperprolactinaemia is
confirmed, imaging with computerised tomography (CT) and magnetic
resonance imaging (MRI) are necessary to define the presence of a
lesion compatible with a pituitary tumour. There is now a general
agreement that medical therapy is of first choice in patients with
prolactinomas. Bromocriptine, the most common drug used in this
condition, is a semisynthetic ergot alkaloid that directly stimulates
specific pituitary cell membrane dopamine D2 receptors and inhibits
prolactin synthesis and secretion. In most patients, a reduction or
normalisation of prolactin levels is usually observed, together with
the disappearance or improvement of clinical symptoms. The sensitivi-
ty to bromocriptine is variable and patients may need different dose
of the drug. Bromocriptine is also able to shrink the tumour in most
patients; however, a few reports of disease progression during
therapy have been described. The need for close follow-up, including
prolactin levels and CT or MRI studies, is therefore emphasised.
Bromocriptine is conventionally given in 2 or 3 daily doses; however,
a single evening dose has been shown to be equally effective.
Bromocriptine is usually well tolerated by the majority of patients;
some adverse effects (nausea, vomiting, postural hypotension) may be
initially present, but they usually wear off in time. To prevent such
adverse effects it is advisable to start treatment with a low dose
during the evening meal and gradually increase the dose over days or
weeks. A few patients are unable to tolerate oral bromocriptine, so
different formulations of bromocriptine or alternative dopamine
agonist drugs (lisuride, terguride, metergoline, dihydroergocryptine,
quinagolide, cabergoline, pergolide) have been proposed. Of
particular clinical relevance because of their good tolerability and
sustained activity are cabergoline and quinagolide. Particular
attention should be paid to pregnancy in prolactinoma patients, as
tumour enlargement has been reported. As the risk for this occurrence
is low in patients with microprolactinoma, there is a general
agreement that the drug can be stopped once pregnancy is diagnosed.
In patients with macroprolactinoma the risk of tumour enlargement is
higher. Therefore, primary therapy with bromocriptine until the
tumour has shrank is suggested before pregnancy is attempted.
Bromocriptine should be stopped as soon as pregnancy is confirmed,
but re (63 Refs)
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