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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