TREATMENT OF PROLACTINOMAS

Citation
A. Colao et al., TREATMENT OF PROLACTINOMAS, Annals of medicine, 30(5), 1998, pp. 452-459
Citations number
77
Categorie Soggetti
Medicine, General & Internal
Journal title
ISSN journal
07853890
Volume
30
Issue
5
Year of publication
1998
Pages
452 - 459
Database
ISI
SICI code
0785-3890(1998)30:5<452:>2.0.ZU;2-T
Abstract
The objectives of the treatment of hyperprolactinaemia are to suppress excessive hormone secretion and its clinical consequences, to remove tumour mass, to preserve the residual pituitary function and to preven t disease recurrence or progression. Prior to the advent of pharmacoth erapy, therapy usually consisted of surgical resection and/or pituitar y irradiation. In microprolactinomas, trans-sphenoidal surgical resect ion normalizes prolactin (PRL) levels, restores normal menses and prod uces the disappearance of galactorrhoea in a great majority of patient s, but normalization of serum PRL levels varies from 35-70%. In macrop rolactinomas, trans-sphenoidal surgery is less successful with only 32 % of patients appearing to be cured initially. However, the recurrence rate is 19%, and the long-term cure rate is only 26%. In more than 80 % of the patients with microprolactinoma, suppression of PRL levels an d tumour shrinkage can be achieved with bromocriptine therapy given at doses of 2.5-5 mg per day. In 5-10% of the patients, the appearance o f side-effects (nausea, dizziness and postural hypotension) is a limit ing factor in continuing the treatment. Dopaminergic compounds cause n otable tumour shrinkage in most macroprolactinomas. Treatment with cab ergoline, a selective and long-lasting dopamine 2-receptor agonist at weekly doses of 0.5-2 mg has been shown to be effective both in normal izing PRL levels and in inducing tumour shrinkage. Pharmacotherapy wit h dopamine (DA) agonists is an appropriate first-line treatment for bo th micro- and macroprolactinomas. Surgery should be recommended for th ose patients who are severely intolerant of or resistant to DA agonist s.