Endocrine Abstracts

Background: The introduction of somatostatin analogues for the treatment of acromegaly has relegated dopamine agonists, once a mainstay of treatment, down the therapeutic ladder. Dopamine agonists are, however, added to somatostatin analogues to control active disease in some patients, in an attempt to achieve biochemical control. There are no reports, however, assessing this practise.

Aim: To assess the effectiveness of adding dopamine agonist therapy to somatostatin analogues in the biochemical control of acromegaly.

Patients: 140 patients are registered on the Sheffield Acromegaly Register. A total of 107 cases were reviewed. Of these patients 24/107 (22%) did not require medical treatment following pituitary surgery alone; 15/107 (14%) had safe GH levels following surgery and radiotherapy; and 52/107 (49%) required medical treatment despite having had surgery, radiotherapy or both. The remaining 16/107 (15%) of patients received only medical treatment.

Methods: In 8 patients a dopamine agonist was added to a somatostatin analogue to control active disease: 5 received bromocriptine, 3 cabergoline. All had previously had both transsphenoidal surgery and radiotherapy. GH day curves and IGF-1 levels were compared before and after the addition of a dopamine agonist to existing somatostatin analogue treatment. All had been on stable maximum dose treatment with a somatostatin analogue, with inadequate biochemical control prior to addition of dopamine agonist therapy. Mean duration of treatment on a dopamine agonist before biochemical assessments were made was 5.6 months.

Results:. All patients exhibited a fall in mean GH levels. Introduction of a dopamine agonist resulted in a 41.8% reduction in mean GH levels on a GH day curve (p=0.018) and a 33.6% reduction in IGF-1 levels (p=0.028).

Conclusion: Addition of dopamine agonists to somatostatin analogues is of benefit in the biochemical control of acromegaly and should be considered in those inadequate controlled.