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Endocrine Abstracts (2015) 37 GP20.08 | DOI: 10.1530/endoabs.37.GP.20.08

ECE2015 Guided Posters Pituitary – Hypopituitarism (9 abstracts)

‘Pseudo-resistance' in macroprolactinomas treated with dopamine agonists; recognising delayed radiological response and a role for 11C-methionine PET-CT in guiding management

Andrew S Powlson 1 , Olympia Koulouri 1 , Andrea Steuwe 2 , Daniel Gillett 2 , Sarah Heard 2 , Andrew Hoole 3 , Miriam Scott 1 , Benjamin G Challis 1 , Nagui Antoun 4 , Heok K Cheow 4 , Richard J Mannion 5 & Mark Gurnell 1


1Metabolic Research Laboratories, Institute of Metabolic Science, University of Cambridge, Cambridge, UK; 2Department of Nuclear Medicine, Addenbrooke’s Hospital, Cambridge, UK; 3Department of Medical Physics, Addenbrooke’s Hospital, Cambridge, UK; 4Department of Radiology, Addenbrooke’s Hospital, Cambridge, UK; 5Department of Neurosurgery, Addenbrooke’s Hospital, Cambridge, UK.

Background: Endocrine Society guidelines classify macroprolactinomas as ‘resistant’ if there is failure to normalise prolactin, or to achieve radiological tumour shrinkage of >50%, on standard doses of dopamine agonist. In this context, escalation of treatment to maximal tolerable doses and/or referral for surgery is advised. However, we have recently observed several ‘discordant responders’, where tumour shrinkage lags significantly (>6 months) behind the biochemical response, but is ultimately achieved without treatment escalation.

Methods: i) A Pubmed search for ‘medical treatment of prolactinomas’ was performed & papers reporting discordance between biochemical and radiological responses identified and ii) We searched our pituitary database for patients treated locally over a 10-year period. A case where 11C-methionine PET-CT was used to guide management is described.

Results: From an initial return of 845 papers, 21 provided sufficient information, describing 340 patients, 92 of whom exhibited a discordant response. Of 89 macroprolactinomas in our local database, we identified 14 patients in whom prolactin normalised, but tumour shrinkage was <50% at >6 months after commencing treatment. One of these, a 36-year-old man (initial prolactin 14,123mU/l) achieved biochemical normalisation within eight weeks; however, despite continued prolactin suppression (28mU/l; 500mcg twice-weekly) at 12 months his tumour showed no reduction in size. Reassuringly, 11C-methionine PET-CT coregistered with MRI demonstrated a complete absence of tracer uptake in the ‘residual adenoma’. With this evidence, contrary to Endocrine Society Guidelines, cabergoline was reduced to 250mcg twice-weekly. 24-months later serum prolactin remained well-controlled (76 mU/l), and substantial (>50%) tumour shrinkage was evident on MRI.

Conclusions: These cases demonstrate that a delayed radiological response may be seen without further dose escalation, once biochemical normalisation has been achieved in prolactinomas; current guidelines may therefore inappropriately categorise such tumours as ‘dopamine agonist resistant’. Our literature and local database review suggests this may be an under-recognised phenomenon. Furthermore, the case described here highlights the utility of functional imaging in aiding management in such patients.

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