Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2006) 11 P541

ECE2006 Poster Presentations Endocrine tumours and neoplasia (116 abstracts)

Differences in the presenting biochemical and imaging data in patients with acromegaly caused by pure GH adenomas, adenomas with GH and PRL cell differentiation and plurihormonal adenomas

A Fernandez 1 , N Karavitaki 1 , O Ansorge 2 , V Fazal-Sanderson 1 , HE Turner 1 & JAH Wass 1


1Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, United Kingdom; 2Neuropathology Department, Radcliffe Infirmary, Oxford, United Kingdom.


Introduction: Pituitary adenomas causing acromegaly are immunocytochemically divided into 3 main groups: growth hormone (GH) cell (A), those with GH and prolactin (PRL) cell differentiation (B) and plurihormonal (C). Recent large series comparing the hormonal and imaging features of these tumours at diagnosis are lacking.

Objectives: To investigate differences in the presenting hormonal and imaging data associated with the above groups of adenomas.

Patients and methods: The patients were recruited from the Acromegaly Database of our Department. Those treated pre-operatively with somatostatin analogues or dopamine agonists were excluded.

Results: Ninety-eight patients were identified [A:27, B:42, C:29, median age 48.5 years (range 17–79), males/females 49/49]. There was no significant difference in the basal, nadir and mean GH values (mU/l) during the oral glucose tolerance test [basal median: A 52.6 (6.4–100), B 30 (4.5–100), C 40.6 (6.9–100) – nadir median: A 35.2 (6–100), B 27 (3–100), C 29.6 (6.4–100) – mean median: A 42.5 (5.1–100), B 31.3 (5.3–100), C 39.9 (8.9–100)] or in the PRL levels (mU/l) [A median: males 206 (100–734)-females 294 (190-638), B median: males 394 (61–3674)-females 359 (162-8335), C median: males 310 (64–4980)-females 301 (87–2430)] among the 3 groups. All but 2 subjects (group B) had insulin-like growth factor-I levels above the reference range. In contrast to tumours of groups A and B, those of C were more frequently microadenomas (micro-/macroadenomas: A 29.6%/70.4%, B 26.2%/73.8%, C 57.1%/52.9%, P=0.02). No difference in the presence of suprasellar extension (A 48%, B 55%, C 43%) or cavernous sinus invasion (A 22%, B 20%, C 7%) between the 3 groups was found.

Conlusions: In this large series of the 3 major immunocytochemical subtypes of adenomas causing acromegaly apart from the size of the tumour, no differences in the investigated hormonal and imaging data at presentation were found.

Volume 11

8th European Congress of Endocrinology incorporating the British Endocrine Societies

European Society of Endocrinology 
British Endocrine Societies 

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