ECE2014 Poster Presentations Pituitary Clinical (<emphasis role="italic">Generously supported by IPSEN</emphasis>) (108 abstracts)
1Department of Medical Endocrinology, Hospital of Copenhagen, Copenhagen, Denmark; 2Department of Neuropathology, University Hospital of Copenhagen, Copenhagen, Denmark.
Hypothesis and aim: Acromegaly is frequently associated with impaired glucose tolerance and diabetes, and concomitant hyperprolactinaemia was suggested to add to this effect. We hypothesized that pituitary prolactin (PRL) histopathology and plasma hyperprolactinaemia has a prognostic value in predicting the risk of glucose metabolic disturbances in acromegalic patients. The aim of this study was to examine glucose metabolic outcomes in acromegalic patients with and without histologically verified PRL and GH co-secreting adenomas (GH+ve; and PRL+ve).
Method: 79 patients (43 men) who had undergone surgical treatment for acromegaly median 8 years (range: 6 months 39 years) earlier were included. Clinical and biochemical baseline data were collected from medical records. Patients were divided into two groups based on histopathological evaluation; i) pure GH+ve or ii) GH+ve;PRL+ve co-secreting adenomas. Patients underwent a follow-up visit between January 2012 and January 2013, where blood samples were drawn and an oral glucose tolerance test was performed.
Results: Thirty-five percent of patients had GH+ve; PRL+ve adenomas, whereas 65% had pure GH-production. Patients with GH+ve; PRL+ve adenomas were older (P=0.04) than patients with pure GH-adenomas. No significant differences were observed between glucose metabolic outcomes of the two groups, neither at baseline nor at long-term follow-up. Also no differences were found in glucose metabolic outcome between patients with hyperprolactinaemia and patients with normal or low prolactin concentrations.
Conclusion: Pituitary histopathology staining for PRL was not useful in predicting long-term glucose metabolic outcome in acromegalic patients. No association was found between glucose metabolic disturbances, plasma hyperprolactinaemia or histologically verified prolactin production.