Searchable abstracts of presentations at key conferences in endocrinology

ea0005s1 | Clinical Endocrinology Trust Visiting Professor Lecture | BES2003

Neuroendocrine regulation of bone mass - GH deficiency and resistance states

Klibanski A

The observation that acquired GnRH deficiency and estrogen deficiency leadsto decreased bone mass in young women was critical evidence thathypothalamic/pituitary disorders could impact on bone metabolism in adults.A three-fold risk of fractures in adults with growth hormone deficiency(GHD) has led to the investigation of the role of the GH/IGF-I axis in bonemetabolism. Two human experimental models, acquired GHD and acquired GHresistance due to severe w...

ea0005s1biog | Clinical Endocrinology Trust Visiting Professor Lecture | BES2003

Clinical Endocrinology Trust Visiting Professor Lecture

, Klibanski A

Anne Klibanski, Massachusetts General Hospital, Boston, MA, USA AbstractAnne Klibanski, M.D, is Professor of Medicine, Harvard Medical School and Chief, Neuroendocrine Unit and Director of the Neuroendocrine Clinical Center at Massachusetts General Hospital, Boston. A leader in the field of neuroendocrinology, Dr. Klibanski's research interests include the pathogenesis of hypogonadal osteoporosis, neuroendocrine contro...

ea0014p610 | (1) | ECE2007

A comparison between the efficacy and safety of pegvisomant to that of octreotide LAR in patients with acromegaly

Harris Philip , D’Souza Gwyn , Good Anthony , Layton Gary , Colao Annamaria , Beverly Biller , Klibanski Anne , Ghigo Ezio

Two medical therapies are now available for the treatment of acromegaly. Pegvisomant is a growth hormone (GH) receptor antagonist. Somatostatin analogues, in contrast, act by inhibiting the release of GH from the pituitary. The primary objective of this study was to compare the efficacy of pegvisomant (P) to that of octreotide LAR (LAR) in terms of IGF-1 normalisation. The secondary objective was to compare safety and tolerability between the two treatments.<p class="abste...

ea0050p249 | Neoplasia, Cancer and Late Effects | SFEBES2017

Multiple endocrine neoplasia type 1 (MEN1) phenocopy due to a P.Leu380Phe cell division cycle 23 (CDC73) mutation

Lines Kate E , Nachtigall Lisa B , Dichtel Laura E , Cranston Treena , Khairi Shafaq , Boon Hannah , Sagvand Babak Torabi , Zhang Xun , Stevenson Mark , Klibanski Anne , Thakker Rajesh V

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterised by the combined occurrence of parathyroid tumours, and neuroendocrine tumours (NETs) of the pituitary and pancreas. MEN1 is caused by mutations of the tumour suppressor gene MEN1, and MEN1 germline mutations are found in >75% of MEN1 patients. The remaining 25% of patients may have mutations involving as yet unidentified gene...

ea0050p249 | Neoplasia, Cancer and Late Effects | SFEBES2017

Multiple endocrine neoplasia type 1 (MEN1) phenocopy due to a P.Leu380Phe cell division cycle 23 (CDC73) mutation

Lines Kate E , Nachtigall Lisa B , Dichtel Laura E , Cranston Treena , Khairi Shafaq , Boon Hannah , Sagvand Babak Torabi , Zhang Xun , Stevenson Mark , Klibanski Anne , Thakker Rajesh V

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterised by the combined occurrence of parathyroid tumours, and neuroendocrine tumours (NETs) of the pituitary and pancreas. MEN1 is caused by mutations of the tumour suppressor gene MEN1, and MEN1 germline mutations are found in >75% of MEN1 patients. The remaining 25% of patients may have mutations involving as yet unidentified gene...