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A V Dreval, I V Trigolosova, I V Misnikova, Y A Kovalyova, R S Tishenina, I A Barsukov, A V Vinogradova and B H R Wolffenbuttel

Introduction Disturbances of glucose metabolism are frequently observed in patients with acromegaly. In one of the first papers to be published on this topic, abnormal glucose tolerance was found in over 60% of patients with acromegaly (1) . The

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Cecilia Follin and Sven Karlsson

Introduction Acromegaly is a rare chronic condition caused by excess growth hormone (GH) secretion – usually from a pituitary tumour – and it has an incidence rate of only 3.3 cases per million people. The mean age at diagnosis is 40 years

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Pinaki Dutta, Bhuvanesh Mahendran, K Shrinivas Reddy, Jasmina Ahluwalia, Kim Vaiphei, Rakesh K Kochhar, Prakamya Gupta, Anand Srinivasan, Mahesh Prakash, Kanchan Kumar Mukherjee, Viral N Shah, Girish Parthan and Anil Bhansali

Introduction Acromegaly is most commonly caused by a growth hormone (GH)-producing pituitary tumor and is potentially life-threatening if untreated. Early diagnosis and treatment of acromegaly result in increased longevity and better quality of life

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A J Varewijck, A J van der Lely, S J C M M Neggers, S W J Lamberts, L J Hofland and J A M J L Janssen

Introduction Acromegaly is characterized by excess secretion of growth hormone (GH) causing multisystem-associated morbidities and increased mortality. GH is considered as the main regulator of circulating total insulin-like growth factor 1 (IGF1

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Elena Valassi, Natalia García-Giralt, Jorge Malouf, Iris Crespo, Jaume Llauger, Adolfo Díez-Pérez and Susan M Webb

of bone matrix and bone mass ( 1 ). Acromegaly (ACRO) is a rare disease caused by excessive GH production from a pituitary adenoma ( 4 ). Chronic elevation of GH and IGF1 in ACRO is associated with severe cardiovascular, respiratory and metabolic

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Gudmundur Johannsson, Martin Bidlingmaier, Beverly M K Biller, Margaret Boguszewski, Felipe F Casanueva, Philippe Chanson, Peter E Clayton, Catherine S Choong, David Clemmons, Mehul Dattani, Jan Frystyk, Ken Ho, Andrew R Hoffman, Reiko Horikawa, Anders Juul, John J Kopchick, Xiaoping Luo, Sebastian Neggers, Irene Netchine, Daniel S Olsson, Sally Radovick, Ron Rosenfeld, Richard J Ross, Katharina Schilbach, Paulo Solberg, Christian Strasburger, Peter Trainer, Kevin C J Yuen, Kerstin Wickstrom, Jens O L Jorgensen and on behalf of the Growth Hormone Research Society

factor-I (IGF-I). Both are used diagnostically; IGF-I is used to monitor the effects of GH replacement in GH deficiency (GHD), and both GH and IGF-I are used in the diagnosis and management of acromegaly. While serum IGF-I level is used as a surrogate

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Anna-Pauliina Iivonen, Johanna Känsäkoski, Atte Karppinen, Leena Kivipelto, Camilla Schalin-Jäntti, Auli Karhu and Taneli Raivio

inputs such as growth hormone-releasing hormone (GHRH) and somatostatin as well as several peripheral hormones. GH-secreting pituitary adenomas, i.e. somatotropinomas, lead to acromegaly in adults and (acro-) gigantism in children and adolescents

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Julie M Silverstein

Introduction Acromegaly is a rare hormonal condition that develops most commonly from benign somatotroph pituitary adenomas and has a prevalence of 36–69 cases per million and an incidence of 3–4 cases per million per year (1, 2, 3, 4) . However

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Adrian Daly, Liliya Rostomyan, Daniela Betea, Jean francois Bonneville, Chiara Villa, Natalia S Pellegata, Beatrice Waser, Jean Claude Reubi, Catherine Waeber Stephan, Emanuel Christ and Albert Beckers

Acromegaly is a rare disease due to chronic excess growth hormone (GH) and IGF-1. Aryl hydrocarbon receptor interacting protein (AIP) mutations are associated with an aggressive, inheritable form of acromegaly that responds poorly to SST2-specific somatostatin analogs (SSA). The role of pasireotide, an SSA with affinity for multiple SSTs, in patients with AIP mutations has not been reported. We studied two AIP-mutation positive acromegaly patients with early-onset, invasive macroadenomas and inoperable residues after neurosurgery. Patient 1 came from a FIPA kindred and had uncontrolled GH/IGF-1 throughout 10 years of octreotide/lanreotide treatment. When switched to pasireotide LAR, he rapidly experienced hormonal control and was associated with marked regression of his tumor residue. Pasireotide LAR was stopped after >10 years due to low IGF-1 and he maintained hormonal control without tumor regrowth for >12 months off pasireotide LAR. Patient 2 had disease onset aged 17 that was not cured by surgery. Chronic pasireotide LAR therapy produced hormonal control and marked tumor shrinkage but control was lost when switched to octreotide. Tumor immunohistochemistry showed absent AIP and SST2 staining and positive SST5. Her AIP-mutation positive sister developed a 2.5 cm follicular thyroid carcinoma aged 21 with tumoral loss of heterozygosity at the AIP locus and absent AIP. Patients 1 and 2 required multi-modal therapy to control diabetes. On stopping pasireotide LAR after >10 years of treatment, Patient 1’s glucose metabolism returned to baseline levels. Long-term pasireotide LAR therapy can be beneficial in some AIP-mutation positive acromegaly patients that are resistant to first-generation SSA.

Open access

Paula Bruna Araujo, Leandro Kasuki, Carlos Henrique de Azeredo Lima, Liana Ogino, Aline H S Camacho, Leila Chimelli, Márta Korbonits and Monica R Gadelha

hydrocarbon receptor-interacting protein ( AIP ) gene mutations ( AIPmut ) were first described by Vierimaa and coworkers in 2006 ( 3 ). This study has found AIPmut in seemingly sporadic acromegaly patients and in familial isolated pituitary adenomas (FIPA