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Johan Verhelst, Anders F Mattsson, Cecilia Camacho-Hübner, Anton Luger, and Roger Abs

881 – 889 . ( ) 21969523 10.1530/EJE-11-0599 4 Claessen KM Appelman-Dijkstra NM Adoptie DM Roelfsema F Smit JW Biermasz NR Pereira AM. Metabolic profile in growth hormone-deficient (GHD) adults

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M Ahmid, C G Perry, S F Ahmed, and M G Shaikh

) has been estimated to be about 1 in 3500–4000 live births, whereas the prevalence of adult onset (AO-GHD) in addition to those with previous CO-GHD is also about 1 in 3000 of the UK adult population ( 1 , 2 ). In addition to linear growth, the GH

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Charlotte Höybye, Erik Wahlström, Petra Tollet-Egnell, and Gunnar Norstedt

replacement therapy with thyroxin, hydrocortisone, sex steroids, and vasopressin for at least 2 years. The characteristics of the patients are given in Table 1 . All had adult-onset GHD, and had not previously been treated with GH. None of the patients had

Open access

Charlotte Höybye, Laia Faseh, Christos Himonakos, Tomasz Pielak, and Jesper Eugen-Olsen

and GH treatment on low-grade inflammation and the level of suPAR in patients with GHD are unknown. The primary aim of this study was to establish baseline suPAR levels in a cohort of adults with GHD. The secondary aims were to measure suPAR during

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Ursula M M Costa, Carla R P Oliveira, Roberto Salvatori, José A S Barreto-Filho, Viviane C Campos, Francielle T Oliveira, Ivina E S Rocha, Joselina L M Oliveira, Wersley A Silva, and Manuel H Aguiar-Oliveira

synergistic anabolic effect on muscle mass, but antagonist effects on insulin action (GH-reducing and IGF1 increasing insulin sensitivity) and lipolysis (GH increasing and IGF1 reducing it) (2) . Adult onset GH deficiency (GHD) has been described as model of

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Mark R Postma, Pia Burman, and André P van Beek

areas that are affected in adults with GHD ( 24 ). The measure consists of 25 questions with ‘yes’ or ‘no’ response choices, with ‘yes’ answer indicating that the patient perceives a problem. The sum of ‘yes’ responses constitute a score, with a high

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Kennett Sprogøe, Eva Mortensen, David B Karpf, and Jonathan A Leff

acceptable PK and pharmacodynamic (PD) profiles in adults with GHD following once-weekly administration ( 29 ). However, a satisfactory IGF-1 profile was not achieved in children with GHD ( 30 ), and as a result, development was discontinued ( 31 , 32

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Thomas Reinehr, Martin Carlsson, Dionisios Chrysis, and Cecilia Camacho-Hübner

height is lower than predicted height. The difference between predicted and achieved adult height depends on bone age retardation in CDGP ( 8 , 9 , 11 ). Since bone age is delayed in children with growth hormone deficiency (GHD) before the initiation

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Laura van Iersel, Sarah C Clement, Antoinette Y N Schouten-van Meeteren, Annemieke M Boot, Hedi L Claahsen-van der Grinten, Bernd Granzen, K Sen Han, Geert O Janssens, Erna M Michiels, A S Paul van Trotsenburg, W Peter Vandertop, Dannis G van Vuurden, Hubert N Caron, Leontien C M Kremer, and Hanneke M van Santen

prevalence and latency times of cRT-induced HP dysfunction vary among patients, with growth hormone deficiency (GHD) usually occurring first and at a prevalence ranging from 29.0 to 39.1% ( 3 ). In contrast, central hypothyroidism primarily occurs after high

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Ekaterina Koledova, George Stoyanov, Leroy Ovbude, and Peter S W Davies

Introduction Recombinant human growth hormone (GH) is approved for use in the treatment of children with various aetiologies, including growth hormone deficiency (GHD), Turner syndrome (TS) and born small for gestational age (SGA) with no