881 – 889 . ( https://doi.org/10.1530/EJE-11-0599 ) 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
Johan Verhelst, Anders F Mattsson, Cecilia Camacho-Hübner, Anton Luger and Roger Abs
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
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
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
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
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
Mark R Postma, Pia Burman and André P van Beek
Introduction: Adult-onset growth hormone deficiency (AGHD) is usually the last deficiency to be substituted in hypopituitarism. In children with documented GH deficiency, treatment without delay is crucial for achieving optimal effects on growth and development. In adults, it is not known whether a delay in treatment initiation influences biochemical response and the favourable physiological effects resulting from GH replacement therapy (GHRT).
Methods: A total of 1085 GH-deficient adults from KIMS (Pfizer International Metabolic Database) were included, adequately replaced with all pituitary hormones except for GH at baseline. Patients were stratified by sex and age (20-50 years and ≥50 years) and subsequently divided into two groups below and above the median duration of unsubstituted AGHD for that subgroup. The median time of unsubstituted GHD for the total cohort was 2.53 years (P5=0.35, P95=24.42).
Results: Beneficial effects of 4 years of GHRT were observed on lipids and quality of life in all subgroups. A decrease in waist circumference was observed only in older (>50 years) patients. There was no difference in IGF-I SDS and in GH dose required to normalize IGF-I in patients with a duration of unsubstituted AGHD above or below the median. No relevant differences were found between the groups for anthropometric measures, cardiovascular risk factors and quality of life scores.
Conclusion: In contrast to GHD in children and adolescents, no difference could be established in treatment response between early or late initiation of GHRT in AGHD in terms of required GH dose, IGF-I, metabolic health and quality of life.
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
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
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