scholarly journals Adolescents with Partial Growth Hormone (GH) Deficiency Develop Alterations of Body Composition after GH Discontinuation and Require Follow-Up

2003 ◽  
Vol 88 (11) ◽  
pp. 5101-5106 ◽  
Author(s):  
Maithé Tauber ◽  
Béatrice Jouret ◽  
Audrey Cartault ◽  
Nadia Lounis ◽  
Michèle Gayrard ◽  
...  

Abstract It is now a consensus to resume GH treatment in adolescents with severe GH deficiency (GHD) at retesting to prevent the occurrence of adult GHD syndrome. However, we do not have any data on the follow-up of adolescents with nonsevere GHD at completion of treatment. This report presents preliminary data from a 1-yr prospective study that includes the first 91 patients retested. Anthropometric data, IGF-I and IGF binding protein-3 levels, glycemia and insulinemia, lipid profile, and body composition using dual x-ray absorptiometry and abdominal computed tomography scan were recorded at completion of GH treatment and 1 yr later. Body composition was significantly different at both evaluations, with increased total body fat and decreased lean body mass in the partial GHD group vs. the normal group. Moreover, these alterations worsened after 1 yr without GH in the partial GHD group, whereas there were no modifications in the normal group. We did not find any metabolic alterations such as elevated triglyceride, total cholesterol, or insulin levels. Adolescents with reconfirmed partial GHD exhibit alterations in body composition after 1 yr without GH, whereas those retested normal do not. These changes are similar to those described in severe GHD, although less marked, and justify a precise follow-up.

1993 ◽  
Vol 128 (4) ◽  
pp. 313-318 ◽  
Author(s):  
Roman Deyssig ◽  
Herwig Frisch ◽  
Werner F Blum ◽  
Thomas Waldhör

The effect of recombinant GH on strength, body composition and endocrine parameters in power athletes was investigated in a controlled study. Twenty-two healthy, non-obese males (age 23.4±0.5 years; ideal body weight 122±3.1%, body fat 10.1±1.0%; mean±sem) were included. Probands were assigned in a double-blind manner to either GH treatment (0.09U (kg BW)−1 day−1 sc) or placebo for a period of six weeks. To exclude concurrent treatment with androgenic-anabolic steroids urine specimens were tested at regular intervals for these substances. Serum was assayed for GH, IGF-I, IGF-binding protein, insulin and thyroxine before the onset of the study and at two-weekly intervals thereafter. Maximal voluntary strength of the biceps and quadriceps muscles was measured on a strength training apparatus. Fat mass and lean body mass were derived from measurements of skinfolds at ten sites with a caliper. For final evaluation only data of those 8 and 10 subjects in the two groups who completed the study were analyzed. GH, IGF-I and IGF-binding protein were in the normal range before therapy and increased significantly in the GH-treated group. Fasting insulin concentrations increased insignificantly and thyroxine levels decreased significantly in the GH-treated probands. There was no effect of GH treatment on maximal strength during concentric contraction of the biceps and quadriceps muscles. Body weight and body fat were not changed significantly during treatment. We conclude that the anabolic, lipolytic effect of GH therapy in adults depends on the degree of fat mass and GH deficiency. In highly trained power athletes with low fat mass there were no effects of GH treatment on strength and body composition.


1998 ◽  
Vol 83 (11) ◽  
pp. 4065-4074
Author(s):  
Hiralal G. Maheshwari ◽  
Bernard L. Silverman ◽  
Josée Dupuis ◽  
Gerhard Baumann

We report, in detail, a new form of familial dwarfism, including its phenotypic features, hormonal profile, and molecular basis. Following a newspaper report of severe dwarfism in two villages in the province of Sindh, Pakistan, we organized an expedition to study its clinical, genetic, and molecular characteristics. We identified 18 dwarfs (15 male, 3 female), all members of a consanguineous kindred, ranging in age from newborn to 28 yr. Mean height was 7.2 sd below the norm, with mean adult heights of 130 cm for males and 113.5 cm for females. Body proportions and habitus were normal; but head circumference was 4.1 sd, and blood pressure approximately 3 sd below the norm. There was no dysmorphism, no microphallus, and no history of hypoglycemia. Serum GH did not respond to provocative stimuli (GHRH, l-dopa, or clonidine). Insulin-like growth factor I (IGF-I) and IGF-binding protein 3 were low (5.2 ± 2.0 ng/mL and 0.42 ± 0.13 μg/mL, respectively; mean ± sd) but rose normally with GH treatment. One affected, dwarfed couple had a son, demonstrating fertility in both sexes. Clinical and endocrinological evidence suggested isolated GH deficiency with a recessive inheritance pattern. The GH-N gene was found to be intact. Linkage analysis of microsatellite chromosomal markers near other candidate genes yielded a high LOD score (6.26) for the GHRH receptor (GHRH-R) locus. DNA sequencing revealed a nonsense mutation (Glu50→Stop) in the extracellular domain of the GHRH-R. This mutation predicts a severely truncated GHRH-R; it is identical to that recently reported in four patients from two other families. Inheritance is autosomal recessive (chromosome 7p) with a high degree of penetrance. Relatives heterozygous for the mutation had moderately decreased IGF-I levels and slightly blunted GH responses to GHRH and l-dopa, but they showed only minimal or no height deficit. This syndrome represents the human homologue of the little (lit/lit) mouse and closely resembles its phenotype. It demonstrates the absolute requirement of GHRH signaling for pituitary GH secretion and postnatal growth in humans, and its relatively minor (but discernible) biological importance in extrapituitary sites. The syndrome is distinct from other forms of GH deficiency with respect to microcephaly, asymptomatic hypotension, and absence of features such as facial dysplasia, significant truncal obesity, microphallus, or hypoglycemia. Its discovery raises the possibility of milder mutations in the GHRH-R gene as potential causes for partial GH insufficiency and idiopathic short stature.


1998 ◽  
pp. 633-639 ◽  
Author(s):  
T Sugimoto ◽  
D Nakaoka ◽  
M Nasu ◽  
M Kanzawa ◽  
T Sugishita ◽  
...  

The present study was performed to investigate the age-dependent changes in body composition and the possible role of growth hormone (GH), insulin-like growth factor (IGF)-I and IGF-binding protein-3 (IGFBP-3) in these changes in postmenopausal Japanese women. A total of 161 Japanese women aged 45-88 years (mean 62) were enrolled in the cross-sectional study. Body composition (bone mineral content (BMC), lean body mass (LBM) and fat) was measured by dual-energy X-ray absorptiometry, and the percentage of BMC, LBM and fat was calculated by dividing each absolute value of body composition by total body mass. Urinary GH concentration divided by creatinine in nocturnal urine samples collected just after waking was used as an index of endogenous GH secretion. Serum levels of IGF-I and IGFBP-3 were measured by RIA. Urinary GH levels as well as serum levels of IGF-I and IGFBP-3 declined with age. BMC, %BMC and LBM also declined with age, while fat mass and %fat did not obviously change with age. Urinary GH levels as well as serum levels of IGF-I and IGFBP-3 correlated positively with BMC, even if age was taken into account. On the other hand, urinary GH correlated negatively with fat and %fat. In contrast, serum levels of IGF-I and IGFBP-3 correlated positively with fat and %fat. LBM did not correlate with either urinary GH or serum IGFBP-3 levels but exhibited a weakly positive correlation with serum IGF-I level. The present study suggests that the GH-IGF-I-IGFBP-3 axis positively regulates bone mass, and that GH and IGF-I-IGFBP-3 inversely regulate fat mass, i.e. GH negatively and IGF-I-IGFBP-3 positively regulates it.


2007 ◽  
Vol 157 (5) ◽  
pp. 597-603 ◽  
Author(s):  
Berthold P Hauffa ◽  
Nils Lehmann ◽  
Markus Bettendorf ◽  
Otto Mehls ◽  
Helmuth-Günther Dörr ◽  
...  

AbstractBackgroundChildhood GH deficiency, suspected in the presence of decreased height velocity and short stature, is usually characterized by low IGF-I and IGF-binding protein-3 (IGFBP-3) serum concentrations and is conventionally confirmed by diminished GH peak responses to pharmacological stimuli.ObjectiveWe evaluated the agreement between different IGF-I (IGFBP-3) assays in predicting GH deficiency and tested whether variability between growth factor screening and pharmacological testing could be diminished by reassessment of growth factor and GH peak concentrations in a single laboratory.DesignUsing the Tuebingen IGF-I (IGFBP-3) RIA, 317 (321) sera from children evaluated for growth disorders in 19 centers were reanalyzed. In 103 children with insulin hypoglycemia and arginine tests, we evaluated how the association between the outcome of growth factor screening and functional testing would change if different assays were employed.ResultsLocally measured IGF-I correlated better than IGFBP-3 with the results of the central laboratory (Tuebingen) assay (slope of the regression curve 1.05; 95% confidence interval (95% CI) 1.01–1.1 versus 1.18; 95% CI 1.09–1.3). Agreement between local and central laboratory assays in predicting GH deficiency was better for IGF-I than for IGFBP-3 assays (κ=0.59 versus κ=0.47). The poor agreement between growth factor screening and GH pharmacological testing was not improved when hormone concentrations were remeasured in the central laboratory (κ local=−0.0031, central=0.12).ConclusionsIn children with impaired growth, growth factor screening reflects different aspects of GH insufficiency than does functional testing. Agreement between these approaches is poor and could not be improved by reduction of assay-related variability.


1995 ◽  
Vol 6 (2-4) ◽  
pp. 377-383 ◽  
Author(s):  
Sylvia ban Buul-Offers ◽  
Ria Reijnen-Gresnigt ◽  
Ruud Bloemen ◽  
Cok Hoogerbrugge ◽  
Jan Leo ban den Brande

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