Currently used growth‐promoting treatment of children results in normal bone mass and density. A prospective trial of discontinuing growth hormone treatment in adolescents<sup>‡</sup>

Fors, Hans; Bjarnason, Ragnar; Wirén, Lena; Albertsson‐Wikland, Kerstin; Bosæus, Ingvar; Bengtsson, Bengt‐Åke; Johannsson, Gudmundur

doi:10.1046/j.1365-2265.2001.01386.x

Cited by 41 publications

(37 citation statements)

References 43 publications

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“…Hypothetically, our findings could be caused by frequent physical activity during adolescence leading to a good peak bone mass despite diminishing secretion of growth hormone. Decreased bone turnover has previously been demonstrated in patients with GHD in some (36,37) but not all (38) studies. Neither this study nor the study of Brennan et al found a correlation between growth hormone and markers of bone turnover (9).…”

Section: Discussionmentioning

confidence: 89%

Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia

Jarfelt¹,

Fors²,

Lannering³

et al. 2006

eur j endocrinol

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Objective: Treatment for childhood leukaemia induces many risk factors for development of decreased bone mineral density (BMD). Physical activity is also known to affect BMD. The aim was to study BMD and markers of bone turnover in a well-defined group of survivors of acute lymphoblastic leukaemia (ALL) who had all reached final height as well as peak bone mass, taking both previous treatment and physical activity into consideration. Design: All patients treated for ALL before the onset of puberty in the region of western Sweden, between 1973 and 1985, in first remission were included. Thirty-five out of forty-seven patients aged 20 -32 years participated. Nineteen patients had received cranial radiotherapy, and the median follow-up time was 20 years. Methods: BMD was assessed using dual-energy X-ray absorbtiometry (DEXA). Serum concentrations of markers of bone turnover were analysed. Physical performance was measured using a performance exercise capacity stress test. Results: BMD was slightly reduced in lumbar spine (2 0.4 SD), but not in femoral neck or total body. BMD in femoral neck was correlated to physical performance and dose of corticosteroid, but no correlation was found with spontaneous growth hormone (GH) secretion. Markers of bone turnover were also correlated to physical performance, but not to GH secretion. Conclusions: Physical fitness seems to be the most important factor in developing and preserving normal bone mineral density in ALL patients. We propose that lifestyle education promoting physical activity is encouraged from an early point in time for these patients.

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Section: Discussionmentioning

confidence: 89%

Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia

Jarfelt¹,

Fors²,

Lannering³

et al. 2006

eur j endocrinol

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“…In vivo, GH administration increases biochemical markers of bone turnover in normal subjects [36], adults with GHD [37]and children with GHD [38]. Furthermore, children with GHD demonstrate reductions in markers of bone turnover after discontinuation of GH at completion of linear growth [39]. …”

Section: Skeletal Health In Adults With Ghd and The Impact Of Gh Replmentioning

confidence: 99%

Impact of Growth Hormone Status on Body Composition and the Skeleton

Mukherjee

Murray

Shalet³

2004

Horm Res Paediatr

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Severe growth hormone (GH) deficiency (GHD) induces a well-defined clinical entity encompassing, amongst the most reported features, abnormalities of body composition, in particular increased fat mass, especially truncal, and reduced lean body mass. The results from virtually all treatment studies are in agreement that GH replacement improves the body composition profile of GHD patients by increasing lean body mass and reducing fat mass. More recently, the observations have been extended to adults with partial GHD, defined by a peak GH response to insulin-induced hypoglycaemia of 3–7 µg/l. These patients exhibit abnormalities of body composition similar in nature to those described in adults with severe GHD; these include an increase in total fat mass of around 3.5 kg and a reduction of lean body mass of around 5.5 kg. The increase in fat mass is predominantly distributed within the trunk. The degree of abnormality of body composition is intermediate between that of healthy subjects and that of adults with GHD. The impact of GH replacement on body composition in adults with GH insufficiency, although predictable, has not been formally documented. The skeleton is another biological endpoint affected by GH status: in adults with severe GHD, low bone mass has been reported using dual energy x-ray absorptiometry (DEXA) and other quantitative methodologies. The importance of low bone mass, in any clinical setting, is as a surrogate marker for the future risk of fracture. Several retrospective studies have documented an increased prevalence of fractures in untreated GHD adults. Hypopituitary adults with severe GHD have reduced markers of bone turnover which normalize with GH replacement, indicating that GH, directly or via induction of insulin-like growth factor-I, is intimately involved in skeletal modelling. Whilst the evidence that GH plays an important role in the acquisition of bone mass during adolescence and early adult life is impressive, the impact of GHD acquired later in adulthood is less clear. Recently we examined the relationship between bone mineral density (BMD) and age in 125 untreated adults with severe GHD using DEXA. A significant positive correlation was observed between BMD (z-scores) and age at all skeletal sites studied. Overall, few patients, except those aged less than 30 years, had significantly reduced bone mass (i.e. a BMD z-score of less than –2); correction of BMD to provide a pseudo-volumetric measure of BMD suggested that reduced stature of the younger patients may explain, at least in part, this higher frequency of subnormal BMD z-scores. Despite normal BMD, however, an increase in fracture prevalence may still be observed in elderly GHD adults as a consequence of increased falls related to muscle weakness and visual field defects.

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“…These results suggest that in young adults with GHD, GH replacement may be needed to support adequate bone mass accumulation in order to maintain bone mass in adult life (21)(22)(23). Furthermore, it seems likely that adolescents with severe GHD may not have achieved their peak bone mass at adult height, when GH treatment is often discontinued, and that GH may play an important role in the acquisition and maintenance of bone mass during this particular period of bone consolidation (3,(24)(25)(26). In addition to reduced BMD, some adults with childhood-onset GHD also have lower lean body mass, diminished quality of life (QoL), abnormal lipids, and impaired cardiac function compared with older adults with adult-onset GHD (27,28).…”

Section: Introductionmentioning

confidence: 99%

Treatment for 24 months with recombinant human GH has a beneficial effect on bone mineral density in young adults with childhood-onset GH deficiency

Conway

Szarras‐Czapnik

Rácz

et al. 2009

European Journal of Endocrinology

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Objective: Discontinuation of growth hormone (GH) therapy on completion of linear growth may adversely affect bone mineral density (BMD) in young adults with childhood-onset GH-deficiency (GHD). In the present study, we analyzed the impact of GH treatment on bone in young adults with GHD. Methods: BMD at the lumbar spine (L2-L4), total hip, and total body was measured at baseline and after 24 months in a cohort of young adults (18-25 years; nZ160) with severe GHD treated with GH during childhood who were randomized to GH (nZ109) or no treatment (nZ51) in a multicenter, multinational, open-label study. GH starting doses (0.2 mg/day (males), 0.4 mg/day (females)) were increased after 1 month to 0.6 mg/day (males) and 0.9 mg/day (females) and then to 1.0 mg/day (males) and 1.4 mg/day (females) at 3 months for the remainder of the study. Results: After 24 months, lumbar spine BMD had increased significantly more in GH-treated patients than in controls (6 vs 2%; estimated treatment difference; 3.5% (95% confidence interval, 1.52-5.51) P!0.001). GH also had a significant positive effect on total hip BMD (PZ0.015). Total body BMD was unchanged from baseline (PZ0.315). Conclusions: In young adults treated for childhood-onset GHD, there is a beneficial effect of continued GH treatment on BMD in adult life. Twenty-four months of GH treatment in these young adults was associated with an estimated 3.5% greater increase in BMD of the lumbar spine compared with controls.

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Currently used growth‐promoting treatment of children results in normal bone mass and density. A prospective trial of discontinuing growth hormone treatment in adolescents^‡

Cited by 41 publications

References 43 publications

Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia

Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia

Impact of Growth Hormone Status on Body Composition and the Skeleton

Treatment for 24 months with recombinant human GH has a beneficial effect on bone mineral density in young adults with childhood-onset GH deficiency

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Currently used growth‐promoting treatment of children results in normal bone mass and density. A prospective trial of discontinuing growth hormone treatment in adolescents‡

Cited by 41 publications

References 43 publications

Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia

Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia

Impact of Growth Hormone Status on Body Composition and the Skeleton

Treatment for 24 months with recombinant human GH has a beneficial effect on bone mineral density in young adults with childhood-onset GH deficiency

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Currently used growth‐promoting treatment of children results in normal bone mass and density. A prospective trial of discontinuing growth hormone treatment in adolescents^‡