Reduced bone mineral density in patients with adult onset growth hormone deficiency.

Holmes, S. J. I.; Economou, G; Whitehouse, Richard W.; Adams, Judith E.; Shalet, Stephen M

doi:10.1210/jcem.78.3.8126140

Cited by 188 publications

(122 citation statements)

References 19 publications

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“…It tends to be more severe in patients with childhood-onset GHD. This is probably attributable to insufficient accumulation of bone mass during childhood and puberty rather than later loss of bone mass (32,33). Low bone mass has been shown to be less frequent with increasing age in patients with GHD (34).…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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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“…Adults with both childhood onset (CO) and adulthood onset (AO) GHD have reduced bone mineral content (BMC) and bone mineral density (BMD) (7)(8)(9)(10). However, the magnitude of the reduction in bone mass is more marked in adult patients with CO disease than in adult patients with AO GHD (11).…”

Section: Introductionmentioning

confidence: 99%

Ten-year GH replacement increases bone mineral density in hypopituitary patients with adult onset GH deficiency

Götherström¹,

Bengtsson²,

Bosæus³

et al. 2007

eur j endocrinol

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There are few studies that have determined the effects of long-term GH replacement on bone mineral density (BMD) in GH-deficient (GHD) adults. In this study, the effects of 10 years of GH replacement on BMD were assessed in 87 GHD adults using dual energy X-ray absorptiometry (DEXA). The results show that GH replacement induced a sustained increase in BMD at all the skeletal sites measured. Introduction: Little is known of the effect of more than 5 years of GH replacement therapy on bone metabolism in GHD adults. Patients and methods: In this prospective, open-label, single-center study, which included 87 consecutive adults (52 men and 35 women; mean age of 44.1 (range 22-74) years) with adulthood onset GHD, the effect of 10 years of GH replacement on BMD was determined. Results: The mean initial dose of GH was 0.98 mg/day. The dose was gradually lowered and after 10 years the mean dose was 0.47 mg/day. The mean insulin-like growth factor-I (IGF-I) SDS increased from 1.81 at baseline to 1.29 at study end. The GH replacement induced a sustained increase in total, lumbar (L2-L4) and femur neck BMD, and bone mineral content (BMC) as measured by DEXA. The treatment response in IGF-I SDS was more marked in men, whereas women had a more marked increase in the total body BMC and the total body z-score. There was a tendency for women on estrogen treatment to have a larger increase in bone mass and density compared with women without estrogen replacement. Conclusions: Ten years of GH replacement in hypopituitary adults induced a sustained, and in some variables even a progressive, increase in bone mass and bone density. The study results also suggest that adequate estrogen replacement is needed in order to have an optimal response in BMD in GHD women.European Journal of Endocrinology 156 55-64

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“…The GH regulatory role in bone remodeling and maintenance of bone mass has been clearly established in clinical studies, where patients with acquired GH deficiency in adulthood (GHD) were found to have secondary osteoporosis, characterized by reduced bone mass, increased fracture risk, and decreased bone remodeling (Holmes et al 1994, Wuster et al 2001. Replacement therapy in GHD patients induces a dose-dependent increase of bone remodeling, as evaluated by relevant biochemical markers that peak at 3-6 months after the start of treatment and remain elevated throughout the 2 years of observation time (Nielsen et al 1991, Joannsson et al 1996.…”

Section: Introductionmentioning

confidence: 99%

Growth hormone stimulates osteoprotegerin expression and secretion in human osteoblast-like cells

Mrak

Villa²,

Lanzi

et al. 2007

Journal of Endocrinology

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It is presently thought that osteoprotegerin (OPG) is a cytokine involved in the regulation of osteoblast/osteoclast crosstalk and maintenance of bone mass. Recent studies showed that GH replacement therapy in GH-deficient patients was able to induce a significant increase of OPG in the plasma, as well as in the cortical and the trabecular bone. In order to determine whether GH could directly modulate OPG secretion, the effect of GH on human osteoblast-like cells (hOB) in primary culture was studied. After detecting the presence of the mRNA for the GH receptor (GHR) by RT-PCR, hOB were exposed to increasing concentrations of GH, from 0 . 1 to 25 ng/ml, for 24 h. The results showed that GH exposure was able to stimulate OPG secretion in a concentration-dependent manner. In addition, the OPG mRNA levels were increased, indicating that the hormone has a stimulatory effect on gene expression. The stimulatory effect on OPG expression and production was prevented by exposing the cells to tyrphostin AG490 (10 mM), an inhibitor of Janus kinase 2, which is one of the kinases involved in the intracellular pathway activated by the binding of GH to its receptor. Similar results were obtained when the cells were exposed to a receptor antagonist of GH, pegvisomant at 50 nM. GH exposure neither induced an increase in IGF-I expression nor secretion in hOB. These results suggest that the stimulation of OPG production induced by GH in hOB is specific and receptor mediated and further support the view that GH is able to modulate bone remodeling by directly influencing osteoblast-osteoclast crosstalk.

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Reduced bone mineral density in patients with adult onset growth hormone deficiency.

Cited by 188 publications

References 19 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

Ten-year GH replacement increases bone mineral density in hypopituitary patients with adult onset GH deficiency

Growth hormone stimulates osteoprotegerin expression and secretion in human osteoblast-like cells

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