The effects of prolonged growth hormone replacement on bone metabolism and bone mineral density in hypopituitary adults*

Beshyah, Salem A.; Kyd, P; Thomas, Elizabeth; Fairney, Angela; Johnston, Desmond G.

doi:10.1111/j.1365-2265.1995.tb01872.x

Cited by 62 publications

(46 citation statements)

References 33 publications

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“…As previously observed (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19), the markers of bone turnover increased in response to GH. To reflect bone formation we measured serum PICP.…”

Section: Discussionsupporting

confidence: 65%

“…To reflect bone formation we measured serum PICP. Serum osteocalcin and total and bone-specific alkaline phosphatase have been used for the same purpose with similar results (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). As a sign of increased bone resorption, serum ICTP rose in our patients in response to GH treatment.…”

Section: Discussionmentioning

confidence: 71%

“…As a sign of increased bone resorption, serum ICTP rose in our patients in response to GH treatment. In previous GH studies, increased bone resorption has been demonstrated using either the same marker (17,18), the urinary excretion of pyridinoline and deoxypyridinoline (8,19), hydroxyproline (10,14) or type I collagen amino-terminal telopeptide (24). Taking all these bone marker findings into account, it seems quite obvious that GH treatment accelerates bone turnover, both bone formation and bone resorption.…”

Section: Discussionmentioning

confidence: 99%

“…GH replacement therapy in GH-deficient adults accelerates whole body bone remodeling, demonstrated not only by biochemical markers of bone resorption and bone formation (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19) but also by histomorphometry (20). After an initial decline (12-14, 21, 22) BMD has increased in studies in which treatment with GH has continued for 12 months or more (14-16, 18, 19, 21, 23, 24).…”

Section: Introductionmentioning

confidence: 99%

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Effects of 42 months of GH treatment on bone mineral density and bone turnover in GH-deficient adults

Välimäki

Pi²,

Salmi³

et al. 1999

European Journal of Endocrinology

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Objective: To study the effects of GH treatment for up to 42 months on bone mineral density (BMD) and bone turnover. Design and methods: BMD with dual energy X-ray absorptiometry, serum type I procollagen carboxyterminal propeptide (PICP), serum type I collagen carboxy-terminal telopeptide (ICTP) and serum IGF-I were assessed in 71 adults with GH deficiency. There were 44 men and 27 women, aged 20 to 59 (median 43) years. Thirty-two patients completed 36 months and 20 patients 42 months of treatment. Results:The BMD increased for up to 30-36 months and plateaued thereafter. In the whole study group, the maximum increase of BMD was 5.0% in the lumbar spine (P < 0.001), 5.9% (P < 0.01) in the femoral neck, 4.9% (NS, P > 0.05) in the Ward's triangle and 8.2% (P < 0.001) in the trochanter area. The serum concentrations of PICP (202.6 Ϯ 11.5 vs 116.3 Ϯ 5.4 mg/l; mean -Ϯ S.E.M.) and ICTP (10.5 Ϯ 0.6 vs 4.4 Ϯ 0.3 mg/l) doubled (P < 0.001) during the first 6 months of GH treatment but returned to baseline by the end of the study (130.0 Ϯ 10.4 and 5.6 Ϯ 0.7 mg/l respectively), despite constantly elevated serum IGF-I levels (39.6 Ϯ 4.1 nmol/l at 42 months vs 11.9 Ϯ 0.9 nmol/l at baseline; P < 0.001). The responses to GH treatment of serum IGF-I, PICP, ICTP (P < 0.001 for all; ANOVA) and of the BMD in the lumbar spine (P < 0.05), in the femoral neck and the trochanter (P < 0.001 for both) were more marked in men than in women. At the end of the study the BMD had increased at the four measurement sites by 5.7-10.6% (P < 0.01-0.001) in patients with at least osteopenia at baseline and by 0.1-5.3% (NS P < 0.05) in those with normal bone status (P < 0.001 for differences between groups; ANOVA). Among patients who completed 36-42 months of treatment, the number of those with at least osteopenia was reduced to more than a half. The response of BMD to GH treatment was more marked in young than in old patients at three measurement sites (P < 0.05-<0.001; ANOVA). In the multiple regression analysis the gender and the pretreatment bone mass appeared to be independent predictors of three measurement sites, whereas the age independently determined only the vertebral BMD. Conclusions: GH treatment in GH-deficient adults increased BMD for up to 30-36 months, with a plateau thereafter. Concurrently with the plateau in BMD the bone turnover rate normalized. From the skeletal point of view GH-deficient patients exhibiting osteopenia or osteoporosis should be considered as candidates for GH supplementation of at least 3-4 years.

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“…As previously observed (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19), the markers of bone turnover increased in response to GH. To reflect bone formation we measured serum PICP.…”

Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effects of 42 months of GH treatment on bone mineral density and bone turnover in GH-deficient adults

Välimäki

Pi²,

Salmi³

et al. 1999

European Journal of Endocrinology

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“…Short-term trials [44,[56][57][58][59], 6-18 months in adults with adult onset GHD, have failed to show any increase in BMC or BMD. In contrast, in the longest placebo-controlled trial reported so far (18 months), Baum et al [60], reported a significant increase in BMD in lumbar spine and Fig.…”

Section: Effects Of Gh Transgenic Micementioning

confidence: 99%

GH and Bone-Experimental and Clinical Studies

et al. 2000

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Regulation of bone mass by growth hormone

Olney

2003

Med. Pediatr. Oncol.

128

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Growth hormone (GH) is a peptide hormone secreted from the pituitary gland under the control of the hypothalamus. It has a many actions in the body, including regulating a number of metabolic pathways. Some, but not all, of its effects are mediated through insulin-like growth factor-I (IGF-I). Both GH and IGF-I play significant roles in the regulation of growth and bone metabolism and hence are regulators of bone mass. Bone mass increases steadily through childhood, peaking in the mid 20s. Subsequently, there is a slow decline that accelerates in late life. During childhood, the accumulation in bone mass is a combination of bone growth and bone remodeling. Bone remodeling is the process of new bone formation by osteoblasts and bone resorption by osteoclasts. GH directly and through IGF-I stimulates osteoblast proliferation and activity, promoting bone formation. It also stimulates osteoclast differentiation and activity, promoting bone resorption. The result is an increase in the overall rate of bone remodeling, with a net effect of bone accumulation. The absence of GH results in a reduced rate of bone remodeling and a gradual loss of bone mineral density. Bone growth primarily occurs at the epiphyseal growth plates and is the result of the proliferation and differentiation of chondrocytes. GH has direct effects on these chondrocytes, but primarily regulates this function through IGF-I, which stimulates the proliferation of and matrix production by these cells. GH deficiency severely limits bone growth and hence the accumulation of bone mass. GH deficiency is not an uncommon complication in oncology and has long-term effects on bone health.

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The effects of prolonged growth hormone replacement on bone metabolism and bone mineral density in hypopituitary adults*

Abstract: Replacement therapy with GH in hypopituitary adults for 6-18 months produced a sustained increase in bone turnover (both formation and resorption). Bone mass was maintained but did not increase over the study period.

Cited by 62 publications

References 33 publications

Effects of 42 months of GH treatment on bone mineral density and bone turnover in GH-deficient adults

Effects of 42 months of GH treatment on bone mineral density and bone turnover in GH-deficient adults

GH and Bone-Experimental and Clinical Studies

Regulation of bone mass by growth hormone

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