The bone mineral density in acquired growth hormone deficiency correlates with circulating levels of insulin‐like growth factor I

Johansson, Amanda; Burman, Pia; Westermark, Kerstin; Ljunghall, Sverker

doi:10.1111/j.1365-2796.1992.tb00613.x

Cited by 119 publications

(65 citation statements)

References 37 publications

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“…Bone mineral density determined by dual-energy X-ray absorptiometry and the plasma IGF-I level positively correlates in adults with aquired GH-deficiency [4]. Basal levels of plasma PICP, a bone formation marker, in GH-deficient adults were similar to those in control subjects in the present study.…”

Section: Discussionsupporting

confidence: 67%

Effect of Growth Hormone (GH) Replacement on Plasma Carboxy-Terminal Propeptide of Type I Procollagen (PICP) and Pyridinoline Cross-Linked Carboxyterminal Telopeptide of Type I Collagen (ICTP) levels in GH-Deficient Adult Patients

et al. 1998

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Section: Discussionsupporting

confidence: 67%

Effect of Growth Hormone (GH) Replacement on Plasma Carboxy-Terminal Propeptide of Type I Procollagen (PICP) and Pyridinoline Cross-Linked Carboxyterminal Telopeptide of Type I Collagen (ICTP) levels in GH-Deficient Adult Patients

et al. 1998

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“…173 Furthermore, both molecules stimulate bone growth and osteoblast activity in animals. 174,175 In some [176][177][178] but not all 179 studies, BMD of the LS was somewhat lower in untreated patients with adult-onset GH deficiency compared with normal subjects. The degree of osteopenia appears to correlate directly to the degree of GH deficiency.…”

Section: Evidence For Potential Usefulness Of Gh or Igf-1 As Anabolicmentioning

confidence: 99%

Targeting the osteoblast: approved and experimental anabolic agents for the treatment of osteoporosis

Toulis¹,

Anastasilakis²,

Polyzos³

et al. 2011

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targeting osteoblast may be the means of effectively improving both bone quality and mass, thus offering an intriguing alternative in the treatment of osteoporosis. Aside from injectable parathyroid hormone (PtH) and its novel preparations, PtH-related peptide (PtHrP), calcilytics, beta-adrenergic receptors, enhancement of Wnt signaling (mainly via sclerostin and Dickkopf-1 neutralization), regulation of low-density lipoprotein receptor-related protein (LPr) 5/osteoblast axis, activin, IGF-1, and bone morphogenic proteins (bMPs) are reviewed for their basic rationale and evidence of bone anabolic potential. sclerostin neutralizing antibody, teriparatide transdermal patch, and PtHrP (1-36) are currently at an advanced stage of research. safety and tissue specificity are the prerequisites in the development of a novel treatment, especially when addressing a chronic condition such as osteoporosis.

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“…Bone mineral density (BMD) is reduced in adults with growth hormone (GH) deficiency (1), especially in those with childhood-onset disease (2), but also in subjects who developed the deficiency in adulthood (3)(4)(5). As a consequence of low BMD, GH-deficient adults have a doubled fracture rate compared with healthy controls (6).…”

Section: Introductionmentioning

confidence: 99%

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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The bone mineral density in acquired growth hormone deficiency correlates with circulating levels of insulin‐like growth factor I

Cited by 119 publications

References 37 publications

Effect of Growth Hormone (GH) Replacement on Plasma Carboxy-Terminal Propeptide of Type I Procollagen (PICP) and Pyridinoline Cross-Linked Carboxyterminal Telopeptide of Type I Collagen (ICTP) levels in GH-Deficient Adult Patients

Effect of Growth Hormone (GH) Replacement on Plasma Carboxy-Terminal Propeptide of Type I Procollagen (PICP) and Pyridinoline Cross-Linked Carboxyterminal Telopeptide of Type I Collagen (ICTP) levels in GH-Deficient Adult Patients

Targeting the osteoblast: approved and experimental anabolic agents for the treatment of osteoporosis

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

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