Effect of growth hormone therapy on bone metabolism of growth hormone deficient children

Stamoyannou, Lela; Karachaliou, Feneli; Gioureli, E.; Voskaki, E.; Mengreli, C; Bartsocas, C. S.; Koutselinis, A.

doi:10.1007/s004310050671

Cited by 8 publications

(6 citation statements)

References 30 publications

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“…In addition, the serum calcium level demonstrated a slight decrease in the patient as in previously reported GHD patients after rhGH therapy [9]. The height velocity of the patient demonstrated improvement after levels of phosphate and vitamin D were increased.…”

Section: Discussionsupporting

confidence: 81%

Growth hormone therapy for a patient with idiopathic Fanconi syndrome and growth hormone deficiency

et al. 2017

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Section: Discussionsupporting

confidence: 81%

Growth hormone therapy for a patient with idiopathic Fanconi syndrome and growth hormone deficiency

et al. 2017

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“…In addition, Tobiume et al [8]found the mean SDS of serum bone-specific ALP in 20 GH-deficient children prior to GH therapy to be 0.6 less than that of controls. However, not all studies have reported reduced levels of bone remodelling markers, and it is thought that the wide range of values in the control groups and the small number of individuals with GHD included in these other studies [5, 11, 12]may have obscured differences between individuals with GHD and controls.…”

Section: Gh and Bone Biochemistrymentioning

confidence: 99%

“…The effects of increases in both bone formation and bone resorption on calcium and phosphate balance have been well studied [9, 11, 12, 15]. The changes are summarized in table 3.…”

Section: Gh and Bone Biochemistrymentioning

confidence: 99%

Bone Markers and Bone Mineral Density during Growth Hormone Treatment in Children with Growth Hormone Deficiency

Cowell¹,

Woodhead²,

Brody

2000

Horm Res Paediatr

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Growth hormone (GH) has a positive impact on muscle mass, growth and bone formation. It is known to interact with the bone-forming unit, with well-documented increases in markers of bone formation and bone resorption within weeks of the start of GH therapy. These changes relate significantly to short-term growth rate, but it is not evident that they predict long-term response to GH therapy. The consequences of GH deficiency (GHD) and GH replacement therapy on bone mineral density (BMD) have been difficult to interpret in children because of the dependency of areal BMD on height and weight. Some studies have tried to overcome this problem by calculating volumetric BMD, but results are conflicting. The attainment of a normal peak bone mass in an individual is considered important for the future prevention of osteoporosis. From the limited data available, it appears difficult to normalize bone mass totally in GH-deficient individuals, despite GH treatment for long periods. Studies to date examining the interaction between GH and bone have included only small numbers of individuals, making it difficult to interpret the study findings. It is hoped that these issues can be clarified in future research by the direct measurement of bone density (using quantitative computer tomography). Mineralization is only one facet of bone strength, however; other important components (e.g. bone structure and geometry) should be addressed in future paediatric studies. Future studies could also address the importance of the degree of GHD in childhood; how GH dose and insulin-like growth factor-I levels achieved during therapy relate to the final outcome; whether or not the continuation of GH therapy after the attainment of final height may further enhance bone mass; whether the timing and dose of other treatments (e.g. sex hormone replacement therapy) are critical to the outcome; and whether GHD in childhood is associated with an increased risk of fracture.

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“…In healthy adult volunteers, rhGH administration corrected acidosis-induced hypophosphatemia due to cumulative renal phosphate retention and raised 1,25D levels while lowering parathyroid hormone (PTH) plasma levels [9]. Treatment with rhGH in GH-deficient children significantly decreased serum calcium levels and increased levels of phosphate, osteocalcin, 1,25D, and IGF-1 [26], while effects on PTH levels were variable [2,26]. Further, in children with idiopathic GH deficiency, rhGH raised plasma levels of osteocalcin, carboxyterminal propeptide of type I collagen (PICP), and alkaline phosphatase, indicators of bone formation, and, simultaneously, also increased levels of cross-linked telopeptide of collagen I (ICTP), a marker of bone reabsorption.…”

Section: Introductionmentioning

confidence: 98%

Growth in X-linked hypophosphatemic rickets

Ariceta

Langman

2006

Eur J Pediatr

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Growth failure appears frequently in children with X-linked hypophosphatemic rickets (XLHR) due to hypophosphatemia, disease severity, body disproportion, and primary bone abnormality. Recombinant human growth hormone (rhGH) increases phosphate tubular reabsorption and phosphate level in blood and, thus, constitutes an attractive but controversial therapy in short children with XLHR, those efficacy was demonstrated in small uncontrolled series. Our aim was to report our experience regarding growth in XLHR. Twenty-seven children with XLHR--20 girls, seven boys--diagnosed at a median (md) of 1.46 years of age, (range 0.39-8.5 years), were studied at 10.12 years of age (1.58-18.56), md (range). All received oral treatment with phosphate and calcitriol. At the first visit, grouped Z-height was -1; (-4.58; 0.54) md (range). After 5 years' follow-up (0.92-15.6), Z-height was -0.91 (- 4.56; 0.17), not different from that at baseline (P = 0.465). In 16 children entirely controlled in our program upon presentation, a "catch up" phenomenon after the rickets had healed (P = 0.823) or throughout the long-term was not observed (P = 0.995). Eight patients had a Z-height 2 years at diagnosis, male gender and non-adherence to treatment. Four children, all boys, received rhGH, and in two cases with sufficient follow up stature normalized. No rhGH side effects were observed, and phosphate and calcitriol doses remained stable. Linear growth failure appeared in a third of XLHR children. Efforts need to be made to reduce the age of diagnosis and to improve adherence to treatment. Treatment with rhGH should be considered early, after the rickets has been controlled, in those patients with impaired growth or delayed diagnosis.

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Effect of growth hormone therapy on bone metabolism of growth hormone deficient children

Abstract: GH treatment significantly influences mineral metabolism and the measurement of TPO4/ GFR after 1 month of GH therapy may serve as a useful predictor of growth response to hGH therapy in GH-deficient children.

Cited by 8 publications

References 30 publications

Growth hormone therapy for a patient with idiopathic Fanconi syndrome and growth hormone deficiency

Growth hormone therapy for a patient with idiopathic Fanconi syndrome and growth hormone deficiency

Bone Markers and Bone Mineral Density during Growth Hormone Treatment in Children with Growth Hormone Deficiency

Growth in X-linked hypophosphatemic rickets

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