Skeletal response to recombinant human growth hormone (rhGH) in children treated with long-term corticosteroids

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Abstract
Corticosteroid therapy causes osteopenia and growth retardation in children; such changes are associated with diminished rates of bone formation and turnover. Since growth hormone activates bone remodeling, the biochemical and skeletal responses to rhGH were evaluated in four pediatric patients, aged 12.8 ± 3 years, with long‐term corticosteroid use (5 ± 2 years). Recombinant human growth hormone (rhGH), 0.125 mg/kg, was given 3 times/week by subcutaneous injection for 12 months. Iliac crest bone biopsies were obtained after double tetracycline labeling before and at the end of rhGH therapy; serum levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone (intact), 25‐hydroxyvitamin D, 1,25‐dihydroxyvitamin D3, osteocalcin (BGP), and insulin‐like growth factor‐1 (IGF‐1) were measured every 3 months during the treatment period. The average dose of prednisone was 0.24 ± 0.05 mg/kg/day initially, and this did not change during the study. Serum calcium, phosphorus, alkaline phosphatase, 25‐hydroxyvitamin D, 1,25‐dihydroxyvitamin D3, and BGP were unchanged during the rhGH therapy, but the serum IGF‐1 level increased by 71%, p < 0.01. Eroded bone perimeter and cancellous bone area did not change significantly during rhGH therapy. Bone formation rates rose from 423 ± 475 to 781 ± 407 μm2/mm2/day, p < 0.05, and the length of double tetracycline‐labeled bone perimeter increased by 85%, p < 0.05. The bone formation rate in the growth hormone group exceeded the values of an age‐matched reference group (143 ± 3 years), 780 ± 407 μm2/mm2/day versus 411 ± 479 μ m2/mm2/day, p < 0.05. Thus, rhGH therapy increases osteoblastic activity, bone formation, and possibly bone turnover despite continued and prolonged corticosteroid administration in children.
Funding Information
  • USPHS (DK-35423, RR-00865, Genentech)
  • National Kidney Foundation of Southern California