title: Effect of long-term growth-hormone substitution therapy on bone mineral density and parameters of bone metabolism in adult patients with growth hormone deficiency.
abstract: Reduced bone mineral density (BMD) and the prevalence for osteoporotic vertebral fractures are symptoms of growth hormone deficiency (GHD) syndrome, and GH replacement therapy is now available for GH-deficient adults. We investigated the long-term effects of GH replacement therapy on bone mineral density (BMD) and bone metabolism in 19 adult patients with GHD over a period of 18 months. In response to GH treatment, the initially decreased IGF-I concentrations rose significantly during 18 months of therapy to levels within the normal range (matched for sex and age) (mean change 158.1 +/- 50.8 ng/ml, P < 0.001). Parameters of bone formation such as osteocalcin (OC) and procollagen I-C-Peptide (PICP) showed a significant increase in the first 6 months of therapy, followed by a slight decrease in the next months. Markers of bone resorption (CrosslapsR and deoxypyridinoline (D-Pyr) also increased significantly with a peak value after 6 months and all parameters except PICP remained above baseline values after 18 months. BMD of the femoral neck (FN) showed an increase after 18 months of therapy (mean change 0.01 +/- 0.03 g/cm2 after 18 months, n.s.). However, the increase in BMD was significant only in the lumbar spine (LS) (mean change 0.03 +/- 0.04 g/cm2, P < 0.05 after 18 months). We conclude that GH replacement therapy in adult patients with GHD over a period of 18 months causes a pronounced increase in bone turnover mainly during the first 12 months of therapy and increases BMD of the lumbar spine and the femoral neck after 18 months.
authors.affiliation: Division of Endocrinology, Department of Medicine III, University of Vienna, Währinger Gürtel 18-20 A-1090 Vienna, Austria.
authors.forename: H
authors.initials: H
authors.lastname: Kotzmann
authors.forename: M
authors.initials: M
authors.lastname: Riedl
authors.forename: P
authors.initials: P
authors.lastname: Bernecker
authors.forename: M
authors.initials: M
authors.lastname: Clodi
authors.forename: F
authors.initials: F
authors.lastname: Kainberger
authors.forename: A
authors.initials: A
authors.lastname: Kaider
authors.forename: W
authors.initials: W
authors.lastname: Woloszczuk
authors.forename: A
authors.initials: A
authors.lastname: Luger
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood / Q000187:drug effects; D000596:Amino Acids / Q000187:drug effects / Q000652:urine; D015519:Bone Density / Q000187:drug effects*; D001846:Bone Development / Q000187:drug effects*; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism*; D003094:Collagen / Q000187:drug effects / Q000652:urine; D003404:Creatinine / Q000652:urine; D004311:Double-Blind Method; D005260:Female; D005272:Femur Neck / Q000187:drug effects; D006130:Growth Disorders / Q000188:drug therapy; D013006:Growth Hormone / Q000172:deficiency* / Q000627:therapeutic use*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000187:drug effects / Q000378:metabolism; D008159:Lumbar Vertebrae / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood / Q000187:drug effects; D010281:Parathyroid Hormone / Q000097:blood; D010446:Peptide Fragments / Q000097:blood / Q000187:drug effects; D011347:Procollagen / Q000097:blood / Q000187:drug effects; D013997:Time Factors; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D000596:Amino Acids; D010281:Parathyroid Hormone; D010446:Peptide Fragments; D011347:Procollagen; C042813:procollagen type I carboxy terminal peptide; D015675:Osteocalcin; D014807:Vitamin D; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; C036020:deoxypyridinoline; D003094:Collagen; C104450:25-hydroxyvitamin D; D003404:Creatinine; D000469:Alkaline Phosphatase