title: Bone mineral density in patients with growth hormone deficiency: does a gender difference exist?
abstract: OBJECTIVE
  The aim of the study was to clarify whether a gender difference exists with respect to bone mineral density (BMD) and bone mineral content (BMC) in adult patients with growth hormone deficiency (GHD).
  
  
  METHODS
  A case-control design.
  
  
  METHODS
  Blood sampling for measurements of calcium, phosphate, creatinine, PTH, vitamin D, IGF-1, markers of bone formation and bone resorption, and dual energy X-ray absorptiometry (DEXA), to determine BMD and BMC of the lumbar spine, hip, distal arm and total body, were performed in 34 patients with GHD (19 females) and 34 sex-, age- and weight-matched healthy control subjects. The patients were well substituted on all pituitary axes, apart from GH.
  
  
  RESULTS
  GH-deficient males had significantly lower BMD in the lumbar spine (P = 0.02), hip (P = 0.01) and total body (P = 0.003) than healthy males while GH-deficient females compared to healthy females had identical BMD values at all regions. This gender difference was even more obvious when BMD values were expressed as Z-scores or as three-dimensional BMD of the total body. The bone formation and bone resorption markers, as well as calcium and vitamin D, were all at the same levels in GH-deficient and healthy males, indicating identical bone turnover. The GH-deficient females, however, had significantly lower levels of bone markers compared to healthy females, indicating a reduced bone turnover. Oestrogen substitution of the GH-deficient females could explain this difference.
  
  
  CONCLUSIONS
  Compared to healthy control subjects GH-deficient males had, in contrast to GH-deficient females, significantly reduced BMD and BMC. This obvious gender difference seems to be caused by the oestrogen substitution given to the females, compensating for the lack of GH, an effect testosterone does not seem to possess.
authors.affiliation: Medical Department, Roskilde County Hospital, Köge, Denmark.
authors.forename: Mette Friberg
authors.initials: MF
authors.lastname: Hitz
authors.forename: Jens-Erik Beck
authors.initials: JE
authors.lastname: Jensen
authors.forename: Peter C
authors.initials: PC
authors.lastname: Eskildsen
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015519:Bone Density; D016723:Bone Remodeling; D002117:Calcitriol / Q000097:blood; D016022:Case-Control Studies; D024042:Collagen Type I / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D011347:Procollagen / Q000097:blood; D012737:Sex Factors; D013004:Somatostatin / Q000097:blood / Q000172:deficiency*; D018709:Statistics, Nonparametric
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D010281:Parathyroid Hormone; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C047202:procollagen Type I N-terminal peptide; D015675:Osteocalcin; D004958:Estradiol; D013004:Somatostatin; D007334:Insulin-Like Growth Factor I; D000469:Alkaline Phosphatase; D002117:Calcitriol