title: Fracture incidence in GH-deficient patients on complete hormone replacement including GH.
abstract: Fracture risk in GHD patients is not definitely established. Studying fracture incidence in 832 patients on GH therapy and 2581 matched population controls, we recorded a doubled fracture risk in CO GHD women, but a significantly lower fracture risk in AO GHD men.
  
  
  BACKGROUND
  The objective of this study was to evaluate fracture incidence in patients with confirmed growth hormone deficiency (GHD) on replacement therapy (including growth hormone [GH]) compared with population controls, while also taking potential confounders and effect modifiers into account.
  
  
  METHODS
  Eight hundred thirty-two patients with GHD and 2581 matched population controls answered a questionnaire about fractures and other background information. Incidence rate ratio (IRR) and 95% CI for first fracture were estimated. The median time on GH therapy for childhood onset (CO) GHD men and women was 15 and 12 yr, respectively, and 6 and 5 yr for adult onset (AO) GHD men and women, respectively.
  
  
  RESULTS
  A more than doubled risk (IRR, 2.29; 95% CI, 1.23-4.28) for nonosteoporotic fractures was recorded in women with CO GHD, whereas no risk increase was observed among CO GHD men (IRR, 0.61) and AO GHD women (IRR, 1.08). A significantly decreased incidence of fractures (IRR, 0.54; 95% CI, 0.34-0.86) was recorded in AO GHD men.
  
  
  CONCLUSIONS
  Increased fracture risk in CO GHD women can most likely be explained by interaction between oral estrogen and the GH-IGF-I axis. The adequate substitution rate of testosterone (90%) and GH (94%) may have resulted in significantly lower fracture risk in AO GHD men.
authors.affiliation: Department of Internal Medicine, Centralsjukhuset, Kristianstad, Sweden.
authors.forename: Helene
authors.initials: H
authors.lastname: Holmer
authors.forename: Johan
authors.initials: J
authors.lastname: Svensson
authors.forename: Lars
authors.initials: L
authors.lastname: Rylander
authors.forename: Gudmundur
authors.initials: G
authors.lastname: Johannsson
authors.forename: Thord
authors.initials: T
authors.lastname: Rosén
authors.forename: Bengt-Ake
authors.initials: BA
authors.lastname: Bengtsson
authors.forename: Marja
authors.initials: M
authors.lastname: Thorén
authors.forename: Charlotte
authors.initials: C
authors.lastname: Höybye
authors.forename: Marie
authors.initials: M
authors.lastname: Degerblad
authors.forename: Margareta
authors.initials: M
authors.lastname: Bramnert
authors.forename: Erik
authors.initials: E
authors.lastname: Hägg
authors.forename: Britt Edén
authors.initials: BE
authors.lastname: Engström
authors.forename: Bertil
authors.initials: B
authors.lastname: Ekman
authors.forename: Karl-Göran
authors.initials: KG
authors.lastname: Thorngren
authors.forename: Lars
authors.initials: L
authors.lastname: Hagmar
authors.forename: Eva-Marie
authors.initials: EM
authors.lastname: Erfurth
mesh_terms: D000293:Adolescent; D000328:Adult; D002648:Child; D005260:Female; D050723:Fractures, Bone / Q000453:epidemiology* / Q000209:etiology / Q000517:prevention & control; D020249:Hormone Replacement Therapy; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D007018:Hypopituitarism / Q000188:drug therapy* / Q000453:epidemiology; D015994:Incidence; D008297:Male; D012307:Risk Factors; D012737:Sex Factors; D013548:Sweden; D013739:Testosterone / Q000627:therapeutic use*
chemical_list: D019382:Human Growth Hormone; D013739:Testosterone