title: Reduced bone density in patients with inflammatory bowel disease.
abstract: BACKGROUND
  Reduced bone mineral density in patients with inflammatory bowel disease is thought to be due to disturbances in calcium homeostasis or the effects of corticosteroid treatment.
  
  
  OBJECTIVE
  To assess the prevalence and mechanism of reduced bone mineral density in 79 patients with inflammatory bowel disease (44 with Crohn's disease, 35 with ulcerative colitis) who did not have significant risk factors for low bone densities.
  
  
  METHODS
  Dual x ray absorptiometry was used to measure bone mineral density and serum and urinary markers of osteoblast (alkaline phosphatase, procollagen 1 carboxy terminal peptide and osteocalcin) and osteoclast (pyridinoline, deoxypyridinoline, and type 1 collagen carboxy terminal peptide) activities to assess bone turnover.
  
  
  RESULTS
  There was a high prevalence of low bone mineral density (prevalence of T scores < -1.0 from 51%-77%; T scores < -2.5 (osteoporosis) from 17%-28%) with hips being more often affected than vertebrae (p < 0.001). Reduced bone mineral density did not relate to concurrent or past corticosteroid intake, or type, site, or severity of disease. Whereas calcium homeostasis was normal, bone markers showed increased bone resorption without a compensatory increase in bone formation.
  
  
  CONCLUSIONS
  The greater prevalence of reduced hip bone mineral density, as opposed to vertebral, mineral density and the pattern of a selective increase in bone resorption contrasts with that found in other known causes of metabolic bone disease.
authors.affiliation: Department of Clinical Biochemistry, King's College Hospital, London.
authors.forename: I
authors.initials: I
authors.lastname: Bjarnason
authors.forename: A
authors.initials: A
authors.lastname: Macpherson
authors.forename: C
authors.initials: C
authors.lastname: Mackintosh
authors.forename: M
authors.initials: M
authors.lastname: Buxton-Thomas
authors.forename: I
authors.initials: I
authors.lastname: Forgacs
authors.forename: C
authors.initials: C
authors.lastname: Moniz
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D000596:Amino Acids / Q000652:urine; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D015519:Bone Density; D001862:Bone Resorption; D003093:Colitis, Ulcerative / Q000378:metabolism / Q000503:physiopathology*; D003424:Crohn Disease / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010384:Pelvic Bones / Q000503:physiopathology; D010446:Peptide Fragments / Q000097:blood; D011239:Prednisolone / Q000627:therapeutic use; D015995:Prevalence; D011347:Procollagen / Q000097:blood; D013131:Spine / Q000503:physiopathology
chemical_list: D000596:Amino Acids; D000893:Anti-Inflammatory Agents; D010446:Peptide Fragments; D011347:Procollagen; C042813:procollagen type I carboxy terminal peptide; D015675:Osteocalcin; C015484:pyridinoline; C036020:deoxypyridinoline; D011239:Prednisolone; D000469:Alkaline Phosphatase