title: Use of risedronate to prevent bone loss following a single course of glucocorticoids: findings from a proof-of-concept study in inflammatory bowel disease.
abstract: CONCLUSIONS
  We performed a randomised controlled trial (RCT) to determine whether risedronate 35 mg once weekly prevents bone loss following an 8-week reducing course of prednisolone given for an exacerbation of inflammatory bowel disease (IBD). The greatest change in bone mineral density (BMD) was at Ward's triangle (WT), which fell by 2.2% in the placebo group, compared with a reduction of 0.8% in the risedronate group.
  
  
  BACKGROUND
  Whether bisphosphonates can prevent bone loss associated with intermittent glucocorticoid (GC) therapy is unknown, reflecting the difficulty in performing RCTs in this context.
  
  
  METHODS
  To explore the feasibility of RCTs to examine this question, lumbar spine (LS; L2-4) and hip dual X-ray absorptiometry (DXA) scans were performed in 78 patients commencing a GC therapy course for a relapse of IBD. They were then randomised to receive placebo or risedronate 35 mg weekly for 8 weeks, after which the DXA scan was repeated.
  
  
  RESULTS
  For LS BMD, there was no change in the placebo group (0.1 +/- 0.4, p = 0.9), but there was an increase after risedronate (0.8 +/- 0.4, p = 0.04; mean% +/- SEM by paired Student's t test). There were small decreases in both groups at the total hip (-0.5 +/- 0.3, p = 0.04; -0.5 +/- 0.3, p < 0.05, placebo and risedronate, respectively). At WT, BMD fell after placebo (-2.2 +/- 0.5, p = 0.001) but not risedronate (-0.8 +/- 0.5, p = 0.09; p = 0.05 for between-group comparison).
  
  
  CONCLUSIONS
  RCTs can be used to examine whether bisphosphonates prevent bone loss associated with intermittent GC therapy, providing metabolically active sites such as WT are employed as the primary outcome.
authors.affiliation: Department of Clinical Sciences at South Bristol, University of Bristol, Bristol, UK.
authors.forename: M H
authors.initials: MH
authors.lastname: Kriel
authors.forename: J H
authors.initials: JH
authors.lastname: Tobias
authors.forename: T J
authors.initials: TJ
authors.lastname: Creed
authors.forename: M
authors.initials: M
authors.lastname: Lockett
authors.forename: J
authors.initials: J
authors.lastname: Linehan
authors.forename: A
authors.initials: A
authors.lastname: Bell
authors.forename: R
authors.initials: R
authors.lastname: Przemioslo
authors.forename: J E
authors.initials: JE
authors.lastname: Smithson
authors.forename: T N
authors.initials: TN
authors.lastname: Brooklyn
authors.forename: W D
authors.initials: WD
authors.lastname: Fraser
authors.forename: C S J
authors.initials: CS
authors.lastname: Probert
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D015519:Bone Density / Q000187:drug effects; D050071:Bone Density Conservation Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D004334:Drug Administration Schedule; D012968:Etidronic Acid / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D006621:Hip Joint / Q000503:physiopathology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy*; D008159:Lumbar Vertebrae / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D011239:Prednisolone / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use; D000068296:Risedronic Acid
chemical_list: D050071:Bone Density Conservation Agents; D005938:Glucocorticoids; D011239:Prednisolone; D000068296:Risedronic Acid; D012968:Etidronic Acid