Rapid hip bone loss in active Crohn’s disease patients receiving short-term corticosteroid therapy J. H. TOBIAS, M. R. SASI, R. GREENWOOD & C. S. J. PROBERT Department of Clinical Science at South Bristol, University of Bristol, Bristol, UK Accepted for publication 6 August 2004 SUMMARY Background: Uncertainty over whether corticosteroids cause bone loss in patients with Crohn’s disease may reflect their short, intermittent use. Aim: We investigated whether a 2-month course of prednisolone is associated with detectable bone loss. Methods: Fifteen patients with active Crohn’s disease and 19 controls with inactive Crohn’s disease were recruited. Bone mineral density of the lumbar spine and hip was measured at baseline and 2 and 8 months. Results: At 2 months, significant bone loss was found in patients with active disease (femoral neck )2.7%, P < 0.002; Ward’s triangle )3.9%, P < 0.01). Although bone mineral density was still lower at 8 months, these differences were no longer significant ()1.3% and )3.4%, femoral neck and Ward’s triangle, respectively). No significant change in hip bone mineral density was observed in controls. Previous corticoster- oid use was not significantly associated with baseline bone mineral density, although significant independent associations were observed between weight, site of disease and lumbar spine bone mineral density, and between dietary calcium deficiency and femoral neck and Ward’s triangle bone mineral density. Conclusion: Significant bone loss at the hip can be detected in patients receiving corticosteroid treatment for 2 months for active Crohn’s disease ; however, it remains unclear whether this is because of disease activity or its treatment. This rapid bone loss may represent a risk factor for fracture and justify bone protective therapy. INTRODUCTION Patients with inflammatory bowel disease (IBD) are at increased risk of sustaining fractures at several sites including the spine and hip. 1, 2 Although Crohn’s disease (CD) and ulcerative colitis (UC) are both associated with an increased fracture risk, the risk of hip fracture appears to be higher in the former. 2 Several studies suggest that IBD patients are at a higher risk of fracture, on the basis of a reduced bone mineral density (BMD), compared with controls. This decrease appears to be the most marked in patients with CD and occurs both at the lumbar spine and hip. 3–5 In terms of the mechanisms responsible for the increased fracture risk in IBD, CS therapy has been found to be associated with an increased risk of fracture in these patients after adjusting for disease severity. 2 That CS therapy contri- butes to the elevated fracture risk in IBD is consistent with previous findings that the risk of fracture is increased in patients receiving CS treatment in a range of disease settings. 6 Several investigations have also found that CS therapy is associated with low BMD in IBD patients. 4, 5, 7–9 However, these effects on BMD are generally small and were not observed in several other studies. 3, 10–12 Any difficulty in detecting bone loss in IBD as a consequence of CS treatment may reflect the short duration of CS therapy used in this condition, which is typically 2 months. Rapid bone loss has previously been Correspondence to: Dr C. S. J. Probert, Department of Gastroenterology, Bristol Royal Infirmary, Bristol BS2 8HW, UK. E-mail: c.s.j.probert@bristol.ac.uk Aliment Pharmacol Ther 2004; 20: 951–957. doi: 10.1111/j.1365-2036.2004.02207.x Ó 2004 Blackwell Publishing Ltd 951