Bone mineral density in patients with inflammatory bowel disease: A population-based prospective two-year follow-up study

Background: Bone loss and osteoporosis are commonly reported in inflammatory bowel disease (CD), especially Crohn disease (CD). The aims of the present study were to evaluate changes in bone mineral density (BMD) in IBD patients during a 2-year follow-up period, and to investigate the role played by possible contributing factors in bone loss. Methods: Sixty patients with CD and 60 with ulcerative colitis (UC) were studied initially. Fifty-five CD and 43 UC patients were re-examined after I year, and 50 CD and 44 UC patients after 2 years. Lumbar spine, femoral neck and total body BMD were measured by dual X-ray absorptiometry (DXA), and Z scores were obtained by comparison with age-matched and sex-matched healthy subjects. Biochemical variables were assessed at inclusion and at the 1-year follow-up visit. Results: Mean BMD values were unchanged in both CD and UC patients. In patients with repeated measurements, significant differences in Z scores (DeltaZ score) were found for femoral neck and total body in CD and for total body in UC. Significant bone loss occurred in 11 CD (22%) and 12 UC (27%) patients. A significant increase in BMD was found in 21 CD (42%) and 20 UC (46%) patients. In CD patients the initial BMD values for lumbar spine and femoral neck were inversely correlated to BMD changes at the same sites and the change in body mass index (BMI) was positively correlated to change in the total body BMD. C-reactive protein was significantly higher in CD patients with bone loss. Biochemical markers of bone metabolism could not be used to predict BMD changes. Although it was not significant, there was a relationship between corticosteroid therapy and bone loss in CD. Conclusions: Only minor changes in BMD were observed in both CD and UC patients during a 2-year period. The multifactorial pathogenesis of bone loss in IBD makes it difficult to assess the importance of each single contributing factor. However, our results indicate that disease activity and corticosteriod therapy are involved in bone loss in CD patients.