Article Text

Bone mineral density in Crohn’s disease
  1. F J COWAN,
  2. J W GREGORY,
  3. H R JENKINS
  1. University Hospital of Wales,
  2. Heath Park,
  3. Cardiff CF4 4XW, UK
  1. Dr Cowan.
  1. J JAHNSEN,
  2. J A FALCH,
  3. E AADLAND
  1. Medical Department,
  2. Aker University Hospital,
  3. Oslo, Norway

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    Editor,—We were interested to read the recent article by Jahnsen et al (Gut 1997;40: 313–9). We have just published a similar study investigating the bone mineral content (BMC) of children with inflammatory bowel disease (IBD),1 and have also found that BMC was reduced in those with Crohn’s disease but not in those with ulcerative colitis. No relation could be found between BMC and disease duration, disease activity, or biomedical markers of bone metabolism. There was, however, a significant relation between reduction in bone mineralisation and steroid usage, as also noted by Jahnsen et al. Although BMC was significantly lower in the children treated with steroids, there was no association with magnitude of steroid use in either dosage or duration. We postulated that the steroid effect was an all or nothing effect, or that the use of steroids acts as a marker for other variables, such as worsening disease activity. We agree that screening of bone mineral status in an important aspect of continuing care in patients with IBD and would like to emphasise that children are not immune to the osteopenic side effects of IBD.

    References

    Reply

    Editor,—We are grateful to Drs Cowan, Gregory and Jenkins for their interest and comments on our study. Crohn’s disease is obviously a more severe systemic disease than ulcerative colitis and surprisingly most studies have failed to demonstrate a difference in bone mineral density between the two patient groups.

    The adverse effects of corticosteroids on bone density are well recognised. However, published studies provide conflicting results on the association between steroid treatment and bone mineral density in patients with IBD.1-1 1-2 The cumulative steroid dose is usually calculated retrospectively from medical records and indeed this method is uncertain as treatment is intermittent and of varying length and dose. Inaccurate estimation of the total steroid dose may have contributed to the conflicting results reported in the literature on this issue.

    We fully agree that steroid use (but also total lifetime dose) might reflect other variables connected to the intestinal illness which impact on bone mineralisation, such as disease activity.

    References

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