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Bone density loss in Crohn’s disease: role of TNF and potential for prevention by bupropion
  1. R E Kast,
  2. E L Altschuler
  1. Department of Psychiatry, University of Vermont, Vermont, USA
  1. Correspondence to:
    Dr R E Kast
    Department of Psychiatry College of Medicine, University of Vermont, 2 Church St, Burlington, Vermont 05401, USA; rekastemail.com

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We note with interest the demonstration by Card et al that the increased hip fracture rate in Crohn’s disease (CD), and by inference the diminished bone density commonly noted in CD, is only to a minor degree secondary to iatrogenic corticosteroid use (Gut 2004;53;251–5). The subject of bone mineral density loss in CD has been recently reviewed; tumour necrosis factor α (TNF-α) is suspected of being an important mediator of this loss.1,2 Evidence has been published for localised overproduction of TNF-α being largely responsible for the bone loss seen in rheumatoid arthritis,3,4 psoriatic arthritis,5 multiple myeloma,6 hip prosthesis loosening,7 periodontal disease,8 and spondyloarthropathies.9 Anti-TNF-α antibody has been shown to slow the bone loss of spondyloarthropy9 and rheumatoid arthritis.3,10

We have found that the commonly used antidepressant bupropion can induce remission in CD11,12 and have found that bupropion can lower TNF-α levels.13 If bupropion is found to be effective in CD and to lower TNF-α levels in large trials, it might be considered for use in bone loss and osteoporosis, in CD or otherwise.

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