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Letter
Authors' response: the role of risedronate in osteopenia in Crohn's disease
  1. Ad A van Bodegraven1,
  2. Birgit I Witte2,
  3. Paul Lips3
  4. for the Crohn and Bone Study Group of the Dutch Initiative on Crohn and Colitis (ICC)
  1. 1 Department of Gastroenterology and Hepatology, VUmc, Amsterdam, The Netherlands
  2. 2 Department of Epidemiology and Biostatistics, VUmc, Amsterdam, The Netherlands
  3. 3 Endocrine Section, Department of Internal Medicine, VUmc, Amsterdam, The Netherlands
  1. Correspondence to Dr Ad A van Bodegraven, Department of Gastroenterology and Hepatology, VUmc, PO Box 7057, Amsterdam 1007 MB, The Netherlands; v.bodegraven{at}vumc.nl

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We read with interest the comments of Buchan and Manuel concerning our risedronate intervention trial in osteopenic patients with Crohn's disease.1 ,2

They stipulated that exclusion of patients with vitamin D deficiency limited the significance of the performed study, as this deficiency is frequently observed in Crohn's disease. It is however well known that replenishment of vitamin D (and calcium) in patients with vitamin D deficiency would lead to a rapid improvement of bone density, irrespective of any effect of risedronate. As assessment of a therapeutic effect of the latter was our primary study aim, we decided to exclude patients with vitamin D deficiency.

In addition to their observation that present-day treatment strategies for osteopenia in patients with Crohn's disease are primarily based on suboptimal study data, a recent meta-analysis from 19 randomised controlled trials concerning low bone mineral density in patients with IBD, though not including our currently published study, was performed leading to the conclusion that particularly bisphosphonates improved bone density, and appeared to reduce the risk of vertebral fractures, in agreement with our assumption that treatment with risedronate in osteopenic patients with Crohn's disease may be beneficial.3 This conclusion was, in a different context, debated in a considered Commentary on our trial in Gut by Bernstein et al.4 These authors questioned whether risedronate might be worthwhile in patients with Crohn's disease, partly based on calculations in a presupposed case using the Dutch FRAX tool, an instrument predominantly validated in 65-year-old and older patients from the Rotterdam study regarding hip fractures, and strongly predisposed by age as the main risk factor.5 Their FRAX-based hip-fracture risk calculation seems, therefore, inapt for the studied Crohn's disease population, in which we observed a predominant favourable effect of risedronate on the vertebral bone density. Although we agree with these authors that the current trial showed limited effects on bone density over a 2-year period, when compared with placebo or anti-inflammatory therapy of Crohn's disease only,6 we underline that, given the increased incidence and prevalence of bone fractures in patients with Crohn's disease,7 adherence to risk stratification applicable to the non-IBD setting may be leading to undertreatment of this population at risk. Timely assessment of bone density (dual X-ray absorptiometry) in these patients appears reasonable. In particular if a combination of established risk factors for osteoporotic fractures and chronically active or aggressive Crohn's disease occurs, early treatment with risedronate may be warranted. As with all intervention trials based on bone density outcome measures, prospective studies assessing fracture rate would be preferable, but undoubtedly, this is challenging to perform because of the high patient number needed.

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Footnotes

  • Correction notice The title of this letter has changed since published Online First.

  • Contributors AAvB, BIW and PL prepared the letter of response. All subsequent authors critically reviewed the letter and approved its contents.

  • Competing interests None.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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