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Increased bone resorption in patients with Crohn’s disease

  1. Robinson1,
  2. Iqbal2,
  3. Abrams3,
  4. Al-Azzawi4,
  5. Mayberry1

Article first published online: 25 DEC 2001

DOI: 10.1046/j.1365-2036.1998.00364.x

Issue

Alimentary Pharmacology & Therapeutics

Alimentary Pharmacology & Therapeutics

Volume 12, Issue 8, pages 699–705, August 1998

Additional Information

How to Cite

Robinson, Iqbal, Abrams, Al-Azzawi and Mayberry (1998), Increased bone resorption in patients with Crohn’s disease. Alimentary Pharmacology & Therapeutics, 12: 699–705. doi: 10.1046/j.1365-2036.1998.00364.x

Author Information

  1. 1

    Gastrointestinal Research Unit, Leicester General Hospital,

  2. 2

    Department of Clinical Chemistry, Leicester Royal Infirmary,

  3. 3

    Department of Epidemiology and Public Health, University of Leicester,

  4. 4

    Department of Obstetrics & Gynaecology, Leicester Royal Infirmary, Leicester, UK

* Robinson Gastrointestinal Research Unit, Leicester General Hospital, Gwendolen Road, Leicester LE5 4PW, UK.

Publication History

  1. Issue published online: 25 DEC 2001
  2. Article first published online: 25 DEC 2001

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Background:

Patients with Crohn’s disease are at risk of osteoporosis and premature fracture. However, the pathophysiology underlying bone loss remains poorly understood and the optimum treatment has not been established.

Aim:

To investigate mechanisms of bone loss in Crohn’s disease using biochemical markers of bone turnover.

Methods:

Bone mineral density was measured at the hip and spine using dual-energy X-ray absorptiometry in 117 patients (48 male) with Crohn’s disease. Bone turnover was assessed by measuring serum osteocalcin (BGP), pro-collagen carboxy-terminal propeptide (PICP), bone specific alkaline phosphatase (BALP) and urinary deoxypyridinoline (DPD); and compared to age-matched healthy controls (n = 28).

Results:

Bone mineral density was reduced (z-score < −1) in 48 (41%) patients with Crohn’s disease. Mean values for bone formation markers in patients with Crohn’s disease were all within the normal reference range (BGP 8.92 (± 3.23) ng/mL (normal range 3.4–10.0), BALP 17.6 (± 12.6) U/L (normal range 11.6–43.3), PICP 95.1 (± 46.5) ng/mL (normal range 69–163)) and were not significantly different to the control population. However, mean urinary DPD was significantly higher in patients with Crohn’s disease compared to healthy controls (10.97 (± 9.22) n M DPD/m M creatinine vs. 5.02 (± 1.03) n M DPD/m M creatinine, difference in means = 5.95, 95% CI: −9.6 to −2.3, P = 0.00001) and compared to the UK reference range DPD levels were increased in 74 (63%) patients.

Conclusions:

Bone resorption as evidenced by urinary DPD was frequently increased in patients with Crohn’s disease and was significantly higher than in an age-matched control population. The high levels of urinary DPD suggest increased bone collagen degradation may contribute to osteoporosis in patients with Crohn’s disease. These results suggest anti-resorptive agents such as the bisphosphonates may be effective treatment for osteoporosis in Crohn’s disease.

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