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Exp Clin Endocrinol Diabetes 1994; 102(1): 44-49
DOI: 10.1055/s-0029-1211264
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© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Bone mineral density and calcium regulating hormones in patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis)

S. H. Scharla1 , H. W. Minne3 , U. G. Lempert1 , G. Leidig1 , M. Hauber1 , R. Raedsch2 , R. Ziegler1
  • 1Department of Internal Medicine I (Endocrinology & Metabolism), Germany
  • 2Department of Internal Medicine IV (Gastroenterology), University of Heidelberg, Germany
  • 3Klinik der Fürstenhof (Klinik für Stoffwechselkrankheiten des Skelettsystems, Endokrinologie, Orthopädie und Gynäkologie), Bad Pyrmont, Germany
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Publication History

Publication Date:
15 July 2009 (online)

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Summary

Inflammatory bowel disease (Crohn's disease and ulcerative colitis) is associated with decreased bone mineral density and increased risk of osteoporosis. However, the pathogenesis of this bone loss is not yet fully understood. In the present study we measured lumbar bone mineral density (by dual photon absorptiometry), serum levels of parathyroid hormone (PTH) and vitamin D metabolites, and serum markers of bone turnover (alkaline Phosphatase and osteocalcin) in 15 patients with Crohn's disease and in 4 patients with ulcerative colitis. The median duration of the disease was 4 years and the median lifetime Steroid dose was 10g of Prednisone. We compared our results to a control group of 19 normal persons, who were matched for age and sex to the patients. We found that lumbar bone density was reduced by 11% in patients compared with control persons (Z-score −0.6 ± 0.6 versus −0.1 ±0.8; p < 0.05). In patients, the serum levels of PTH, 25-hydroxyvitamin D3, and calcitriol (l,25(OH)2D3) were significantly reduced compared with control persons. Serum alkaline Phosphatase activity (AP) was significantly higher in the patients and was inversely related to lumbar bone density. Osteocalcin values were not different between patients and control persons. There was also no difference in serum levels of calcium between the two groups, whereas phosphorus levels were higher in patients. We conclude that malabsorption of calcium was not a primary cause of bone loss in our patients, because we did not find secondary hyperparathyroidism. Accordingly, we did not find a severe vitamin D deficiency, since 25hydroxyvitamin D3 levels were within the normal range. Therefore, our results favor the hypothesis that glucocorticoid therapy and/or the inflammatory process itself caused changes in bone metabolism leading to a negative bone balance with secondary reduction of PTH and calcitriol levels.

Key words

bone density - osteoporosis - Crohn's disease - parathyroid hormone - calcitriol

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