Assessment of bone and mineral metabolism in inflammatory bowel disease: case series and review.

OBJECTIVE

To determine the prevalence of low bone mass, fractures, and vitamin D deficiency and the levels of biochemical markers of mineral metabolism in patients with inflammatory bowel disease (IBD).

METHODS

Our retrospective study consisted of 30 patients with Crohn's disease (CD) and 18 patients with ulcerative colitis (UC). Dual-energy x-ray absorptiometry was performed to determine bone mineral density at the lumbar spine and hip. Serum calcium, phosphorus, parathyroid hormone, 25-hydroxyvitamin D (25-OHD), and 1,25-dihydroxyvitamin D, urinary N-telopeptide cross-linked collagen type I, and 24-hour urinary calcium levels were evaluated.

RESULTS

On the basis of Z-score definitions of low bone mass in the IBD group as a whole, 13 patients (27%) had low bone mass at the lumbar spine. Similarly, at the femoral neck, 13 patients (27%) had low bone mass. There was a higher prevalence of low bone mass in the UC group than in the CD group, consistent with a high prevalence of fractures in that group. Of all patients with IBD, 65% had a history of fractures, of which 23% were atraumatic. Deficiency of 25-OHD was high, with a prevalence of 55% in patients with UC and 83% in patients with CD. Secondary hyperparathyroidism, defined as a parathyroid hormone level >55 pg/mL in conjunction with a low or normal serum calcium and a low 25-OHD level, was present in 50% of patients with CD and only 7% of patients with UC.

CONCLUSION

Metabolic bone disease and fractures are common in IBD. The mean bone mineral density of the spine or femoral neck did not differ significantly between patients with CD and those with UC. Patients with UC had a higher prevalence of low bone mass, as defined by a Z-score of less than -2, than did patients with CD, consistent with a high prevalence of fractures in the UC group. In contrast, hyperparathyroidism attributable to vitamin D deficiency was more prevalent in patients with CD than in those with UC. This finding suggests a different etiologic mechanism of low bone mass in patients with CD.