Negative impact of Crohn's disease on bone mineral mass.
Prolonged chronic inflammation and corticosteroid therapy increase the risk of osteoporosis in patients with Crohn's disease. It has been estimated that 30% of these patients, who take steroids for prolonged periods, will suffer a vertebral fracture. Patients with Crohn's disease are difficult to wean from corticosteroids and therefore are at risk of developing bone complications. The purpose of this cross-sectional study was to examine the relationship between cumulative steroid dose, duration of the disease and the development of osteopenia in patients with Crohn's disease. We studied 28 patients (17 men, 11 women) with Crohn's disease: eight had one or more bowel resections and all the women were premenopausal. Serum calcium, phosphate, total alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), 25(OH)Vitamin D(3) and 1,25 (OH)(2) Vitamin D(3) were measured by autoanalyser methods or radioimmunoassay. Bone mineral density (BMD) was studied using dual energy X-ray bone absorptiometry of the lumbar spine (L2-L4) and the femoral neck. Of these 28 patients, 27 received an average of 17.3 +/- 21.7 g (range 1 to 80) g of prednisone over a period of 4 to 216 months. Fourteen out of the 28 patients had mildly diminished bone density (z-score >-2.5 SD and < -1 SD) of the spine and 15/28 of the hip. We found a greater decrease in bone density (z-score < -2.5 SD) in 2 out of 28 patients at the spine and in 5 out of 28 at the femoral neck. Those in whom the duration of the disease was less than two years (12 patients) had significantly higher vertebral z-scores (-0.096 +/-0.91) than those who had the disease for over two years (-1.31 +/- 2.37), (p<0.05). We found no significant correlation between lumbar spine and femoral neck z-scores and cumulative steroid therapy. Six out of 28 patients (four women and two men), of mean age 47.2+/-11.7, had one vertebral fracture. The mean cumulative dose of steroids (prednisone or budesonide) in patients with vertebral fractures was higher but not significantly different from that in patients without fractures -20.1+/-18.2 versus 14.1+/-11.2 g of prednisone, respectively (p>0.05). No correlation was found between various serum hormones and other biochemical parameters of bone turnover or bone density. We conclude that a large proportion of patients with Crohn's disease have reduced bone mineral density (58% at the spine and 75% at the femoral neck). The pathogenesis of bone loss is probably multifactorial. Although steroid therapy might be an important contributory factor, we were unable to find a significant correlation between it and bone loss. On the contrary, we observed that the duration of the disease makes a significant contribution to bone loss.
Thodis
E
E
Division of Nephrology and Gastroenterology, Toronto, Canada.
Rossos
P
P
Habal
F
F
Oreopoulos
D
D