Scharla S H, Minne H W, Lempert U G, Leidig G, Hauber M, Raedsch R, Ziegler R
Department of Internal Medicine I (Endocrinology & Metabolism), University of Heidelberg, Germany.
Exp Clin Endocrinol. 1994;102(1):44-9. doi: 10.1055/s-0029-1211264.
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 (1,25(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 25-hydroxyvitamin D3 levels were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
炎症性肠病(克罗恩病和溃疡性结肠炎)与骨矿物质密度降低及骨质疏松风险增加相关。然而,这种骨质流失的发病机制尚未完全明确。在本研究中,我们测量了15例克罗恩病患者和4例溃疡性结肠炎患者的腰椎骨矿物质密度(采用双能光子吸收法)、血清甲状旁腺激素(PTH)水平、维生素D代谢产物水平以及骨转换血清标志物(碱性磷酸酶和骨钙素)。疾病的中位病程为4年,终身类固醇剂量的中位数为10克泼尼松。我们将结果与19名年龄和性别与患者匹配的正常对照组进行了比较。我们发现,与对照组相比,患者的腰椎骨密度降低了11%(Z值为-0.6±0.6对-0.1±0.8;p<0.05)。与对照组相比,患者的血清PTH、25-羟维生素D3和骨化三醇(1,25(OH)2D3)水平显著降低。患者的血清碱性磷酸酶活性(AP)显著更高,且与腰椎骨密度呈负相关。患者与对照组之间的骨钙素值没有差异。两组之间血清钙水平也没有差异,而患者的磷水平更高。我们得出结论,钙吸收不良不是我们患者骨质流失的主要原因,因为我们未发现继发性甲状旁腺功能亢进。因此,我们未发现严重的维生素D缺乏,因为25-羟维生素D3水平在正常范围内。(摘要截选至250字)