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

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

炎症性肠病(克罗恩病和溃疡性结肠炎)患者的骨矿物质密度和钙调节激素。

DOI:
--
复制
发表时间:
2009
期刊:
Experimental and clinical endocrinology
影响因子:
--
通讯作者:
Reinhard Ziegler
Reinhard Ziegler
中科院分区:
--
文献类型:
--
作者:
S. Scharla;Helmut W. Minne;U. Lempert;G. Leidig;M. Hauber;R. Raedsch;Reinhard Ziegler

文献摘要

被引文献

相似文献

炎症性肠病(克罗恩病和溃疡性结肠炎)与骨密度降低和骨质疏松症风险增加有关。然而,这种骨丢失的发病机制尚未完全了解。在本研究中,我们测量腰椎骨密度(双光子吸收法),血清甲状旁腺激素(PTH)和维生素D代谢产物的水平,和骨转换的血清标志物(碱性磷酸酶和骨钙素)在15例克罗恩病和4例溃疡性结肠炎患者。疾病的中位持续时间为4年,中位终生类固醇剂量为10 g泼尼松。我们将我们的结果与19名年龄和性别与患者相匹配的正常人对照组进行了比较。我们发现,与对照组相比,患者的腰椎骨密度降低了11%(Z评分-0.6 +/-0.6 vs-0.1 +/-0.8; p < 0.05)。在患者中,与对照组相比,PTH、25-羟基维生素D3和骨化三醇(1,25(OH)2D 3)的血清水平显著降低。患者血清碱性磷酸酶活性(AP)显著升高,且与腰椎骨密度呈负相关。骨钙素值患者和对照组之间没有差异。两组之间的血清钙水平也没有差异,而患者的磷水平较高。我们的结论是,钙吸收不良不是我们患者骨丢失的主要原因,因为我们没有发现继发性甲状旁腺功能亢进。因此,我们没有发现严重的维生素D缺乏症,因为25-羟基维生素D3水平在正常范围内。(250字处删节)
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)