Sinnott Bridget P, Licata Angelo A
Division of Endocrinology, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
Endocr Pract. 2006 Nov-Dec;12(6):622-9. doi: 10.4158/EP.12.6.622.
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).
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.
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.
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.
确定炎症性肠病（IBD）患者低骨量、骨折及维生素D缺乏的患病率，以及矿物质代谢生化标志物水平。
我们的回顾性研究纳入了30例克罗恩病（CD）患者和18例溃疡性结肠炎（UC）患者。采用双能X线吸收法测定腰椎和髋部的骨密度。评估血清钙、磷、甲状旁腺激素、25-羟维生素D（25-OHD）、1,25-二羟维生素D、尿I型胶原N-端肽交联物以及24小时尿钙水平。
根据IBD组整体低骨量的Z评分定义，13例患者（27%）腰椎骨量低。同样，在股骨颈，13例患者（27%）骨量低。UC组低骨量的患病率高于CD组，这与该组骨折的高患病率一致。所有IBD患者中，65%有骨折史，其中23%为非创伤性骨折。25-OHD缺乏率较高，UC患者中患病率为55%，CD患者中为83%。继发性甲状旁腺功能亢进定义为甲状旁腺激素水平>55 pg/mL，同时血清钙低或正常且25-OHD水平低，50%的CD患者存在，而UC患者中仅7%存在。
代谢性骨病和骨折在IBD中很常见。CD患者和UC患者的脊柱或股骨颈平均骨密度无显著差异。根据Z评分小于-2定义，UC患者低骨量的患病率高于CD患者，这与UC组骨折的高患病率一致。相比之下，CD患者中因维生素D缺乏导致的甲状旁腺功能亢进比UC患者更普遍。这一发现提示CD患者低骨量的病因机制不同。
