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炎症性肠病患者骨矿物质密度降低及骨代谢失衡。

Reduced bone mineral density and unbalanced bone metabolism in patients with inflammatory bowel disease.

作者信息

Schulte C, Dignass A U, Mann K, Goebell H

机构信息

Department of Internal Medicine, University of Essen, Germany.

出版信息

Inflamm Bowel Dis. 1998 Nov;4(4):268-75. doi: 10.1002/ibd.3780040403.

Abstract

Patients with chronic inflammatory bowel diseases (IBD) are at increased risk to develop osteopenia and osteoporosis. New parameters for the assessment of bone formation and especially bone resorption have significantly improved the diagnostic procedures to characterize bone metabolism. Biochemical characterization of bone turnover in IBD patients may provide important information about the pathogenesis of osteoporosis in this patient population. A cross-sectional study was performed. One hundred forty-nine patients (77 men, 52 premenopausal, and 20 postmenopausal women) with IBD (104 with Crohn's disease [CD] and 45 with ulcerative colitis [UC]) underwent clinical, osteodensitometric, and metabolic bone assessment. Bone mineral density was determined by dual energy X-ray absorptiometry. Bone formation (bone alkaline phosphatase), bone resorption (N-terminal telopeptide of type-I collagen, free desoxypyridinoline, total pyridinoline, and desoxypyridinoline), vitamin D, and parathyroid hormone were assessed. Thirty-six percent of patients with CD and 32% with UC showed osteopenia, 15% with CD and 7% with UC showed osteoporosis. Bone resorption was significantly increased in IBD patients compared to normal controls, whereas bone formation did not show a compensatory increase. Bone formation was even more suppressed in the subset of patients currently treated with corticosteroids. Our data confirm the high prevalence of osteopenia and osteoporosis reported in IBD patients. Furthermore, we provide evidence for an increased bone resorption accompanied by low bone formation in IBD patients. This imbalance of bone metabolism is likely to be one of the reasons for increased bone loss in IBD patients.

摘要

患有慢性炎症性肠病(IBD)的患者发生骨质减少和骨质疏松的风险增加。用于评估骨形成尤其是骨吸收的新参数显著改善了表征骨代谢的诊断程序。IBD患者骨转换的生化特征可能为该患者群体骨质疏松的发病机制提供重要信息。进行了一项横断面研究。149例IBD患者(77名男性、52名绝经前女性和20名绝经后女性)(104例克罗恩病[CD]和45例溃疡性结肠炎[UC])接受了临床、骨密度测定和代谢性骨评估。通过双能X线吸收法测定骨矿物质密度。评估了骨形成(骨碱性磷酸酶)、骨吸收(I型胶原N端肽、游离脱氧吡啶啉、总吡啶啉和脱氧吡啶啉)、维生素D和甲状旁腺激素。36%的CD患者和32%的UC患者表现为骨质减少,15%的CD患者和7%的UC患者表现为骨质疏松。与正常对照组相比,IBD患者的骨吸收显著增加,而骨形成未显示出代偿性增加。在目前接受皮质类固醇治疗的患者亚组中,骨形成受到更明显的抑制。我们的数据证实了IBD患者中报告的骨质减少和骨质疏松的高患病率。此外,我们提供证据表明IBD患者骨吸收增加且伴有骨形成减少。这种骨代谢失衡可能是IBD患者骨量丢失增加的原因之一。

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