A controlled study of bone mineral density in patients with inflammatory bowel disease.

A controlled study of bone mineral density in patients with inflammatory bowel disease.
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炎症性肠病患者骨矿物质密度的对照研究。

DOI:
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发表时间:
1995
期刊:
Gut
影响因子:
24.5
通讯作者:
J. Lehtola
J. Lehtola
中科院分区:
医学1区
文献类型:
--
作者:
J. Silvennoinen;T. Karttunen;S. Niemela;J. Manelius;J. Lehtola

文献摘要

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为了评估炎症性肠病 (IBD) 患者骨密度低的患病率和危险因素,对 152 名 IBD 患者和 73 名健康对照进行了研究。 67 名患者患有溃疡性结肠炎,78 名患者患有克罗恩病(其中 52 名患者(66.7%)患有回肠疾病),7 名患者患有不确定性结肠炎。通过双能 X 射线吸收法测量脊柱 (L2-L4)、股骨颈、Ward 三角和转子的骨矿物质密度值 (g/cm2) 分别为 1.177、0.948、0.850 和 0.838,患者为 1.228 (p = 0.034)、1.001 (p = 0.009)、对照组分别为 0.889 (NS) 和 0.888 (p = 0.012)。疾病的类型或程度或既往小肠切除术对骨密度值没有任何显着影响。骨矿物质密度与终生皮质类固醇剂量之间存在微弱但具有统计学意义的负相关性(腰椎 r = -0.164,p = 0.04,股骨颈 r = -0.185,p = 0.02,Ward 三角 r = -0.167,p = 0.04,转子 r = -0.237,p = 0.003)。终生皮质类固醇剂量(泼尼松/泼尼松龙)超过 10 g 的患者骨密度特别低(与没有皮质类固醇或少于 5 g 的组相比,p < 0.05)。从未口服皮质类固醇的患者骨密度并未降低。总之,IBD 患者的骨密度值显着低于健康对照,但差异并不像之前报道的那么大。这些患者的低骨密度值与高终生皮质类固醇剂量有关。
To assess the prevalence of and risk factors for low bone mineral density in inflammatory bowel disease (IBD), 152 IBD patients and 73 healthy controls were studied. Sixty seven patients had ulcerative colitis, 78 had Crohn's disease (52 of them (66.7%) had ileal disease), and seven had indeterminate colitis. Bone mineral density values (g/cm2) measured by dual energy x ray absorbtiometry at the spine (L2-L4), the femoral neck, Ward's triangle, and the trochanter were 1.177, 0.948, 0.850, and 0.838 in the patients and 1.228 (p = 0.034), 1.001 (p = 0.009), 0.889 (NS), and 0.888 (p = 0.012) in the control group, respectively. The type or extent of the disease or previous small bowel resection did not have any significant effect on the bone mineral density values. There was a weak, but statistically significant negative correlation between bone mineral density and the total lifetime corticosteroid dose (in the lumbar spine r = -0.164, p = 0.04, the femoral neck r = -0.185, p = 0.02, Ward's triangle r = -0.167, p = 0.04, and the trochanter r = -0.237, p = 0.003). The patients whose lifetime corticosteroid dose (prednisone/prednisolone) was more than 10 g had especially low bone mineral density (p < 0.05 compared with the groups with no or less than 5 g of corticosteroid). The patients who had never taken peroral corticosteroids did not have decreased bone mineral density. In conclusion, IBD patients have significantly lower bone mineral density values than healthy controls, but the difference is not so great as has been reported previously. Low bone mineral density values in these patients are related to high lifetime corticosteroid doses.