Schett Georg, Kiechl Stefan, Weger Siegfried, Pederiva Angelo, Mayr Agnes, Petrangeli Manuele, Oberhollenzer Friedrich, Lorenzini Rolando, Redlich Kurt, Axmann Roland, Zwerina Jochen, Willeit Johann
Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany.
Arch Intern Med. 2006;166(22):2495-501. doi: 10.1001/archinte.166.22.2495.
Chronic inflammatory diseases are associated with bone loss and an enhanced fracture risk. It is unknown, however, whether low-grade inflammation in healthy individuals, as estimated by the high-sensitivity C-reactive protein (hs-CRP) level, interferes with bone metabolism and affects the risk of nontraumatic fractures.
Lifetime bone fractures were carefully recorded in the cohort of the population-based Bruneck Study (n = 919) along with information on the date of occurrence and associated circumstances. The serum level of hs-CRP was measured from blood samples collected during the 1990 baseline examination and the 1995, 2000, and 2005 follow-up examinations. In addition, lifestyle and demographic characteristics, bone ultrasonographic data at the heel, and variables of bone metabolism were assessed.
Between September 1, 1990, and August 31, 2005, 69 subjects experienced nontraumatic hip or vertebral fractures. The incidence of nontraumatic fractures was 1.3, 3.8, and 13.9 per 1000 person-years in the tertile groups for hs-CRP. In multivariate pooled logistic regression analysis, the adjusted relative risk (95% confidence interval) of nontraumatic fracture in the highest vs lowest tertile group for hs-CRP was 9.4 (3.6-24.8) (P < .001). The exclusion of subjects with cardiovascular disease, dementia, malignancies, and chronic inflammatory disease had little effect on the results obtained. The hs-CRP level was unrelated to ultrasonographic measures of bone density, but showed an inverse relation to laboratory markers of bone turnover, like beta-crosslaps and osteocalcin concentration (P < .001).
The hs-CRP level is a significant and independent risk predictor of nontraumatic fracture. This finding is consistent with the hypothesis of a tight interplay between low-grade inflammation and bone turnover.
慢性炎症性疾病与骨质流失及骨折风险增加相关。然而，尚不清楚健康个体中通过高敏C反应蛋白（hs-CRP）水平估算的低度炎症是否会干扰骨代谢并影响非创伤性骨折的风险。
在基于人群的布伦内克研究队列（n = 919）中仔细记录终生骨折情况，同时记录发生日期及相关情况。在1990年基线检查以及1995年, 2000年和2005年随访检查期间采集的血样中测量hs-CRP的血清水平。此外，评估生活方式和人口统计学特征、足跟部骨超声数据以及骨代谢变量。
在1990年9月1日至2005年8月31日期间，69名受试者发生了非创伤性髋部或椎体骨折。hs-CRP三分位数组中非创伤性骨折的发病率分别为每1000人年1.3、3.8和13.9例。在多变量合并逻辑回归分析中，hs-CRP最高三分位数组与最低三分位数组相比，非创伤性骨折的调整相对风险（95%置信区间）为9.4（3.6 - 24.8）（P <.001）。排除患有心血管疾病、痴呆、恶性肿瘤和慢性炎症性疾病的受试者对所得结果影响不大。hs-CRP水平与骨密度的超声测量值无关，但与骨转换的实验室标志物如β-交联C末端肽和骨钙素浓度呈负相关（P <.001）。
hs-CRP水平是非创伤性骨折的重要独立风险预测指标。这一发现与低度炎症和骨转换之间紧密相互作用的假设一致。
