Neumann T, Lodes S, Kästner B, Franke S, Kiehntopf M, Lehmann T, Müller U A, Wolf G, Sämann A
Department of Internal Medicine III, Jena University Hospital, Erlanger Allee 101, 07747, Jena, Germany,
Osteoporos Int. 2014 May;25(5):1527-33. doi: 10.1007/s00198-014-2631-7. Epub 2014 Mar 6.
Fracture risk in type 1 diabetes (T1D) is supposed to be underestimated by bone mineral density (BMD). Individuals with T1D had more prevalent fractures in a cross-sectional study. Serum levels of pentosidine, an advanced glycation end product, and poor glycaemic control were associated with prevalent fractures independent of BMD.
Type 1 diabetes (T1D) is associated with increased fracture risk. Bone mineral density (BMD) underestimates the risk of fractures in some individuals. The accumulation of advanced glycation end products (AGEs) impairs bone matrix and reduces bone strength.
In a cross-sectional study, 128 men and premenopausal women with T1D were evaluated. We compared traditional risk factors for fractures, BMD, parameters of bone metabolism and AGEs in individuals with and without prevalent fractures. An independent association of serum AGE levels with prevalent fractures was investigated.
Individuals with prevalent fractures exhibited a longer duration of T1D, higher HbA1c and more diabetic-related complications. BMD at the femoral neck (z-score -0.76 ± 0.94 vs. -0.23 ± 1.02; p = 0.031) and total hip (z-score -0.54 ± 0.93 vs. 0.11 ± 1.11; p = 0.017) was lower in those with prevalent fractures. Individuals with fractures had higher pentosidine levels (164.1 ± 53.6 vs. 133.2 ± 40.4; p = 0.002). The levels of N-ε-(carboxymethyl)-lysine (CML) and endogenous secretory receptor for AGEs (esRAGE) did not significantly differ. Multivariate logistic regression analysis adjusted for age, BMI, family history of fractures, smoking, vitamin D deficiency, BMD at lumbar spine, femoral neck and total hip identified pentosidine levels and HbA1c as independent factors associated with prevalent fractures (odds ratio 1.02, 95% CI 1.00-1.03/pmol/ml increase of pentosidine; p = 0.008 and odds ratio 1.93, 95% CI 1.16-3.20 per percentage increase of HbA1c; p = 0.011).
The pentosidine levels but not BMD are independently associated with prevalent fractures. Impaired bone quality in T1D may result from increased AGE formation.
1型糖尿病（T1D）患者的骨折风险可能被骨密度（BMD）低估。在一项横断面研究中，T1D患者的骨折更为普遍。血清中晚期糖基化终产物戊糖苷水平以及血糖控制不佳与骨折的发生相关，且独立于骨密度。
1型糖尿病（T1D）与骨折风险增加有关。骨密度（BMD）会低估某些个体的骨折风险。晚期糖基化终产物（AGEs）的积累会损害骨基质并降低骨强度。
在一项横断面研究中，对128名患有T1D的男性和绝经前女性进行了评估。我们比较了有和没有骨折的个体的传统骨折风险因素、骨密度、骨代谢参数和AGEs。研究了血清AGE水平与骨折发生的独立关联。
有骨折的个体T1D病程更长、糖化血红蛋白（HbA1c）更高且糖尿病相关并发症更多。有骨折的个体股骨颈骨密度（z值 -0.76±0.94 vs. -0.23±1.02；p = 0.031）和全髋骨密度（z值 -0.54±0.93 vs. 0.11±1.11；p = 0.017）更低。有骨折的个体戊糖苷水平更高（164.1±53.6 vs. 133.2±40.4；p = 0.002）。N-ε-（羧甲基）-赖氨酸（CML）和内源性AGE分泌受体（esRAGE）水平无显著差异。多因素逻辑回归分析对年龄、体重指数、骨折家族史、吸烟、维生素D缺乏、腰椎、股骨颈和全髋骨密度进行校正后，确定戊糖苷水平和HbA1c为与骨折发生相关的独立因素（戊糖苷每增加1 pmol/ml，优势比为1.02，95%置信区间为1.00 - 1.03；p = 0.008；HbA1c每增加1个百分点，优势比为1.93，95%置信区间为1.16 - 3.20；p = 0.011）。
戊糖苷水平而非骨密度与骨折发生独立相关。T1D患者的骨质量受损可能是由于AGE形成增加所致。
