背景:神经病变和骨折是1型糖尿病(T1D)的常见并发症。尽管在临床文献中相关,目前尚不清楚神经病变是否会在疾病的早期阶段导致骨丢失。
方法:我们执行了单中心,横断面研究,以量化T1D青春期女孩(n=21)和相关对照(n=12)的神经和骨骼健康参数。群体在年龄上很匹配,高度,力量,和身体活动。
结果:通过HR-pQCT,T1D患者桡骨远端骨小梁体积分数较低(-14.6%,p-adj=0.095)和胫骨(-12.8%,p-adj=0.017)和小梁厚度减小(-8.3%半径,p-adj=0.007;-7.5%胫骨,调整车身尺寸后,p-adj=0.034)。仅在胫骨中,T1D的皮质骨矿物质密度增加了8.6%(p-adj=0.024),孔隙率降低了52.9%(p-adj=0.012)。DXA对骨密度没有显著差异。患有T1D的参与者的骨钙蛋白循环水平也较低(-30%,p=0.057),和I型胶原交联C端肽(-36%,p=0.035),提示T1D中骨形成和更新较低。根据密歇根神经病筛查仪器,9.5%的T1D患者有糖尿病周围神经病变的临床证据。然而,对神经病变状态的考虑未能解释广泛的T1D相关骨变化.
结论:我们的研究定义了小梁骨微结构的早期缺陷,胫骨皮质孔隙度降低,和抑制T1D青春期女孩骨转换的生物标志物,在症状性周围神经病变发作之前。这些发现使我们了解了T1D年轻女孩骨骼疾病的快速发展,并表明早期发现和管理策略可能有助于预防以后的骨折和相关合并症。
BACKGROUND: Neuropathy and fracture are prevalent complications of type 1 diabetes (T1D). Although correlated in the clinical literature, it remains unknown whether neuropathy contributes to the initiation of bone loss at the earliest stages of disease.
METHODS: We performed a single-center, cross-sectional study to quantify parameters of nerve and bone health in adolescent girls with T1D (n=21) and associated controls (n=12). Groups were well matched for age, height, strength, and physical activity.
RESULTS: By HR-pQCT, participants with T1D had lower trabecular bone volume fraction at the distal radius (-14.6%, p-adj=0.095) and the tibia (-12.8%, p-adj=0.017) and decreased trabecular thickness (-8.3% radius, p-adj=0.007; -7.5% tibia, p-adj=0.034) after adjustment for body size. In the tibia only, cortical bone mineral density was increased by 8.6% (p-adj=0.024) and porosity was decreased by 52.9% with T1D (p-adj=0.012). There were no significant differences in bone density by DXA. Participants with T1D also had lower circulating levels of osteocalcin (-30%, p=0.057), and type I collagen cross-linked C-telopeptide (-36%, p=0.035), suggesting low bone formation and turnover in T1D. Based on the Michigan Neuropathy Screening Instrument, 9.5% of those with T1D had clinical evidence of diabetic peripheral neuropathy. However, consideration of neuropathy status failed to explain the widespread T1D-associated changes in bone.
CONCLUSIONS: Our study defines early deficits in trabecular bone microarchitecture, decreased cortical porosity in the tibia, and suppression of biomarkers of bone turnover in adolescent girls with T1D, prior to the onset of symptomatic peripheral neuropathy. These findings inform our understanding of the rapid progression of skeletal disease in young girls with T1D and suggests that early detection and management strategies may help to prevent fracture and related co-morbidities later in life.