Diabetes mellitus a risk for osteoporosis?
Diabetes mellitus a risk for osteoporosis?
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DOI：
10.1055/s-2001-18605
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发表时间：
2001-01-01
影响因子：
1.8
通讯作者：
Ziegler, R
中科院分区：
文献类型：
--
作者：
Leidig-Bruckner, G;Ziegler, R
足部骨骼局限性病变是糖尿病常见的严重并发症，严重影响患者的临床预后。相反，与糖尿病相关的全身性骨病或骨质疏松症的存在较少被承认，其临床相关性不太明显。本文是一个临床重点审查的文献骨质疏松症与糖尿病。由于1型和2型糖尿病的发病机制不同，因此没有统一的糖尿病骨病实体并不奇怪。在1型糖尿病受试者中进行的大多数临床研究显示，前臂骨量中度降低，而股骨或腰椎骨量降低或与非糖尿病对照无差异。在2型糖尿病患者中，骨质减少的风险不像1型糖尿病那样明确。与对照组相比，2型糖尿病患者前臂的骨密度降低、不变甚至增加，而椎骨或股骨颈的骨密度没有显著差异或增加，但很少降低。触发1型和2型糖尿病患者骨量变化的潜在机制尚不清楚。在大多数研究中，糖尿病的代谢控制和骨密度之间没有一致的关系。钙和骨代谢的生化参数与骨密度测量值无明显关系。从少数人类骨组织学研究和实验研究中，有证据表明骨形成减少是导致糖尿病患者骨量减少的一个主要机制。骨组织微血管病变也被认为是糖尿病骨质减少的可能原因。研究表明，胰岛素和胰岛素样生长因子（IGF-1、IGF-2）对骨代谢本身有影响，其他生长因子、细胞因子和激素可能决定糖尿病骨代谢的变化。最近的研究表明，瘦素参与成骨细胞功能和骨量的调节，这是2型糖尿病的特殊利益。骨质疏松症或骨质减少的临床相关性取决于功能不全骨折的风险增加。很少有研究发现骨折风险增加，特别是在1型糖尿病的老年女性中，而其他研究没有显示骨折风险增加，甚至发现2型糖尿病女性的骨折率降低。有必要进行进一步的纵向研究，包括骨化性骨折的发病率和危险因素。在临床常规中，1型或2型糖尿病患者全身性骨病或糖尿病性骨质减少的诊断和治疗活动程度应基于个体状况和骨质疏松症的风险特征。
Localized lesions at the foot skeleton are a serious and well recognized complication of diabetes mellitus which may impair the clinical outcome of the patients remarkably. In contrast, the presence of a generalized bone disease or osteoporosis related to diabetes mellitus is less acknowledged and its clinical relevance is less obvious. This paper is a clinically focused review of the literature on osteoporosis related to diabetes mellitus. Due to the different pathogenesis of diabetes mellitus type 1 and type 2 it is not surprising that there is no uniform entity of diabetic osteopathy. The majority of clinical studies in subjects with diabetes mellitus type 1 showed a moderately decreased bone mass at the forearm, while bone mass at the femur or lumbar spine was either decreased or not different from non-diabetic controls. In patients with diabetes mellitus type 2 the risk of osteopenia is not as clear as in type 1 diabetes. Bone mineral density at the forearm in patients with type 2 diabetes mellitus was decreased, unchanged or even increased in comparison to controls, while bone mineral density at the vertebrae or femoral neck was either not significantly different or increased, but rarely decreased. The underlying mechanisms triggering changes in bone mass in patients with diabetes mellitus type 1 and type 2 are not well known. In most studies there was no consistent relationship between the metabolic control of diabetes and bone mineral density. Biochemical parameters of the calcium and bone metabolism showed no clear relationship to the bone mineral density measurements. From few bone histology studies in humans and experimental studies there is evidence that a decreased bone formation is one major mechanism leading to reduced bone mass in diabetics. Microangiopathy at the bone tissue was also discussed as a possible reason for diabetic osteopenia. It was shown that insulin and insulin like growth factors (IGF-1, IGF-2) have an influence on bone metabolism itself and other growth factors, cytokines and hormones may determine changes in diabetic bone metabolism. Recent findings suggest that leptin is involved in the regulation of osteoblast function and bone mass, which is of special interest in diabetes mellitus type 2. The clinical relevance of osteoporosis or osteopenia is determined by the increased risk for insufficiency fractures. Few studies found an increased fracture risk, especially in older women with type 1 diabetes mellitus, while others did not show an increased risk for fractures or even found a decreased rate of fractures in women with diabetes mellitus type 2. There is a need for further longitudinal studies, including the incidence and risk factors for osteoporotic fractures. In clinical routine the extent of diagnostic and therapeutic activities in patients with type 1 or type 2 diabetes mellitus in respect to generalized bone disease or diabetic osteopenia should be based on individual conditions and risk profile for osteoporosis.