论文部分内容阅读
临床上常用糖皮质激素(glucocorticoids,GCs)来治疗多种疾病,但GCs诱导的骨质疏松症(glucocorticoid-induced osteoporosis,GIO)是其严重副作用之一。目前已知高剂量GCs可以抑制成骨细胞(osteoblast,OB)的增殖和分化,诱导OB的凋亡,减少骨形成,而导致骨质疏松(osteoporosis,OP)。而低剂量GCs体外却刺激了OB的增殖和分化。在动物体内实验中发现:一定的条件下,GCs在未影响松质骨的情况下,即可造成皮质骨骨量的丢失,这种GCs的双向作用是由于体内骨转移和GCs对骨组织作用的部位特异性造成的,目前还没有统一的结论。笔者主要从临床、实验和机理这3方面的研究入手,综述GCs对成骨的双向作用与OP之间关系的研究现状,以便更深入地了解GIO的发病机理,并为临床合理使用该类药物提供指导意见。
Glucocorticoids (GCs) are commonly used clinically to treat a variety of diseases, but one of the serious side effects of GCs-induced osteoporosis (GIO) is GCs. It is known that high-dose GCs can inhibit the proliferation and differentiation of osteoblast (OB), induce the apoptosis of OB, reduce the formation of bone and lead to osteoporosis (OP). However, low dose GCs stimulated the proliferation and differentiation of OB in vitro. In animal experiments found: under certain conditions, GCs in the absence of cancellous bone, can cause the loss of cortical bone mass, the two-way effect of GCs is due to bone metastases in vivo and GCs on bone tissue Of the site-specific caused, there is no unified conclusion. The author mainly from the clinical, experimental and mechanism of these three aspects of the study, review GCs on the two-way osteogenesis and the relationship between the current status of research in order to more in-depth understanding of the pathogenesis of GIO, and clinical rational use of such drugs Provide guidance.