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骨质疏松(ostceporosis)是最常见的骨骼代谢性疾病,其特征包括正常骨密度的减少、骨质脆弱以及骨折的风险性增加。糖皮质激素(glucocorticoids,GCs)治疗的病人容易并发糖皮质激素性骨质疏松症(glucocorticoids-induced osteoporosis,GCOP)。糖皮质激素受体(glucocorticoidreceptor,GR)基因多态性能可改变其受体对糖皮质激素的敏感性,而激素高敏感病人极容易被临床医生所忽视而使用常规剂量糖皮质激素,所以存在更高的糖皮质激素性骨质疏松症风险,甚至出现病理性骨折。糖皮质激素性骨质疏松症最明显的表现为体内的骨代谢水平升高,体内骨代谢敏感性变化能反映骨质疏松的进展情况。然而,近来对糖皮质激素受体基因多态性与骨代谢敏感性的研究缺乏统一的认识。作者对文献进行检索分析发现,糖皮质激素受体基因的多态性可能增强或者减弱其对糖皮质激素敏感性,进而促进或抑制骨代谢,其作用结果和基因多态性位点、受体作用通路等有关。
Osteoporosis (ostceporosis) is the most common bone metabolic disease characterized by a decrease in normal bone density, bone fragility and an increased risk of fractures. Patients treated with glucocorticoids (GCs) are prone to develop glucocorticoids-induced osteoporosis (GCOP). Glucocorticoid receptor (GR) gene polymorphism can change its sensitivity to glucocorticoid receptors, and hormone-sensitive patients can easily be ignored by clinicians and the use of conventional doses of glucocorticoid, so there is more High risk of glucocorticoid osteoporosis, and even pathological fractures. The most obvious manifestation of glucocorticoid-induced osteoporosis is an increase in the level of bone metabolism in the body, and a change in susceptibility to bone metabolism in vivo can reflect the progress of osteoporosis. However, recent studies on glucocorticoid receptor gene polymorphism and bone metabolism have been lacking in common understanding. The author of the literature search and analysis found that glucocorticoid receptor gene polymorphisms may enhance or reduce its glucocorticoid sensitivity, thereby promoting or inhibiting bone metabolism, and its role in the results and genetic polymorphism sites, receptors The role of access and other related.