阿仑膦酸钠对2型糖尿病合并骨质疏松患者骨代谢标志物的影响

摘要

目的 观察阿仑膦酸钠对2型糖尿病合并骨质疏松症患者骨代谢标志物的影响,以评价该药的治疗效果.方法 收集2011年1月至2012年6月门诊及住院患者共103例.对所有患者均早晨空腹采血.测量空腹血糖(FPG)、血钙、血磷、碱性磷酸酶(ALP)、糖化血红蛋白(HbA1c)、血清抗酒石酸酸性磷酸酶-5b(TRACP-5b)、血清Ⅰ型胶原C末端肽(s-CTX)、血清骨源性碱性磷酸酶(BAP)和血清骨钙素(OC).利用双能X线吸收法进行腰椎和髋骨的骨密度检测.使用阿仑膦酸钠治疗6个月后复查上述各项生化指标和骨密度.将每例样本治疗前后的检测结果进行对比分析,统计学方法为配对t检验.结果 治疗前后血钙、血磷、碱性磷酸酶的差异无统计学意义;TRACP-5b、s-CTX治疗后较治疗前升高,BAP与OC较治疗前降低.治疗后腰椎和髋部的骨密度较治疗前均有不同程度升高.结论 阿仑膦酸钠对2型糖尿病合并骨质疏松症的治疗效果明显,其机制可能与抑制骨吸收,促进骨形成有关.%Objective To observe the effect of alendronate on bone metabolic markers in type 2 diabetes mellitus patients with osteoporosis, in order to evaluate the therapeutic effect of this drag. Methods One hundred and three out -patient and hospitalized patients were selected from January 2011 to June 2012. After fasting, blood of all patients was collected in the next morning. Fasting plasma glucose ( FPG ), serum calcium, serum phosphorus, alkaline phosphatase ( ALP), glycosylated hemoglobin (HbAlc), serum tartrate-resistant acid phosphatase-5b (TRACP-5b), serum type Ⅰ collagen C-terminal peptide (s-CTX), serum bone alkaline phosphatase (BAP), and serum osteocalcin (OC) were detected. Bone mineral density ( BMD) of the lumbar' vertebrae and the hip was measured using dual -energy X-ray absorptiometry (DEXA). Detection of all these biochemical markers and BMD was repeated after 6-month alendronate treatment. The results of each sample before and after treatment were comparatively analyzed. Paired t-test was used for statistical analysis. Results The results of serum calcium, serum phosphorus, and alkaline phosphatase showed no significant difference before and after the treatment. The levels of TRACP 5b and s-CTX after treatment were higher than those before the treatment. While the levels of BAP and OC after the treatment were lower than those before the treatment. BMD of the lumbar vertebrae and the hip increased to a different extent after the treatment than that before the treatment. Conclusion Alendronate has obvious therapeutic effect on type 2 diabetes mellitus patients with osteoporosis. Its possible mechanism may be related to inhibiting bone resorption and promoting bone formation.