骨标志物检测在预测糖皮质激素诱发自身免疫疾病骨质疏松中的意义

The significance of bone markers in the prediction of glucocorticoid-induced osteoporosis in patients with autoimmune diseases

目的自身免疫疾病患者长期应用糖皮质激素可以诱发骨质疏松,但是往往在应用早期尚无显著骨密度变化,为寻找在应用激素早期即可观察到的骨代谢变化,我们对98例自身免疫病患者进行了骨标志物检测,并研究其与激素应用的关系。方法对2011年4月1日至2013年1月31日于我院住院的98例自身免疫病患者进行骨标志物——血清骨钙素、I型原胶原N端前肽(PINP)β胶原降解产物(βCTX)的检测,采用电化学发光法检测。并对该98例患者的临床资料进行收集。应用SPSS13.5软件进行统计分析。结果 98例患者RA52例,SLE14例,SPA10例,其他自身免疫疾病22例。其中入院前已经接受糖皮质激素治疗患者39例,尚未接受激素治疗患者59例,两组患者的性别构成比及平均年龄均无统计学差异。激素治疗组患者血清骨钙素、βCTX和PINP均显著低于未接受激素治疗组,分别为[(7.57±4.46)μg/L vs(20.06±10.40)μg/L,P<0.01]、[(0.31±0.22)μg/L vs.(0.52±0.26)μg/L,P<0.01]和[(22.71±13.98)μg/Lvs.(49.86±35.46)μg/L,P<0.01],有显著统计学差异。而两组间血钙、血磷、血尿素氮、血肌酐和C反应蛋白水平,以及股骨颈和腰椎骨密度值均无统计学差异。其中RA52例患者中,有应用糖皮质激素治疗组患者的骨钙素、βCTX和PINP亦均显著低于未接受激素治疗组,且βCTX和DAS28正相关(r=0.456,P<0.01),提示βCTX和疾病活动度相关。结论糖皮质激素治疗可以导致自身免疫疾病患者骨代谢异常,而骨标志物的降低可以较早提示骨代谢的变化,对早期预防骨质疏松治疗有指导意义,而RA患者βCTX的水平升高可提示潜在疾病活动度升高。

Objective Long-term use of glucocorticoid in patients with autoimmune diseases could induce osteoporosis. However, we can not detect any change in bone mineral density （ BMD ） at the early stage of glucocorticoid usage. In order to observe the changes of bone metabolism as early as possible, we detected the bone markers of 98 patients with autoimmune diseases and further investigated their relationships with the application of steroid. Methods Ninety-eight patients with autoimmune diseases, who were hospitalized in our hospital from April 1st, 2011 to January 31st, 2013, were included in this study. The expression of bone markers, including serum osteocalcin, PINP, and 13 CTX, was detected using elctrochemiluminescence. The clinical data of 98 patients were collected. Statistical analysis was performed using a SPSS 13.5 software. Results Among the 98 patients, 52 patients had RA, 14 had SLE, 10 had SPA, and 22 had other autoimmune diseases. Thirty-nine patients received glucocorticoid therapy before admitted to our hospital, and the other 59 patients did not receive such treatment. No statistical difference of gender composition ratio and mean age between the two groups was observed. The serum concentrations of osteocalcin, 13 CTX, and PINP in glucocorticoid treated group were significantly lower than those in non-glucocorticoid treated group [ （7.57 ± 4.46） μg/L vs. （20.06±10.40） μg/L; （0.31 ±0.22） μg/Lvs. （0.52±0.26） μg/L; （22.71 ±13.98） μg/L vs. （49.86 ± 35.46） μg/L; P 〈 0.01 ]. But the serum calcium, phosphorus, blood urea nitrogen, serum creatinine, and C-reactive protein levels, and BMD of the femoral neck and the the lumbar vertebrae had no statistical difference between the two groups. In 52 patients with RA, the serum levels of osteocalcin, 13 CTX, and PINP in glucocorticoid treated group were also significantly lower than those in non-glucocorticoid treated group, respectively. Furthermore, 13 CTX was positively correlated with DAS28 （ r = 0. 456,P 〈 0.01 ）, suggesting that 13 CTX may be associated with the disease activity in RA patients. Conclusion Bone metabolic abnormalities can be induced by glucocorticoid treatment for autoimrnune diseases. The decrease of bone markers can predict early changes in bone metabolism, which may have an important significance in preventing osteoporosis. In addition, the increased 13 CTX level may be a potential indicator for the assessment of disease activity in RA patients.