肾素-血管紧张素系统与儿童糖皮质激素性骨质疏松患者骨密度的相关性分析

Correlation analysis between renin-angiotensin system and bone mineral density in children with glucocorticoid-induced osteoporosis

目的探讨肾素-血管紧张素系统(renin-angiotensin system,RAS)与儿童糖皮质激素性骨质疏松(glucocorticoids-induced osteoporosis,GIOP)患者的骨密度相关性分析。方法2020年4月至2021年5月在太原市妇幼保健院市儿童医院就诊的53例GIOP患儿纳入观察组,47例接受糖皮质激素治疗但未患GIOP的患儿纳为对照组。检测两组患儿血清RAS成分水平与骨密度并进行对比,分析影响骨密度与GIOP的危险临床指标。结果观察组与对照组的性别、年龄、身体质量指数(BMI)、疾病类型、糖皮质激素使用种类、是否使用抗骨质疏松(osteoporosis)药物、血管紧张素转换酶2(angiotensin converting enzyme 2,ACE2)、血管紧张素Ⅱ(angiotensin Ⅱ,AngⅡ)表达水平的差异无统计学意义(均P>0.05)。观察组的骨密度数值均低于对照组,血管紧张素转换酶(angiotensin converting enzyme,ACE)(1.19±0.23)、血管紧张素受体1(angiotensin receptor 1,AT1R)(1.24±0.24)、血管紧张素受体2(angiotensin receptor 2,AT2R)(1.14±0.17)、Mas受体(Mas receptor,MasR)(1.11±0.28)水平较对照组(1.00±0.23,1.00±0.25,1.00±0.21,1.00±0.20)显著升高,差异有统计学意义(均P<0.05)。pearson分析显示骨密度与ACE(r=-0.34,P=0.013)、AT1R(r=-0.41,P=0.002)、AT2R(r=-0.34,P=0.014)的水平呈负相关,逐步回归模型显示ACE(t=-2.21,P=0.032)、AT1R(t=-2.92,P=0.005)为影响骨密度的主要因素。Logistic回归模型分析显示骨密度(OR=0.85,P<0.001)、AngⅡ(OR=0.53,P=0.041)、AT2R(OR=2.00,P=0.024)是影响GIOP的独立临床危险因素。结论RAS成分ACE、AT1R是影响儿童GIOP的骨密度的独立危险因素,与患儿骨密度显著相关。

Objective To investigate the relationship between renin-angiotensin system(RAS)and bone mineral density in children with glucocorticoids-induced osteoporosis(GIOP).Methods From Apr.2020 to May.2021,53 children with GIOP were recruited in the Children’s Hospital of Taiyuan Maternal and Child Health Hospital and included in the observation group,and 47 children who received glucocorticoid therapy but did not suffer from GIOP were included in the control group.The levels of serum RAS components and bone mineral density of the two groups of pediatric patients were detected and compared,and the risk clinical indicators affecting bone mineral density and GIOP were analyzed.Results There were no significant differences between the observation group and the control group in terms of gender,age,BMI,disease type,type of glucocorticoid use,use of anti-osteoporosis(OP)drugs,expression levels of Angiotensin converting enzyme 2(ACE2)or angiotensin Ⅱ(AngⅡ)(all P>0.05).The bone density value of the observation group was lower than those of the control group,and the levels of angiotensin converting enzyme(ACE)(1.19±0.23),angiotensin receptor 1(AT1R)(1.24±0.24),angiotensin receptor 2(AT2R)(1.14±0.17),and Mas receptor(MasR)(1.11±0.28)were significantly higher than those of the control group(1.00±0.23,1.00±0.25,1.00±0.21,1.00±0.20),and the differences were statistically significant(all P<0.05).Pearson analysis showed that bone mineral density was negatively correlated with the levels of ACE(r=-0.34,P=0.013),AT1R(r=-0.41,P=0.002)and AT2R(r=-0.34,P=0.014),and stepwise regression model showed that ACE(t=-2.21,P=0.032)and AT1R(t=-2.92,P=0.005)were the main factors affecting bone mineral density.Logistic regression model analysis showed that bone mineral density(OR=0.85,P<0.001),AngⅡ(OR=0.53,P=0.041)and AT2R(OR=2.00,P=0.024)were independent clinical risk factors affecting GIOP(all P<0.05).Conclusion RAS components ACE and AT1R are independent risk factors affecting bone mineral density in children with GIOP,and are significantly correlated with bone mineral density in children.