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目的探讨肺表面活性物质蛋白B(SP-B)缺陷是否为新生儿呼吸窘迫综合征(RDS)发病的影响因素。方法选择无血缘关系的30例RDS死亡新生儿为RDS组,其中<34周、34~36周及≥37周每组各纳入10例;选择无血缘关系的30例其他疾病死亡新生儿为对照组,胎龄与RDS组以1∶1相匹配分成3个亚组(P>0.05)。所有研究对象均在死后半小时内取肺组织浸入4%多聚甲醛固定,石蜡包埋后5μm连续切片,采用免疫组织化学技术检测各组患儿SP-B在肺部的表达;计算两组SP-B缺陷的频率。结果 SP-B位于细胞胞浆中,部分分泌至气道及肺泡表面,着色深浅不一、范围不同,随组别、胎龄、疾病严重程度而变化;RDS组肺部SP-B蛋白未随胎龄增加而增加,对照组除2例26周患儿SP-B明显低于同组同胎龄外,肺部SP-B蛋白随胎龄增加而增加。RDS组SP-B阳性表达细胞明显低于对照组(t=10.205,P<0.001),RDS组SP-B缺陷13例,缺陷频率43.3%,对照组SP-B缺陷2例,缺陷频率6.7%,RDS组高于对照组(χ2=60.00,P<0.001)。结论 SP-B缺陷参与了新生儿RDS的发病。
Objective To investigate whether pulmonary surfactant protein B (SP-B) deficiency is the influencing factor of neonatal respiratory distress syndrome (RDS). Methods Thirty unrelated neonates with RDS death were selected as the RDS group, of which 10 were enrolled in each group at 34 weeks, 34-36 weeks and ≥37 weeks. Thirty newborns with no other blood-related disease were selected as controls Group, gestational age and RDS group were divided into 3 subgroups according to 1: 1 matching (P> 0.05). All subjects were taken lung tissue immersed in 4% paraformaldehyde within half an hour after death, 5μm serial sections after paraffin embedding, immunohistochemistry was used to detect SP-B expression in the lungs of each group; two Group SP-B defect frequency. Results SP-B was located in the cytoplasm of cells, partially secreted to the airways and alveolar surface, with different shades of color, different ranges, with the group, gestational age, severity of the disease; SP-B protein in the RDS group did not The gestational age increased and increased in the control group except 2 cases 26 weeks of children with SP-B was significantly lower than the same group with the same gestational age, lung SP-B protein increased with increasing gestational age. The SP-B positive cells in RDS group were significantly lower than those in control group (t = 10.205, P <0.001). There were 13 cases of SP-B deficiency in RDS group, the frequency of defect was 43.3% , RDS group was higher than the control group (χ2 = 60.00, P <0.001). Conclusion SP-B deficiency is involved in the pathogenesis of neonatal RDS.