肺表面活性物质蛋白 B、C 基因变异与蒙古族早产儿 呼吸窘迫综合征相关性研究

目的研究肺表面活性物质蛋白(SP)B、SP-C基因外显子4(exon4)区域基因变异与蒙古族早产儿呼吸窘迫综合征(RDS)的相关性。方法选择住院治疗的无血缘关系的蒙古族RDS早产儿50例(男31例,女19例),同期、同民族和同群体中无血缘关系的非RDS早产儿50例为对照组(男27例,女23例),分别用聚合酶链式反应(PCR)基因多态性分析和基因检测技术对SP-B、SP-C基因exon4区域基因进行测序,并比较两组患儿SP-B基因exon4区域1580位点基因变异及基因型频率、SP-C基因exon4区域c.571C A(T138N)位点基因变异及基因型频率的差异。结果检测出SP-B基因exon4区域1580位点基因变异,RDS组14例,变异率为28%,非RDS组11例,变异率为22%,两组差异无统计学意义(χ2=0.480,P 0.05)。RDS组1580位点CC、TT、CT基因型频率分别为16%、72%和12%,非RDS组则分别为10%、78%和12%;RDS组C等位基因频率为22%、T等位基因频率为78%,非RDS组则分别为16%、84%;两组间基因型频率差异无统计学意义(χ~2=1.170,P 0.05)。检测出SP-C基因exon 4区域c.571 C A(T 138 N)位点基因变异,RDS组41例,变异率为82%,非RDS组6例,变异率为12%,两组间差异有统计学意义(χ~2 =49.177,P 0.05)。RDS组c.571C A(T138N)位点CC、AA、AC三种基因型频率分别为18%、50%和32%,非RDS组分别为88%、8%和4%;RDS组C等位基因频率为34%、A等位基因频率为66%,非RDS组则分别为90%、10%,两组间A等位基因型频率的差异有统计学意义(χ~2=66.553,P 0.05)。结论携带SP-C基因exon 4区域c.571 C A(T 138 N)位点A等位基因的蒙古族早产儿患RDS的风险更高,而SP-B基因exon 4区域1580位点基因变异与蒙古族早产儿发生RDS无关。     

肺表面活性物质蛋白B基因多态性与新生儿呼吸窘迫综合征易感性的研究

目的 探讨肺泡表面活性物质蛋白B（SPB）基因多态性与新生儿呼吸窘迫综合征易感性的关系。方法 收集华中科技大学同济医学院附属同济医院的新生儿呼吸窘迫综合征（NRDS）诊断病例为病例组,并按1∶2比例收集胎龄和出生体重相匹配的无明显感染症状早产儿为对照组。应用聚合酶链反应 限制性片段长度多态（PCR RFLP）分析技术及基因测序技术检测SPB 18A/C及SPB1580C/T多态性,观察两组间基因型频率和等位基因频率的差异。并复习文献比较本研究汉族与其他种族人群等位基因频率的差异。结果 2008至2010年NRDS组91例,对照组182名进入分析。 ①SPB－18A/C基因在NRDS组AA,AC,CC基因型频率分别为11.0%、40.7%和48.4%,对照组分别为6.6%、31.3%和62.1%;两组基因型频率差异无统计学意义（P>0.05）;NRDS组A等位基因频率显著高于对照组（31.3% vs 22.3%）。②SPB1580C/T基因在NRDS组TT、TC和CC基因型频率分别为5.5%、63.7%和45.1%,对照组分别为30.8%、6.6%和48.4%;两组基因型频率差异无统计学意义（P>0.05）;NRDS组C等位基因频率显著高于对照组（79.1% vs 70.9%）。③本研究汉族人、美国人、巴西人和丹麦人SPB1580等位基因C频率分别为79%、35%、41%和46%,差异有统计学意义（P<0.05）,与日本人群等位基因C频率（72%）差异无统计学意义（P>0.05）;本研究汉族人、巴西人、美国人和丹麦人SPB－18等位基因A频率分别为31%、58%、57%和61%,差异有统计学意义（P<0.05）。结论 本研究汉族人群SPB－18A/C及SPB1580C/T基因多态性是NRDS的危险因素。不同种族人群SPB1580C/T和SPB－18A/C基因多态性分布存在明显差异。     

信号转导和转录激活因子6基因多态性与支气管哮喘易感性的关系

目的研究信号转导和转录激活因子6(STAT6)基因rs324015位点多态性与青岛汉族支气管哮喘(哮喘)患儿易感性的关系。方法应用PCR-限制性片段长度多态性(RFLP)的方法对青岛汉族113例哮喘患儿(哮喘组)、87例无血缘关系的汉族无变应性疾病及其他疾病的健康儿童(健康对照组)进行STAT6基因rs324015位点多态性分析;Hardy-Weinberg遗传平衡检验方法进行基因分布遗传平衡吻合度检验。结果 1.健康对照组和哮喘组STAT6基因rs324015位点各基因型频率分布均符合Hardy-Weinberg平衡检验,具有群体代表性。2.哮喘组GG、GA及AA 3种基因型分布频率分别为15.9%、46.9%和37.2%,健康对照组儿童其分布频率分别为21.8%、59.8%和18.4%,2组间基因型分布差异具有统计学意义(χ2=8.445,P<0.05),且不同基因型患哮喘的危险性不一样,AA基因型与GA、GG基因型比较患哮喘的危险性明显增加[OR(AA/GA)=2.575,95%CI:1.290～5.141,P<0.01;OR(AA/GG)=2.771,95%CI:1.167～6.577,P<0.05];基因型GA与GG间,患哮喘的危险性无统计学差异(OR=1.076,95%CI:0.508～2.277,P>0.05)。哮喘组患儿G、A等位基因分布频率分别为39.3%和60.6%,对照组分别为51.7%、48.2%,2组等位基因分布频率比较,差异有统计学意义(χ2=6.058,P<0.05),且A等位基因携带者哮喘患病率是非携带者的1.649倍[OR(A/G)=1.649,95%CI:1.106～2.459,P<0.05]。结论 STAT6基因rs324015位点多态性可能与汉族儿童哮喘易感性相关,突变纯合子AA携带者患哮喘的危险性大,A等位基因为导致哮喘患儿发病的优势等位基因。     

COL9A1基因在单纯性马蹄内翻足中的表达及其多态性分析

目的：COL9A1 基因是位于单纯性马蹄内翻足（ICTEV）易感区域(6q12-13)的已知基因。本研究探讨 COL9A1 基因在 ICTEV 患者中的表达及其单核苷酸多态 (SNP) 位点在ICTEV 和正常人中的分布情况。方法：应用免疫组化方法检测 25 例 ICTEV 患儿及 5 例正常对照组肌肉及肌腱组织中 COL9A1 的表达;应用限制性片段长度多态性技术结合测序法,分析 118 例 ICTEV 患者及 100 名正常人 COL9A1 基因的 2 个 SNP位点基因型。结果：88%（22/25）的 ICTEV 患者 COL9A1蛋白表达阳性,明显高于正常对照组。位于 COL9A1 基因编码区的 SNP 位点 rs1135056 的基因型频率和等位基因频率在两组人群中的分布差异有统计学意义（P<0.05）：ICTEV 组 G 等位基因频率高于对照组;与对照组相比,AA 基因型频率降低,AG、GG 基因型频率增高。结论：COL9A1 基因在 ICTEV 中高表达,rs1135056多态位点G等位基因和ICTEV的发生相关。     

肺表面活性物质蛋白B基因多态性与新生儿呼吸窘迫综合征易感性的相关性研究

目的：研究肺表面活性物质蛋白（SP）B基因单核苷酸多态性分布以及与新生儿呼吸窘迫综合征（RDS）的关系。方法：选择88例RDS早产儿和未并发RDS的早产儿103例作为研究对象,采用DNA提取试剂盒提取DNA,应用聚合酶联反应-限制性片段长度多态性技术检测SP-B-18A/C、SP-B 1580C/T两个位点的单核苷酸多态性,分析两个位点多态性与RDS的关系。结果：SP-B -18A/C、SP-B 1580C/T两个位点在病例组和对照组中均存在多态性,与未并发RDS的早产儿对照组比较,RDS患儿SP-B 1580C/T位点基因型以CC型明显增多,（χ2=12.26,P0.05）。结论：SP-B 1580 位点C/T多态性与RDS有关,SP-B 1580C/T可能是RDS的易感基因,携带SP-B 1580位点C等位基因的个体患RDS的风险增加。SP-B-18A/C与RDS无关。     

中国汉族人群RET基因多态性与先天性巨结肠的遗传易感性研究

目的 建立中国汉族人群RET基因密码子45和769的基因型和等位基因频率的分布背景，探讨其基因多态性与先天性巨结肠的关系。方法应用PCR-RELP在中国人群中检测对照组（n=122）及散发性先天性巨结肠组（n=94）G45A和T769G的单核苷酸多态性（single nucleotide polymorphisms，SNPs）。结果45位密码子和769位密码子在中国人群中均存在多态性。G45A在正常对照和疾病组中基因型频率分别为：对照组，AA0．17、AG0．72、GG0．11，突变型A和野生型G等位基因的频率为0．53、0．47；HD组，AA0．61、AG0．35、GG0．04，突变型A和野生型G等位基因的频率为0．78、0．22；T769G在正常对照和疾病组中基因型频率分布分别为：对照组，GG0．30、GT0．52、TT0．18，突变型G和野生型T等位基因的频率为0．56、0．44；HD组，GG0．49、GT0．36、TT0．15，突变型G和野生型T等位基因的频率为0．67、0．33。两个位点的基因型和等位基因的分布频率在两组间均有显著性差异（X^2=28．64，P〈0．001；X^2=5．27，P=0．022）。结论RET密码子45和769的基因多态性可能与中国汉族人群先天性巨结肠相关。     

PVRL2基因多态性与维吾尔族非综合征性唇腭裂相关性研究

目的 探讨脊髓灰质炎病毒相关受体2基因（poliovirus receptor-related 2, PVRL2） rs2075642位点多态性与新疆地区维吾尔族非综合征性唇腭裂（non-syndromic cleft lip with or without cleft palate, NSCL/P）的关系。方法 2014年1月至2015年6月乌鲁木齐市第一人民医院随机抽取维吾尔族NSCL/P病例120例, 正常对照100名, 运用Snapshot分型法测定PVRL2基因rs2075642多态性。χ2检验基因型分布是否符合Hardy-Weinberg遗传平衡, 分析基因型和等位基因型频率分布在病例组和对照组的差异。结果 资料符合Hardy-Weinberg平衡（P＞0.05）; PVRL2基因rs2075642位点的GA基因型、 等位基因A频率在维吾尔族病例组和对照组间的分布差异均具有统计学意义（分别为χ2＝5.829; P＜0.05和χ2＝5.642; P＜0.05）。结论 新疆地区维吾尔族NSCL/P的发生与PVRL2 基因rs2075642位点多态性相关; 人群携带杂合突变型 GA和等位基因A可能降低NSCL/P的发生风险。     

特发性矮小患儿胰岛素样生长因子受体基因单核苷酸多态性研究

目的：探讨胰岛素样生长因子-I受体（IGF-IR）基因单核苷酸多态性（SNP）与特发性矮小（ISS）的发病危险的相关性。方法：2008~2011年确诊为ISS患儿804例,正常对照组575例,用Snapshot法检测两组 IGF-IR基因相关位点SNP。结果：两组rs1976667基因型分布频率差异无统计学意义（P>0.05）;rs1976667 A等位基因分布频率较正常对照组高,差异有统计学意义（P<0.01)。结论：IGF-IR基因rs1976667位点等位基因A是ISS发病的危险因素。     

血小板活化因子乙酰水解酶基因多态性与早产儿颅内出血的关联性

目的：本研究从基因水平探讨血小板活化因子乙酰水解酶（PAF-AH）基因第9外显子Val279Phe单核苷酸多态性与早产儿颅内出血是否具有关联性,为有效预防颅内出血的发生提供理论依据。方法：选取颅内出血早产儿58例作为出血组,无颅内出血早产儿65例作为对照组,应用聚合酶链式反应（PCR）检测PAF-AH第9外显子Val279Phe单核苷酸多态性位点的基因型及等位基因的分布情况,进行病例对照研究分析。结果：出血组和对照组PAF-AH第9外显子Val279Phe基因型分布频率差异有统计学意义（P＜0.05）,其中出血组正常基因型频率（63.8%）明显低于对照组（81.5%）;出血组突变杂合子基因型（34.5%）明显高于对照组（16.9%）。两组PAF-AH等位基因分布频率差异亦有统计学意义（P＜0.05）,其中出血组T 等位基因频率（19.0%）明显高于对照组（10.0%）。结论：PAF-AH第9外显子Val279Phe的单核苷酸基因多态性与早产儿颅内出血有关。     

维生素D受体基因ApaI位点多态性与维生素D缺乏性佝偻病的研究

目的研究山西汉族儿童维生素D受体(VDR)基因ApaI位点多态性与维生素D缺乏性佝偻病的关系,探讨个体遗传因素在佝偻病发病中的意义,为临床防治探索一条新途径。方法以血清25(OH)D3水平、骨源性碱性磷酸酶(BALP)以及临床症状和体征作为分组指标,确定佝偻病组(40例)、对照组(68例)作为研究对象。应用酶联免疫和放射免疫方法,采用聚合酶链反应和限制性片段长度多态性技术(PCRRFLP)检测VDR基因ApaI位点多态性,HardyWeinberg遗传平衡检验方法进行基因分布遗传平衡吻合度检验。结果佝偻病组AA、Aa、aa基因型分布频率分别为5.0%、52.5%和42.5%。对照组AA、Aa、aa基因型分布频率分别为4.4%、55.9%、39.7%。佝偻病组等位基因A、a分布频率分别为31.3%、68.7%,对照组等位基因A、a分布频率分别为32.3%、67.7%。VDR基因型分布频率、等位基因分布频率两组间差异无统计学意义(χ2=0.089,P>0.05;χ2=0.028,P>0.05)。两组间血清25(OH)D3水平差异有统计学意义(t=-8.919,P<0.01)。结论(1)本组汉族儿童VDR基因ApaI位点多态性分布相对较均衡,a等位基因频率为67.7%,是优势基因。(2)本组人群VDR基因多态性分布与高加索人种相比明显不同,存在种族差异。(3)提示VDR基因ApaI位点多态性在个体是否发生维生素D缺乏性佝偻病方面可能没有意义。     

Polymorphisms of surfactant protein A genes and the risk of bronchopulmonary dysplasia in preterm infants

The pathophysiology of bronchopulmonary dysplasia (BPD) as an inflammatory disorder secondary to neonatal respiratory distress syndrome (RDS) is not yet fully understood and still represents a major complication of prematurity. The main pathophysiologic feature of RDS is a primary surfactant deficiency in a structurally immature lung. Pulmonary surfactant contains 90 percent phospholipids and 10 percent proteins (surfactant proteins A, B, C, and D). As surfactant protein A (SP-A) has several major immunological and metabolic intrapulmonary functions, we aimed at investigating an association of polymorphisms of SP-A1 and SP-A2 encoding genes and the risk of BPD. We performed a case-control study exclusively including Caucasian preterm infants below 32 weeks of gestation matched for the degree of immaturity and the year of birth. Venous cord blood was taken prospectively and analyzed by polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP), cloning and sequencing. BPD was defined as oxygen dependency or need for mechanical ventilation at day 28. Twenty-three infants with BPD were enrolled (mean gestational age 26.2 weeks; mean birth weight 760.4 g) and compared with 23 infants matched on the basis of gestational age (mean gestational age 27.9 weeks; mean birthweight 1015 g). We observed a significantly increased frequency of the SP-A1 polymorphism 6A6 in infants with BPD compared with controls. In addition to previously established risk factors for BPD, 6A6 polymorphism for SP-A1 gene is an independent co-factor. We believe treatment of neonatal RDS should also include stratification according to genetic risk factors.     

Prediction of respiratory distress syndrome by the level of pulmonary surfactant protein A in cord blood sera

The purpose of this study was to determine the utility of measuring the level of pulmonary surfactant protein A (SP-A) in cord blood sera to predict for respiratory distress syndrome (RDS). SP-A levels in cord blood sera from 48 infants born at gestational ages < 32 weeks were measured by a sandwich ELISA system. Mean value of SP-A in cord blood was 5.8 ng/ml in cases with RDS and 15.1 ng/ml in those without RDS (p = 0.002). The best cut-off point of cord blood SP-A to predict RDS was determined as 10 ng/ml. The sensitivity and the specificity of the cut-off point for predicting RDS were 81 and 76%, respectively. Multivariate regression analysis showed that high SP-A level in cord blood, premature rupture of the membranes longer than 24 h and heavy birth weight were all significantly related to the non-RDS outcome.     

Usefulness of stable microbubble test of tracheal aspirate for the diagnosis of neonatal respiratory distress syndrome

Objectives: To compare the overall accuracy of the stable microbubble test (SM test) with measurement of level of surfactant protein A (SP-A) of tracheal aspirate for the diagnosis of respiratory distress syndrome (RDS).
Methodology: Tracheal aspirates were obtained from neonates on ventilatory support. The SM test was carried out on specimens of tracheal aspirate immediately after collection. Levels of SP-A in tracheal aspirates were determined by enzyme-linked immunosorbent assay (ELISA) method. The results of the SM test and SP-A level of the tracheal aspirates were compared against the clinical diagnosis of RDS based on clinical, radiological and bacteriological findings.
Results: Both the median microbubble counts (6 microbubbles/mm,² range = 0–90) and median SP-A levels (100μg/L, range = 0–67 447) of infants with RDS were significantly lower than those of infants with no obvious lung pathology ( P <0.0001), and pneumonia ( P <0.0001). The SM test of tracheal aspirates had higher overall accuracy for the diagnosis of RDS than measurement of SP-A levels (94.6% vs 82.4%). When the receiver operating characteristic (ROC) curves of both tests for RDS were compared, the area under the ROC curve of the SM test was larger (0.9689) than that of the SP-A method (0.8965).
Conclusions: This study showed that the SM test of tracheal aspirate was a useful bedside diagnostic test for RDS. It could be carried out at any time after birth on infants requiring ventilatory support.     

Surfactant Apoprotein A (SP-A) in Tracheal Aspirates of Newborn Infants with RDS

Human pulmonary surfactant contains four groups of apoproteins, SP-A, B, C and D. We determined the concentration of SP-A in the tracheal aspirate of newborn infants by a two-site simultaneous immunoassay with monoclonal antibodies, and used this assay to assess changes in surfactant in various clinical situations. SP-A concentrations were standardized per milligram of albumin in the aspirate. The ratio of SP-A/albumin (µg/mg) in tracheal aspirates of 18 preterm infants with respiratory distress syndrome (RDS), in which samples were obtained within 12 hours of birth, was significantly lower (0.2 ± 0.1/µg/mg, mean ± S.D.) compared to a group of 20 non-RDS preterm infants of similar gestational age (15.8±7.4µg/mg) (p<0.05). None of the RDS infants had a SP-A/albumin ratio above l/µg/mg within 12 hours of birth, but the ratio exceeded 5µg/mg in all samples from non-RDS infants. The SP-A/albumin ratio significantly increased, however, at 48 to 72 hours after birth in infants with RDS (15.7 ± 9.5µg/mg). During the recovery phase of RDS, no difference was evident in the SP-A/albumin ratio in babies treated with artificial surfactant compared to those not treated .     

Inherited disorders of neonatal lung diseases

Although genetic factors are assumed to have a role in the etiology of respiratory distress syndrome (RDS), specific genes underlying this susceptibility are incompletely known. The most promising candidates are the genes coding for the lung-specific protein components of the surfactant. In congenital absence of surfactant protein A in mice, lung mechanics or surfactant homeostasis is normal. However, there is an increased susceptibility to infections. The major surfactant protein A alleles, 6A(2) and 1A(0), are the general high-risk RDS alleles, while the allele 6A(3) carries a decreased risk of RDS. The allele 6A(6) is also over-represented in infants with bronchopulmonary dysplasia. To date, no human infants who lack surfactant protein A have been identified, and the human respiratory phenotype associated with the 1A(0) allele has been demonstrated to be variable, therefore, surfactant protein A polymorphisms are not currently useful for estimation of individual risk of having an affected infant. Surfactant protein B (SP-B) plays an essential role in the structure of tubular myelin. Mutations resulting in an absence of surfactant protein B have been identified. They cause a recessively inherited, progressive respiratory disease. More than 27 loss of function mutations have been identified in the surfactant protein B gene that result in lethal neonatal respiratory failure. Of the several known common variants of the surfactant protein B gene, the most common mutation is 121ins22 that accounts for 60-70% of the mutant cases. Although the frequency of the 121ins2 mutation is rare, the consistent phenotype is exhibited by infants with a homozygous genotype. The clinical presentation in infants homozygous for the 121ins2 mutation is full-term infants who develop respiratory distress within the first 12-24 hours of life. Surfactant replacement therapy fails to reverse this outcome, and without lung transplantation, they expire within the first 1-6 months of life. Surfactant protein B gene mutations may also result in milder phenotypes. These mutations resulting in reduced synthesis of SP-B appear to be family-specific and result in respiratory distress, but sometimes with more gradually progressive or chronic respiratory failure. Surfactant protein C plays a role in the stabilization of surfactant and may also have a role in the intracellular processing of the surfactant complex. Surfactant protein B is important in the intracellular processing and production of surfactant protein C. Although surfactant protein C-deficient mice are viable and survive to adulthood without obvious pulmonary abnormalities, their lung have reduced viscoelasticty. Human respiratory disease in the neonatal period caused by loss-of-function mutations in the surfactant protein C gene has not been identified. However, an autosomal dominant inherited mutation at the surfactant protein C gene causes chronic interstitial lung disease. Surfactant protein D is a member of the collectin family like surfactant protein A, therefore it opsonizes pathogens and enhances their phagocytosis by alveolar macrophages and neutrophils. Unlike surfactant protein A, it does not contribute to lowering surface tension. Surfactant protein D-deficient mice have no respiratory abnormalities at birth, but it causes development of emphysema and predisposition to specific infections. No human infant or child with respiratory distress and mutation in the surfactant protein D gene has been identified.     

Endogenous pulmonary surfactant metabolism is not affected by mode of ventilation in premature infants with respiratory distress syndrome

OBJECTIVE: To determine if high frequency oscillatory ventilation (HFOV) decreases surfactant production in premature infants with respiratory distress syndrome (RDS). STUDY DESIGN: We randomized 19 infants <28 weeks of gestation to either HFOV (n = 8) or conventional ventilation (CV, n = 11) at 24 hours of life. After a 24-hour continuous infusion of uniformly labeled carbon 13 glucose (U-(13)C(6)) glucose, we measured (13)C enrichment in surfactant phosphatidylcholine (PC) in tracheal aspirate samples using gas chromatography/mass spectrometry. We calculated the fractional synthetic rate (FSR) of surfactant PC from labeled glucose and its half-life of clearance (T(1/2)). RESULTS: FSR did not differ between groups (4.7% +/- 2.7%/day CV vs 4.2% +/- 3.1%/day HFOV, P =.7). T(1/2) was 79 +/- 18 hours in the CV group and 76 +/- 23 hours in the HFOV group (P =.7). Neither degree of ventilatory support nor supplemental oxygen exposure correlated with surfactant metabolic indices. Three of 4 infants who died from RDS within the first month of life had a shorter T(1/2) than 14 of 15 infants who survived. CONCLUSION: Surfactant metabolism is similar in preterm infants ventilated with HFOV and CV. Shortened surfactant half-life may characterize a subset of preterm infants with lethal RDS.     

Pulmonary surfactant protein A in sera for assessing neonatal lung maturation

To examine whether surfactant protein A (SP-A) in postnatal serum can predict the development of respiratory distress syndrome (RDS), we analyzed the relationship between serum concentrations of SP-A and the risk of RDS using sera from neonates within 24 h after birth. A total of 104 blood samples including 23 samples from newborn infants with RDS were obtained. SP-A content in sera was measured with an enzyme-linked immunosorbent assay system consisting of a standard of native SP-A and two monoclonal antibodies against human SP-A. The level of serum SP-A increased with advancing gestation. Since the mean level of serum SP-A in patients with RDS (3.8 ng/ml) was significantly lower than those without RDS (12.0 ng/ml) (P<0.001), we calculated the diagnostic index values at various cutoff points and chose cutoff values to predict the risk of RDS. Maximum diagnostic value of 85% was obtained at a cutoff point of 3.8 ng/ml (sensitivity 57% and specificity 93%). We also chose a cutoff value of 2.1 ng/ml for definitive diagnosis of RDS, and 8.3 ng/ml for exclusive diagnosis of RDS. The adjusted odds ratios of RDS was significantly elevated when SP-A concentration in serum was under the cutoff values. The presence of SP-A in cord blood serum was also confirmed by immunoblotting analysis. We emphasize the value of SP-A examination in cord blood or postnatal serum from infants who exhibited respiratory difficulties at birth. We believe that our results are consistent with the hypothesis that SP-A is a useful serum marker in predicting the development of RDS.     

不同胎龄新生儿胃液卵磷脂／鞘磷脂比值变化及其临床意义

应用薄层层析法检测１１０例［足月儿５０例，其中正常新生儿３０例，窒息１２例，妊娠高血压综合征（简称好高征）母亲所生新生儿８例；早产儿６０例］新生儿胃液卵磷脂／鞘磷脂（Ｌ／Ｓ）比值。结果显示，足月儿Ｌ／Ｓ比值＞２．０，早产儿＜２．０，早产儿Ｌ／Ｓ比值与胎龄、体重有非常显著正相关（ｒ分别为０．８６、０．６５，Ｐ均＜０．０１）。足月窒息儿Ｌ／Ｓ比值明显低于正常对照组（ｔ＝２．６０，Ｐ＜０．０５）；患妊高征母亲所生新生儿Ｌ／Ｓ比值明显高于对照组（ｔ＝３．０３，Ｐ＜０．０１），提示母亲患妊高征有使胎儿肺成熟加速的倾向。６０例早产儿并发呼吸窘迫综合征７例，Ｌ／Ｓ比值均在１．０９以下，５例死亡，其中４例Ｌ／Ｓ比值在０．４以下。提示胃液Ｌ／Ｓ比值对评价肺成熟度及预估呼吸窘迫综合征发生及预后有重要参考价值。     

Pulmonary haemodynamics after surfactant replacement in severe neonatal respiratory distress syndrome.

Aortopulmonary pressure difference and pulmonary blood flow velocity were studied during the first 48 hours of life in 12 premature neonates with severe respiratory distress syndrome (RDS), treated by natural surfactant, and in 25 premature neonates with mild RDS. A non-invasive Doppler ultrasound method was used to estimate aortopulmonary pressure difference and pulmonary blood flow velocity from the left pulmonary artery. Aortopulmonary pressure difference was significantly lower at 6 hours of age in the infants with severe RDS and was not increased one hour after surfactant therapy. Aortopulmonary gradient started to rise at 24 hours of age and was equal to that of neonates with mild RDS at 48 hours. Pulmonary blood flow velocity was significantly lower, initially in the severe RDS group, and was not increased one hour after surfactant therapy. Left pulmonary artery flow velocity began to rise after 24 hours and reached the values of the mild RDS group at 48 hours. These data indicate that aortopulmonary pressure difference and pulmonary blood flow are low in the acute phase of RDS and that surfactant treatment does not seem to affect these values.