新生儿缺氧缺血性脑病患儿血清sFas/sFasL水平的变化

目的观察缺氧缺血性脑病(HIE)新生儿血清可溶性Fas(sFas)和可溶性Fas配体(sFasL)的动态变化及其与头颅CT改变程度的相关性。方法选择HIE新生儿48例,按临床分度及头颅CT分度分为轻、中、重度3组。应用双抗体夹心酶联免疫吸附法(ELISA)测定其血清sFas、sFasL含量。结果1.HIE患儿急性期、恢复早期血清sFas、sFasL水平均明显高于对照组(P均<0.01);二者急性期均显著高于恢复早期(P均<0.01)。2.轻、中、重度HIE患儿急性期血清sFas与sFasL水平均明显高于对照组(P<0.05,0.01)。3.HIE患儿急性期血清sFas与sFasL水平呈密切正相关(r=0.51 P<0.01)。结论HIE患儿血清sFass、FasL水平增高与其病程和病情密切相关,血清sFasL和sFas水平可作为判断HIE病情的实验室指标之一。     

病毒性心肌炎患儿血清sFas、sFasL的表达水平

目的 探讨可溶性Fas(sFas)及其配体(sFasL)在小儿病毒性心肌炎中的表达以及与细胞凋亡和免 疫反应的关系。方法 采用ELISA法对21例病毒性心肌炎患儿和20例健康儿童进行血清sFas和sFasL的浓度 测定。结果 病毒性心肌炎患儿血清sFas和sFasL表达水平较健康儿童明显增高(P均<0.01);病毒性心肌炎患 儿血清sFas与sFasL表达水平呈正相关(P<0.01)。结论 血清sFas及sFasL表达增高与病毒性心肌炎疾病过 程有关,其作用机制可能通过抑制或减弱激活的T淋巴细胞凋亡造成免疫性心肌损害;病毒性心肌炎患儿血清 sFas表达增高进一步证实其发病与免疫因素有关;血清中sFas和／或sFasL表达增高可望作为T淋巴细胞激活的 标志和病毒性心肌炎的诊断依据之一。     

病毒性心肌炎患儿血清巨噬细胞移动抑制因子、肿瘤坏死因子-α、白细胞介素-1β表达及其意义

目的 探讨巨噬细胞移动抑制因子(MIF)、TNF-α、IL-1β在病毒性心肌炎(VM)患儿血清中表达的意义.方法 收集衡阳市中心医院和南华大学第一附属医院收治的30例急性期和20例恢复期VM患儿及30例健康儿童血清,采用ELISA测定其血清MIF、TNF-α、IL-1β水平,采用日立7180型全自动生化分析仪检测磷酸肌酸激酶同工酶(CK-MB),并与30例健康儿童作对照.结果 VM急性期患儿血清MIF[(136.7±32.2) ng/L]、TNF-α[(247.6±48.2) ng/L]、IL-1β[(19.7±4.4) ng/L]及CK-MB[(34.2±9.7) U/L]水平均明显高于恢复期及健康对照组,有显著性差异(F=17.2,21.4,13.5,14.1 Pa＜0.01),且血清MIF、TNF-α、LI-1β及CK-MB水平随病情加重而增高,MIF与CK-MB,TNF-α与CK-MB、IL-1β与CK-MB均呈正相关(r=0.68,0.82,0.73 Pa＜0.05);VM恢复期MIF[(41.8±8.2) ng/L]、TNF-α[(67.5±12.1) ng/L]、IL-1β[(6.4±1.2) ng/L]及CK-MB[(12.6±4.1) U/L]水平与健康对照组比较,无显著性差异(Pa＞0.05),且MIF、TNF-α、IL-1β与CK-MB无相关性(Pa＞0.05).结论 VM患儿存在细胞免疫功能紊乱,MIF、TNF-α、IL-1β可能参与VM发病过程,并可作为病情判断及疗效的观察指标之一.     

病毒性心肌炎患儿血清肿瘤坏死因子-α的变化及维生素E、C的干预作用

目的探讨病毒性心肌炎(VM)患儿TNFα的变化及维生素E、C的干预作用。方法将31例VM患儿随机分为A组16例,予抗感染、营养心肌药物及对症治疗;B组15例,在A组治疗基础上加用维生素E胶囊50mg/d口服,维生素C注射液100mg/(kg·d)静脉点滴,疗程均为1个月,采用ELISA双抗体夹心法测定VM患儿及健康儿童外周血清TNFα含量,采用美国贝克曼公司生产的CX7型全自动化分析仪测定31例VM心肌酶。结果VM组TNFα水平显著高于健康儿童(P<0.01),VM组TNFα升高者其各项心肌酶异常百分数均显著增高(P均<0.05);B组TNFα水平较A组显著下降(P<0.05)。结论TNFα参与VM发生发展的病理生理过程,检测血清TNFα水平有助于VM的诊断、病情判断和预后,维生素E、C可降低VM患儿血清TNFα的水平。     

颗粒酶B和可溶性Fas配体在病毒性心肌炎血清中的表达与心脏超声心功能的关系

目的探讨病毒性心肌炎(VM)患儿急性期血清颗粒酶B(GrB)和可溶性FasL(sFasL)水平变化及其与心脏超声和心脏收缩功能的关系。方法采用ELISA方法检测60例VM和40例健康儿童血清GrB和sFasL水平,同时对VM患儿行心脏超声及心功能检查。测定心脏指数(CI)、射血分数(EF)、心轴缩短率(SF)、每搏指数(SI)、左室内径(LV)、左房内径(LA)、右室内径(RV)。结果VM组GrB和sFasL水平显著高于对照组(P均<0.01);VM患儿血清GrB与sFasL水平呈正相关(r=0.7608 P<0.05);VM组GrB和sFasL升高者,心脏超声检查示心脏扩大、心肌动度减弱和心功能下降发生率明显增加(P均<0.05)。结论血清GrB和sFasL可作为判断VM患儿心肌损害程度及评估心功能的辅助指标。     

过敏性紫癜患儿血清可溶性血管细胞黏附分子-1及可溶性细胞间黏附分子-1表达的意义

目的 检测过敏性紫癜(HSP)患儿血清可溶性血管细胞黏附分子-1(sVCAM-1)及可溶性细胞间黏附分子-1(sICAM-1)表达,并探讨其临床意义.方法 酶联免疫吸附法(ELISA)测定53例HSP患儿(其中急性期37例,恢复期16例)及25例健康儿童血清sVCAM-1、sICAM-1水平,分别比较其急性期和恢复期及有或无肾损害HSP患儿上述因子表达水平.结果 HSP急性期患儿血清sVCAM-1和sICAM-1水平明显高于恢复期和健康对照组(Pa＜0.01);肾损害组血清sVCAM-1、sICAM-1明显高于无肾损害组(Pa＜0.01).结论 sVCAM-1、sICAM-1参与HSP病理生理过程,与疾病分期相关;血清sVCAM-1、sICAM-1水平增高可作为儿童HSP肾损害的判断指标之一.     

恙虫病患儿Th1/Th2/Th17细胞特征性细胞因子表达研究

目的观察恙虫病患儿Th1/Th2/Th17细胞特征性细胞因子在病程不同时期血清的表达,并探讨其在儿童恙虫病中的作用。方法收集2005年1月至2010年11月于广州市妇女儿童医疗中心住院治疗的恙虫病患儿,参照文献建立儿童恙虫病危重症评分系统。用双抗体夹心酶连免疫吸附(ELISA)法分别测定高评分组(≥5分)和低评分组(5分)恙虫病患儿急性期(起病7 d内)和恢复期(病程14 d)血清中细胞因子干扰素(IFN)-γ、白细胞介素(IL)-4和IL-17表达水平。选择10例健康体检患儿标本作为对照。结果急性期高评分组和低评分组血清IL-17表达水平与对照组比较显著增高(P0.01),恢复期高评分组和低评分组血清IL-17表达下降与对照组比较差异无统计学意义(P0.05);血清IL-4表达水平在急性期和恢复期与对照组比较差异无统计学意义(P0.05);血清IFN-γ表达水平在恢复期与急性期比较差异无统计学意义(P0.05)。不同时期血清IL-17表达水平与儿童恙虫病评分呈显著正相关(r=0.92,P=0.031)。结论检测血清中细胞因子IL-17水平对儿童恙虫病病情评估有重要临床应用价值,可作为疗效用预后的监测指标之一。     

病毒性心肌炎患儿免疫状况的研究

目的：探讨病毒性心肌炎 (VMC)患儿在细胞免疫、体液免疫和自身免疫方面的改变,从而指导免疫治疗。方法：用流式细胞技术分别测定 30例急性期、2 2例迁延期VMC患儿及30例对照的血清CD2 3,CD3/HLA DR,用比浊法测IgG,IgA和IgM。 结果：VMC患儿急性期、迁延期的CD2 3,IgG ,IgA ,IgM及CD3+ /HLA -DR+,CD3-/HLA -DR+ 细胞比例均高于正常对照组 (P均 <0 .0 1)。VMC患儿CD2 3和IgG ,IgA ,IgM呈正相关 (r分别=0.30,0.17,0.40,P<0.0 5),而急性期、迁延期VMC患儿的CD3+ /HLA DR-细胞表达率与正常对照组相比均无明显差异 (P均 >0 .0 5 )。迁延期患儿的各项指标和急性期相比无明显差异(P均>0.05)。结论：病毒性心肌炎患儿急性期、迁延期的细胞免疫、体液免疫均处于增强状态,提示细胞免疫、体液免疫可能参与了VMC患儿的心肌损伤。     

过敏性紫癜患儿不同时期血清D-二聚体与病程的关系

目的探讨儿童过敏性紫癜血清D-二聚体数值与病程之间的关系。方法检测诊断且未经治疗的过敏性紫癜单纯型的47例患儿及39例混合型患儿病程初期与发病两周后的血清D-二聚体,并进行对比、判断。结果入院时诊断单纯型和混合型的患儿初期血清D-二聚体对比,差异有显著性;两组患儿发病两周后血清D-二聚体对比,差异无显著性;将病程初期与病程超过两周后两组血清D-二聚体增高患儿的例数分别与最终病程超过3月的例数进行对比,有显著性差异。结论过敏性紫癜患儿初期血清D-二聚体增高不能提示病程迁延;而病程超过两周后血清D-二聚体增高多提示病程迁延。     

急性毛细支气管炎患儿血清白细胞介素13、γ-干扰素表达的意义

目的 探讨急性毛细支气管炎患儿血清IL-13、IFN-γ表达及其临床意义.方法 用酶联免疫吸附法(ELISA)检测42例急性期毛细支气管炎患儿(其中轻症组22例,重症组20例)和20名健康婴儿血清IL-13、IFN-γ水平.采用方差分析和成组t检验,检测各组间差异.结果 1.急性毛细支气管炎患儿血清IL-13[(6.88±2.12 )ng/L]明显高于对照组[(5.48±1.28 )ng/L](P＜0.05).2.急性期毛细支气管炎患儿IFN-γ[(10.71±2.44 )ng/L]明显高于对照组[(9.20±1.54)ng/L](P＜0.05);轻症组明显高于重症和对照组(P＜0.05),而重症与对照组则无显著性差异(P＞0.05).结论 1.IL-13参与毛细支气管炎的发病过程,但其水平不能反映病情严重程度;2.IFN-γ水平在轻症毛细支气管炎组明显增高,而重症组不增高,可能与急性重症毛细支气管炎患儿IFN-γ产生受抑制有关.     

病毒性心肌炎患儿微小病毒B19感染的研究

目的探讨病毒性心肌炎患儿微小病毒B19（HPV B19）感染的状况及其相关性。方法应用巢式聚合酶链反应法对60例病毒性心肌炎患儿（观察组）及30例健康体检儿童（对照组）血浆中微小病毒B19-DNA进行检测,并对观察组中HPV B19-DNA检测阳性与阴性两组中血CK、CK-MB及心功能指标进行比较。结果观察组B19-DNA检测阳性率为26．7％（16／60例）,对照组B19-DNA检测均为阴性,两组比较差异有显著性（P〈0．01）。观察组中HPV B19-DNA检测阳性与阴性的两组中血CK、CK—MB值差异无显著性（P〉0．05）。心功能指标LVSF比较差异有显著性（P〈0．01）,SV比较差异亦有显著性（P〈0．05）。结论小儿病毒性心肌炎与HPV B19感染有关,HPV B19可能是小儿病毒性心肌炎主要病原之一;HPV B19感染所致小儿病毒性心肌炎的心功能改变中左室功能受累程度较重。     

病毒性脑炎患儿血清心肌肌钙蛋白的临床意义

目的　研究血清心肌肌钙蛋白I(CTnI)水平对病毒性脑炎 (病脑 )并心肌炎或心肌损害患儿的诊断价值。方法　用酶联免疫吸附试验 (ELISA)测定 4 0例病脑患儿 (意识障碍组 12例 ,无意识障碍组 2 8例 ;惊厥组18例 ,无惊厥组 2 2例 )及 4 0例对照组血清心肌酶谱及CTnI水平。结果　病脑组血清心肌酶谱及CTnI阳性率明显高于对照组 (P <0 .0 5 ) ,同时有意识障碍组血清心肌酶谱及CTnI阳性率明显高于无意识障碍组 (P <0 .0 5 ) ,有惊厥组血清心肌酶谱和CTnI阳性率高于无惊厥组 (P均 <0 .0 5 )。结论　CTnI对病脑并心肌损害诊断有较高的特异性、敏感性 ,是治疗及预后判断的指标之一     

神经生长因子在小鼠病毒性心肌炎心肌中表达的意义

目的探讨病毒性心肌炎(VMC)发病过程中,心肌组织神经生长因子(NGF)表达的动态变化及发病机制中作用。方法70只4周龄雄性BALB/C小鼠腹腔接种0.1ml的CVB3建立VMC模型,10只同周龄同品系小鼠腹腔接种Eagle’s液作为对照组。VMC组于接种后3、7、15、30d,对照组于30d处死,采用RT-PCR、免疫组化检测心肌NGF mRNA及蛋白表达,并对NGF表达水平与心肌病变积分进行相关性分析。结果VMC组3~30d各时点心肌NGF mRNA及蛋白表达水平均明显增高,以7d时为最高,与对照组比较,差异均有显著性(P<0.05或0.01),而且NGF蛋白表达水平与心肌病变积分呈显著正相关(r=0.90,P<0.05)。结论NGF过度表达可能在病毒性心肌炎的发病机制中起重要作用。     

Expression of neurotrophic factors in cerebrospinal fluid and plasma of children with viral and bacterial meningoencephalitis

Aim: To evaluate the expression of neurotrophic factors (nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF)) and their association with the clinical-radiological characteristics and outcome of children with viral and bacterial meningoencephalitis (ME). Methods: Prospective observational clinical study performed on 13 children with ME and 12 controls with non-inflammatory obstructive hydrocephalus. Neurotrophic factor levels in the cerebro-spinal fluid (CSF) and plasma were measured using an immunoenzymatic assay. Results: High levels of NGF and BDNF were demonstrated in all patients, while GDNF levels did not undergo significant variations. NGF expression in the CSF was higher in viral ME than in bacterial ME and was correlated with CSF cellularity (particularly mononuclear cells). BDNF expression in the CSF was higher in bacterial ME than in viral ME and was correlated with CSF cellularity and blood platelet count. No relationships were noted between CSF protein or serum C-reactive protein levels and the expression of neurotrophic factors. Regarding clinical and radiological features, elevated NGF/BDNF levels in the CSF correlated with higher incidence of seizures and prolonged comatose state and with specific radiological lesions. No correlation was found between NGF/BDNF levels and final outcome.

Conclusions: The variations in neurotrophic factor levels may reflect an endogenous attempt at neuroprotection against biochemical and molecular changes during both viral and bacterial ME. The expression of these factors is likely to play a neuro-immunomodulatory or neurosurvival role in ME infections.     

Circulating cardiac troponins levels and cardiac dysfunction in children with acute and fulminant viral myocarditis

Objectives: To study the correlation between cardiac Troponins blood levels and degrees of cardiac dysfunction in children with acute and fulminant viral myocarditis and to study their prognostic role in predicting the outcomes and risk of having dilated cardiomyopathy. Methodology: Troponin I & T blood levels were measured in 65 children with acute or fulminant viral myocarditis. The cardiac functions of RV & LV were assessed by Doppler echocardiography. Results: The levels of cTnI & CTnT were significantly higher in patients with fulminant myocarditis than in controls and children with acute myocarditis (p < 0.05 & <0.001* respectively). The cardiac functions were significantly impaired in fulminant myocarditis than in acute myocarditis (p < 0.001*). There were negative correlations between the cardiac troponins levels and the cardiac functions measured by echocardiography in children with acute and fulminant myocarditis. There were 3 deaths (7.5%), and 10 (25%) children developed dilated cardiomyopathy in acute myocarditis while there were eight deaths (32%) and one patient (4%) who developed dilated cardiomyopathy in fulminant myocarditis group. Conclusion: Cardiac troponins levels can predict the severity of myocarditis and the prognosis on the short‐term level. Fulminant myocarditis was associated with higher levels of both cTn I & cTn T than acute myocarditis. Despite that fulminant myocarditis has a more aggressive course, the risk of developing cardiomyopathy was less than in acute myocarditis.     

三种不同类型抗心磷脂抗体在小儿病毒性心肌炎中的价值

采用酶联免疫吸附试验（ＥＬＩＳＡ）法测定６２例ＣｏｘＢ组病毒引起的病毒性心肌炎（ＶＭ）患儿和４０名健康儿童的血清抗心磷脂抗体（ＡＣＡ）。结果：ＶＭ组ＡＣＡ－ＩｇＧ、ＡＣＡ－ＩｇＡ、ＡＣＡ－ＩｇＭ阳性率（分别为４５．２％、３０．６％、３３．９％）均显著高于正常对照组（分别为２．５％、０、０）;ＶＭ发病早期ＡＣＡ－ｉｇＡ、ＡＣＡ－ＩｇＭ阳性显著多于ＡＣＡ－ｉｇＧ阳性恩赐 ＡＣＡ－ＩｇＧ阳性者的ＣＫ－Ｍ     

病毒性心肌炎患儿血清可溶性白细胞介素2受体检测的临床意义

目的探讨心肌炎患儿免疫功能的改变。方法应用单克隆抗体夹心酶联免疫吸附试验（ＥＬＩＳＡ）法对３０例病毒性心肌炎急性期患儿可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）进行检测,并与２２例健康儿童对照进行比较。结果病毒性心肌炎患儿血清ｓＩＬ－２Ｒ水平明显升高,为６３２．５６±２９３．４５Ｕ／ｍｌ,在急性期病人中,病程小于１个月者与病程２～６个月者血清ｓＩＬ－２Ｒ无显著性差异。当病毒感染时,机体免疫功能处于紊乱状态,随着病程的延长,病情的迁延不愈,血清ｓＩＬ－２Ｒ一直处于高水平状态。ｓＩＬ－２Ｒ升高可使白细胞介素２（ＩＬ－２）产生受体抑制,从而进一步加重机体的免疫功能紊乱。结论动态观察血清ｓＩＬ－２Ｒ水平对判定病情变化和预后有意义,亦可评估机体的免疫状态。     

sFas and sFas ligand and pediatric sepsis-induced multiple organ failure syndrome

The Fas-Fas ligand system is important for apoptosis of activated immune cells. Perturbation of this system occurs in diseases with dysregulated inflammation. Increased soluble Fas (sFas) occurs in systemic inflammatory response syndrome (SIRS) and can block apoptosis. Increased shedding of FasL (sFasL) occurs in viral infection and hepatitis. Although dysregulated inflammation is associated with sepsis-induced multiple organ failure (MOF) in children, a role for Fas has not been established. We hypothesize that 1) sFas will be increased in children with severe and persistent sepsis-induced MOF and will correlate with inflammatory markers suggesting a role for sFas in inflammatory dysregulation in severe sepsis, and 2) sFasL will be increased when viral sepsis or sepsis-induced liver failure-associated MOF is present in children. Plasma sFas, sFasL, IL-6, IL-10, nitrite + nitrates, and organ failure scores were measured on d 1 and d 3 in 92 children with severe sepsis and 12 critically ill control children. sFas levels were increased in severe sepsis, continued to increase in persistent MOF and nonsurvivors, and were correlated with serum inflammatory markers (IL-6, IL-10, nitrite + nitrate levels). In contrast, sFasL was not increased in severe sepsis and did not correlate with inflammation. sFasL was, however, increased in liver failure-associated MOF and in nonsurvivors, and was associated with viral infection. At autopsy, hepatocyte destruction and lymphocyte infiltration were associated with increased sFas and sFasL levels. sFas may interfere with activated immune cell death and contribute to dysregulation of inflammation, worsening outcome from severe sepsis. sFasL may contribute to hepatic injury and the development of liver failure-associated MOF.     

病毒性心肌炎患儿血清心肌钙蛋白I检测阳性与时间的关系

目的探讨病毒性心肌炎(VM)患儿血清心肌钙蛋白I(cTnI)检测阳性与时间的关系。方法临床诊断为急性VM患儿21例,分别于入院后不同时间静脉采血,动态检测血清cTnI,并与35例正常对照组比较。结果正常对照组血清cTnI均阴性;VM患儿刚入院时阳性6例(28.6%),至入院后6、12、18、24、48、72 h,10~14 d分别为7例(33.3%)、8例(38.1%)、9例(42.9%)、9例(42.9%)、13例(61.9%)、4例(19%)。入院后48、72 h cTnI累计阳性率分别较刚入院时和入院后10~14 d有显著性差异(P均<0.05)。结论对临床上拟诊VM发病不久患儿,通过不同时间段反复多次采血,能提高cTnI检出阳性率。