实用临床医学
實用臨床醫學
실용림상의학
Practical Clinical Medicine
2015年
9期
50-53
,共4页
莫坤梅%黎远团%谢建红%陈雨彬%梁伯泉%陈忠其%邓玲
莫坤梅%黎遠糰%謝建紅%陳雨彬%樑伯泉%陳忠其%鄧玲
막곤매%려원단%사건홍%진우빈%량백천%진충기%산령
早产儿%脑损伤%宫内感染%细胞因子
早產兒%腦損傷%宮內感染%細胞因子
조산인%뇌손상%궁내감염%세포인자
preterm infants%brain damage%intrauterine infection%cytokine
目的:研究宫内感染与早产儿脑损伤的因果关系,从细胞因子网络反应角度探讨宫内感染早产儿脑损伤机制,为防治早产儿脑损伤提供新途径。方法将100例早产儿根据头颅超声及 CT 检查结果分为早产脑损伤组(31例)和早产无脑损伤组(69例)。通过对2组胎膜、胎盘的病理检测(主要以检测绒毛膜羊膜炎为主),判断是否有宫内感染导致的早产儿脑损伤。采用酶联免疫吸附试验(ELISA)检测2组血清中细胞因子[IL-1β、IL-6、IL-10及肿瘤坏死因子(TNF-α)]的水平。结果100例患儿中发生宫内感染40例,60例为非宫内感染,宫内感染患病率为40.0%。宫内感染患儿脑损伤的患病率为47.5%(19/40),非宫内感染患儿脑损伤的患病率为20.0%(12/60)。宫内感染患儿脑损伤患病率显著高于非宫内感染患儿(χ2=8.485,P <0.05)。早产脑损伤组 IL-1β、IL-6、IL-10及TNF-α分别为(6.33±2.17)(8.20±4.10)(1.46±0.25)及(5.35±2.00)μg·L-1;早产无脑损伤组 IL-1β、IL-6、IL-10及 TNF-α分别为(1.44±1.01)(1.58±2.33)(1.65±0.30)及(3.57±1.33)μg·L-1。早产脑损伤组 IL-1β、IL-6、TNF-α显著高于早产无脑损伤组,IL-10低于早产无脑损伤组(均 P <0.05)。结论早产儿脑损伤与宫内感染关系密切,细胞因子网络反应可能介导该损伤过程。
目的:研究宮內感染與早產兒腦損傷的因果關繫,從細胞因子網絡反應角度探討宮內感染早產兒腦損傷機製,為防治早產兒腦損傷提供新途徑。方法將100例早產兒根據頭顱超聲及 CT 檢查結果分為早產腦損傷組(31例)和早產無腦損傷組(69例)。通過對2組胎膜、胎盤的病理檢測(主要以檢測絨毛膜羊膜炎為主),判斷是否有宮內感染導緻的早產兒腦損傷。採用酶聯免疫吸附試驗(ELISA)檢測2組血清中細胞因子[IL-1β、IL-6、IL-10及腫瘤壞死因子(TNF-α)]的水平。結果100例患兒中髮生宮內感染40例,60例為非宮內感染,宮內感染患病率為40.0%。宮內感染患兒腦損傷的患病率為47.5%(19/40),非宮內感染患兒腦損傷的患病率為20.0%(12/60)。宮內感染患兒腦損傷患病率顯著高于非宮內感染患兒(χ2=8.485,P <0.05)。早產腦損傷組 IL-1β、IL-6、IL-10及TNF-α分彆為(6.33±2.17)(8.20±4.10)(1.46±0.25)及(5.35±2.00)μg·L-1;早產無腦損傷組 IL-1β、IL-6、IL-10及 TNF-α分彆為(1.44±1.01)(1.58±2.33)(1.65±0.30)及(3.57±1.33)μg·L-1。早產腦損傷組 IL-1β、IL-6、TNF-α顯著高于早產無腦損傷組,IL-10低于早產無腦損傷組(均 P <0.05)。結論早產兒腦損傷與宮內感染關繫密切,細胞因子網絡反應可能介導該損傷過程。
목적:연구궁내감염여조산인뇌손상적인과관계,종세포인자망락반응각도탐토궁내감염조산인뇌손상궤제,위방치조산인뇌손상제공신도경。방법장100례조산인근거두로초성급 CT 검사결과분위조산뇌손상조(31례)화조산무뇌손상조(69례)。통과대2조태막、태반적병리검측(주요이검측융모막양막염위주),판단시부유궁내감염도치적조산인뇌손상。채용매련면역흡부시험(ELISA)검측2조혈청중세포인자[IL-1β、IL-6、IL-10급종류배사인자(TNF-α)]적수평。결과100례환인중발생궁내감염40례,60례위비궁내감염,궁내감염환병솔위40.0%。궁내감염환인뇌손상적환병솔위47.5%(19/40),비궁내감염환인뇌손상적환병솔위20.0%(12/60)。궁내감염환인뇌손상환병솔현저고우비궁내감염환인(χ2=8.485,P <0.05)。조산뇌손상조 IL-1β、IL-6、IL-10급TNF-α분별위(6.33±2.17)(8.20±4.10)(1.46±0.25)급(5.35±2.00)μg·L-1;조산무뇌손상조 IL-1β、IL-6、IL-10급 TNF-α분별위(1.44±1.01)(1.58±2.33)(1.65±0.30)급(3.57±1.33)μg·L-1。조산뇌손상조 IL-1β、IL-6、TNF-α현저고우조산무뇌손상조,IL-10저우조산무뇌손상조(균 P <0.05)。결론조산인뇌손상여궁내감염관계밀절,세포인자망락반응가능개도해손상과정。
ABSTRACT:Objective To explore the causality relationship between intrauterine infection and brain damage in premature infants,to observe the mechanism of brain damage in premature in-fants with intrauterine infection from the perspective of cytokine network response,and to provide a new way of preventing premature brain damage.Methods According to head ultrasound and CT results,100 premature infants were divided into brain damage group(n = 31)and non-brain damage group (n = 69 ).Intrauterine infection-induced premature brain damage was observed through pathological examinations of fetal membranes and placenta(mainly chorioamnionitis).In addition,serum levels of cytokines interleukin-1β(IL-1β),interleukin-6 (IL-6 ),interleukin-10 (IL-10)and tumor necrosis factor-α(TNF-α)were detected by ELISA.Results The prevalence of intrauterine infection was 40.0%(40/100).The incidence of brain damage in infants with intrau-terine infection(47.5%,19/40)was significantly higher than that in infants without intrauterine infection(20.0%,12/60)(χ2 =8.485,P <0.05).Moreover,infants with brain damage had higher levels of IL-1β,IL-6 and TNF-αand lower levels of IL-10 than infants with non-brain damage((6. 33±2.17),(8.20±4.10),(1.46±0.25)and(5.35±2.00)μg·L-1 vs(1.44±1.01),(1.58±2. 33),(1.65±0.30)and(3.57 ± 1.33)μg· L-1 ,respectively;P <0.05).Conclusion Premature brain damage is positively associated with intrauterine infection,and the cytokine network re-sponse may mediate the damage process.