机构地区:[1]徐州医学院徐州临床学院儿科,221009 [2]徐州医学院附属医院儿科医院新生儿科,221002 [3]徐州医学院徐州临床学院中心实验室,221009
出 处:《中国新生儿科杂志》2016年第1期2-8,共7页Chinese Journal of Neonatology
基 金:徐州市社会发展科技计划(XZZD1238)
摘 要:目的探讨口服布洛芬与对乙酰氨基酚治疗早产儿症状性动脉导管未闭(sPDA)时血浆和尿前列腺素E_2(PGE_2)水平的变化。方法选择2012年10月至2015年6月徐州医学院徐州临床学院儿科新生儿病房收治的生后15 h^10天诊断sPDA的早产儿,随机分为布洛芬组和对乙酰氨基酚组。布洛芬组口服布洛芬10 mg/kg,24 h及48 h后再各给予5 mg/kg;对乙酰氨基酚组口服对乙酰氨基酚每次15 mg/kg,每6 h一次,共3天。首剂给药后72 h复查超声心动图,并检测治疗前后血浆和尿PGE_2水平,观察患儿尿量及并发症发生情况,分析血浆和尿PGE_2水平相关性。应用SPSS 20.0统计软件,分别采用卡方检验、t检验、非参数检验之Mann-Whitney U法、Pearson相关分析。结果布洛芬组43例,对乙酰氨基酚组44例。两组治疗后血浆和尿PGE_2水平均明显低于治疗前[布洛芬组血浆:(47.3±24.7)比(70.0±35.7)ng/L,对乙酰氨基酚组血浆:(59.9±32.9)比(74.2±35.5)ng/L,布洛芬组尿:(115.4±46.3)比(189.0±62.4)ng/L,对乙酰氨基酚组尿:(139.3±54.0)比(184.4±73.8)ng/L,P<0.05];对乙酰氨基酚组治疗后血浆和尿PGE_2水平下降幅度[12.6(5.7,19.5)ng/L、(45.0±36.9)ng/L]明显小于布洛芬组[18.5(10.1,33.8)ng/L、(73.5±44.8)ng/L,P=0.031、0.002]。对乙酰氨基酚组动脉导管闭合率与布洛芬组差异无统计学意义(70.5%比76.7%,P=0.506);虽然对乙酰氨基酚组少尿发生率明显低于布洛芬组(2.3%比14.0%),但差异无统计学意义(P=0.108)。两组治疗后大便隐血阳性率、脑室内出血、新生儿坏死性小肠结肠炎、支气管肺发育不良发生率差异无统计学意义(P>0.05)。两组治疗后血小板、血肌酐、谷丙转氨酶均无明显变化(P>0.05)。成功组与失败组治疗后血浆和尿PGE_2水平下降幅度差异无统计学意义(P>0.05),少尿组治疗后血浆和尿PGE_2水平下降幅度[35.0(26.3,49.8)ng/L、(135.0±38.0)ng/L]明显大于非少尿组[13.3(6.7,20.8)ng/L、(52.5±37.0)ng/L,P=0Objective To study the changes of plasma and urinary prostaglandin E2 (PGE2 ) levels in preterm infants with symptomatic patent ductus arteriosus (sPDA) treated with oral ibuprofen and acetaminophen. Methods Preterm infants with sPDA admitted to the neonatal ward of Xuzhou Clinical School of Xuzhou Medical College from Oct 2012 to Jun 2015 were randomly divided into two groups: Ibuprofen group (oral ibuprofen suspension was given with an initial dose of 10 mg/kg, followed by 5 mg/kg 24 and 48 hr later), acetaminophen group ( oral acetaminophen suspension was given at doses 15 mg/kg every 6 hours for three days). Echocardiography was repeated 72 hr after initial drug dose. The level of plasma and urinary PGE2 were monitored pre- and post-treatment. The urine volume and complications were recorded during treatment. SPSS 20. 0 software was used for data analysis. Data were compared by chi-square test, student's t test, Mann-Whitney U method of nonparametric test, Pearson correlation analysis. Results The post-treatment plasma PGE2 level in the ibuprofen group was In =43, (47.3 ±24. 7) ng/L] and acetaminophen group was In =44, (59. 9 ±32. 9) ng/L], and the post-treatment urinary PGE2 level in ibuprofen group was ( 115.4 ± 46. 3 ) ng/L and acetaminophen group was (139. 3 ±54. 0) ng/L. These results were significantly lower when compared to the pre-treatment plasma PGE2 level in ibuprofen group (70. 0± 35.7 ) ng/L and acetaminophen group (74. 2±35.5) ng/L, and significant lower when compared to the urinary PGE2 level in ibuprofen group ( 189. 0± 62. 4 ) ng/L and acetaminophen group ( 184. 4± 73.8 ) ng/L ( all P 〈 0. 05 ). After the treatment, the level of plasma and urinary PGE2 reduction of acetaminophen group was [ 12. 6 (5.7, 19. 5) ng/L, (45.0± 36. 9) ng/L] which was significantly lower than that of ibuprofen group [18.5 (10. 1, 33.8) ng/L, (73.5 ±44.8) ng/L] (P=0.031,0.002). The closure rate of sPDA in acetaminophen group (31
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