前列腺素E_2是否是新生儿肥厚性幽门梗阻的致病因素?  

IF PROSTAGLANDIN E_2 IS ONE ETIOLOGICAL FACTOR OF INFANTILE HY-PERTROPfflC PYLORIC STENOSIS?

作　　者：倪庆宾[1] 时继东[2] 张凯[2] 吕秀芝[2] 

机构地区：[1]山东大学山东省立医院小儿科,250021 [2]泰山医学院第一教学医院小儿外科

出　　处：《新生儿科杂志》2003年第2期49-51,共3页The Journal of Neonatology

摘　　要：研究先天性肥厚性幽门梗阻(HPS),对患儿胃液中PGE_2术前、术后的变化,以探讨其与HPS发病的关系。测定HPS患儿术前、术后24小时、术后72小时胃液中PGE_2和PH值及其相关关系,并设立正常对照组。结果显示:HPS组术前PGE_2测定(220.10±68.20mg/L)明显高于对照组(98.75±50.20mg/L,P<0.01);术后24小时(150.33±45.10mg/L)明显下降(P<0.05),72小时(102.25±40.55mg/L)降至正常(P>0.05)。胃液pH值术前、术后24小时、72小时分别为1.95±0.45、2.25±0.38、3.15±0.42;而对照组3.10±0.55,术前明显低于对照组(P<0.01),术后很快升高,72小时与对照组无差异(P>0.05)。PGE_2水平与术前、术后胃液为pH值呈负相关(R=0.73),即与胃酸水平呈正相关。结论:HPS患儿胃液中PGE_2水平明显高于对照组,术后显著下降;PGE_2与胃液pH值呈负相关,即胃酸浓度越高,PGE_2分泌越增加。说明,PGE_2的升高是由胃酸分泌增加引起的继发现象,与HPS的发病无关。HPS患儿幽门梗阻、胃排空延迟,刺激胃酸分泌从而引起PGE_2升高,反之梗阻解除后PGE_2下降。To study the role of prostaglandin E2 (PGE2) in the pathogenesis of hypertrophic pyloric stenosis (HPS), the levels of PGE2 and pH of gastric fluid in HPS patients were measured before and after a Ramstedt operation. Results showed the PGE2 concentration in the gastric fluid of 35 HPS patients before the Ramstedt operation was sinificantly higher(220.10 ±68. 20 mg/L) than that of 18 controls(98.75 ± 50.20 mg/L, P < 0.01), and the concentration which was 150.33 ± 45. 10 mg/L at 24 hours and 102.25 ± 40.55 mg/L at 72 hours after the operation which decreased significantly (P < 0.05). The pH level in the gastric fluid in HPS patients was 1.95 ± 0.45 before the operation and 2.25 ± 0.38 and 3.15 ± 0.42 24 h and after the operation 72 h. It was significantly lower than that of the controls (3.10 ± 0.55, P<0.01) before the operation, and elevated markedly after the operation. A significant inverse correlation between the PGE2 and the pH level in the gastric fluid was shown in HPS cases (R = 0.73). Conclusion: The results showed that the level of PGE2 in gastric fluid of HPS patients before the operation was higher than that of the controls, and decreased markedly after the operation. The PGE2 was correlated inversely with the pH level in the gastric fluid. The enhanced generation of PGE2 in gastric mucosa in cases of HPS was a secondary phenomenon caused by hyperacidity and was unreponsible for the pathogenesis of HPS. Prolonged gastric emptying time caused by pyloric stenosis may result in hyperacidity in HPS patients, it can enhance the PGE2 secretion. It would be inverse if the stenosis was released.

关 键 词：前列腺素E2 新生儿 肥厚性幽门梗阻 致病因素 术前 术后 胃泌素 

分 类 号：R726.5[医药卫生—儿科]