Abstract
ObjectiveAlthough intra-amniotic(IA) infection is present in both preterm labor and intact membranes(PTL) and preterm premature rupture of membranes(preterm-PROM), it is more common in preterm-PROM than in PTL. Microorganisms and their products in the amniotic-cavity can elicit an inflammatory-response in fetus as well as in amniotic-cavity in the progression of acute histologic chorioamnionitis(acute-HCA). A fundamental question is whether a fetal and an IA inflammatory-response is more severe in preterm-PROM than in PTL, in the same-context of acute-HCA with or without fetal-involvement. The purpose of current-study was to answer this-question.Study-DesignStudy population consisted of 213 singleton preterm-gestations(<34 weeks) delivered within 4 days of amniocentesis due to PTL(120 cases) or preterm-PROM(93 cases). The intensity of fetal and IA inflammatory-responses was compared between PTL and preterm-PROM, according to placental inflammatory conditions:1)placenta without inflammatory-lesion;2)acute-HCA without funisitis;3)acute-HCA with funisitis. IA inflammatory response was assessed by amniotic-fluid(AF) matrix metalloproteinase-8(MMP-8), and fetal inflammatory response(FIR) by umbilical-cord plasma(UCP) C-reactive protein(CRP) at birth.Results1) Patients with preterm-PROM had higher rates of IA infection, acute-HCA, and acute-HCA with funisitis than those with PTL did(p<.01 for each);2) there were no significant differences in the intensity of fetal and IA inflammatory-responses and the rate of cervical dilatation≥3 cm or 4 cm between patients with PTL and those with preterm-PROM in the context of both placenta without inflammatory-lesion and acute-HCA without funisitis(p>.05 for each);3) however, acute-HCA with funisitis was associated with a significantly higher median AF MMP-8 and UCP CRP concentration and higher rate of cervical dilatation≥3 cm or 4 cm in PTL than in preterm-PROM(AF MMP-8, 675 ng/mlvs.417 ng/ml; UCP CRP, 969 ng/mlvs.397 ng/ml;each for p<.05), despite less common IA infection in PTL than in preterm-PROM(29%vs.57%;p<.05).ConclusionsA fetal and an IA inflammatory-response is more severe in PTL than in preterm-PROM in the context of funisitis, despite less common IA infection. This unexpected observation may indicate the fundamental difference in the pathogenesis between PTL and preterm-PROM.
Highlights
Microbial invasion of amniotic cavity (MIAC) can be present in both patients with preterm labor and intact membranes (PTL) and those with preterm premature rupture of membranes [1,2,3,4,5,6,7,8]
1) Patients with preterm-PROM had higher rates of IA infection, acute-HCA, and acute-HCA with funisitis than those with PTL did(p,.01 for each);2) there were no significant differences in the intensity of fetal and IA inflammatory-responses and the rate of cervical dilatation$3 cm or 4 cm between patients with PTL and those with preterm-PROM in the context of both placenta without inflammatory-lesion and acute-HCA without funisitis(p..05 for each);3) acute-HCA with funisitis was associated with a significantly higher median Amniotic Fluid (AF) Matrix Metalloproteinase-8 (MMP-8) and UCP Creactive protein (CRP) concentration and higher rate of cervical dilatation$3 cm or 4 cm in PTL than in preterm-PROM(AF MMP-8, 675 ng/mlvs.417 ng/ml; UCP CRP, 969 ng/mlvs.397 ng/ ml;each for p,.05), despite less common IA infection in PTL than in preterm-PROM(29%vs.57%;p,.05)
A fetal and an IA inflammatory-response is more severe in PTL than in preterm-PROM in the context of funisitis, despite less common IA infection
Summary
Microbial invasion of amniotic cavity (MIAC) can be present in both patients with preterm labor and intact membranes (PTL) and those with preterm premature rupture of membranes (pretermPROM) [1,2,3,4,5,6,7,8]. It is more common in preterm-PROM than in PTL [1,2,4,5,9,10,11,12,13,14] It remains unclear which first develops between substantial bacterial infection in the chorioamniotic membranes or that in the amniotic cavity [15,16,17,18,19,20,21], ascending intrauterine infection is known to cause an inflammatory change in the chorio-amniotic membranes and sequentially elicit an inflammatory response in the amniotic cavity and fetus during the progression of acute histologic chorioamnionitis (acuteHCA).
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