Etiology And Pathology Of Premature Rupture Of Fetal Membranes' Placenta

Objective:Placenta is an intermediary organ between pregnant women and embryo. Certain diseases of pregnant women may be transmissed from the embryo through placenta. It can be found in placenta some evidences of pregnant women and embryo's diseases,death causes and etiopathogenisis of embryo and newborn.PROM (premature rupture of fetal membranes) is a common obstetrical neopathy. Many studies have been conducted for PROM, but most of them are limited to the analysis of clinical data, we can not see, especially the systematic study of placenta of microorganism infections pathological changes and the correlation with peripartum pregnant women and embryo's infectious diseases with PROM. This study though observing etiology and pathology of placenta with PROM and, to discuss correlation with newborn early infectious diseases to provide placental evidences about early newborn infectious diseases'diagnosis, treatment, prevention and prognosis.Methods:We analyze the etiology and pathology of 50 pieces of placenta with PROM, using methods of Gram staining, FQ-PCR, microscope frozen section, HE, transmission electron microscope and immunohistochemistry S-P, linking to the clinical data.Results:1.Gram-positive bacteria: amniotic membrane smear 90%(45/50p), amniotic fluid smear 96%(48/50p), gular swab smear 94%(47/50p), antrum auris fluid smear 78% (39/50p). Gram-negative bacteria: amniotic membrane smear 24%(12/50p), amniotic fluid smear 16%(8/50p), gular swab smear22%(11/50p), antrum auris fluid smear 12%(6/50p).2.Uu positive rate through FQ-PCR :cord blood 8%(4/50p), amniotic fluid smear 10%(5/50p),placenta 2%(1/50).HPVDNA: find one pou only in amniotic fluid smear.3.TEM show:Uu distribute individually dispersely. Villus dging, thicking basal membrane, growing collagen,et al.4.Placental histomorphology change with PROM: membranitis trend to serious along with time lengthening(RS = 0.3114,0.4685),syneytiotrophoblast tuberoses, expanding,syneytiotrophoblast membrane of villus blood vessel.5.Placental immunohistochemistry with PROM: apoptosis factor of bcl-2,fas/fasl are found to be positively localized in syncytial trophoblast(Bcl-2:Chi-Square = 5.7971 p= 0.0161;Fas:Chi-Square =70.6731 p <0.0001;Fas1:Chi-Square=17.7037 p<0.0001),MMP-9 is mainly localized in infiltrated inflammatory cell within fatal membranes,with the levels higher than that in control group(the rate of positive area:16.87±10.58,6.59±7.14,p= 0.0077).No positive protein was found in amnioepithelial cell and trophocyte.Conclusion:1.Microorganism infection is the initiative or important reason of premature rupture of fetal membranes.2.Ureaplasma urealyticum(Uu) can permeate placental barrier, cryptoreplicate in placenta , and then cause placental and intrauterine infection.3.Antepartum screening and the check of placenta with premature rupture of fetal membranes for pathogen is necessary. It can guide the medication before and after parturition period, to prevent the occurrence of premature rupture of fetal membranes) and pregnant women and embryo's infection.4.Placenta with premature rupture of fetal membranes may occur morphological changes because of pathogen infection, which are related to direct damages and immunity harms of pathogen.5.Frozen sectioncan make a early diagnosis of Membrantitis. Pathological changes of premature rupture of fetal membranes will provide some preventive factors for diagnosing and curing pregnant women and embryo's infection and intrauterine infection6.It is the most direct evidence that, there find Uu through transmission electron microscope(TEM), Uu can be found through TEM.7.Apoptosis is the functional placental barrier) important factor of infectious turnover, which can effect intrauterine infection and maternal-infant transmission.