Prediction of short-term newborn infectious morbidity based on maternal characteristics in patients with PPROM and Ureaplasma species infection.

OBJECTIVES: Preterm premature rupture of membranes (PPROM) complicates about 5% of pregnancies. Ureaplasma species is the most common pathogen found in the amniotic fluid in pregnancieneonatal outcome. The aim of the following study was to evaluate the impact of colonization with the Ureaplasma spp. on pregnant women with PPROM, coin fection with different microorganisms, and antimicrobial treatment on neonatal outcome. MATERIAL AND METHODS: The study included 30 women with PPROM hospitalized in Division of Reproduction in s complicated by PPROM. It is speculated that it requires a coin fection to produce unfavorable Poznan's K. Marcinkowski University of Medical Sciences. Swabs from cenvical canal were obtained for the identifidation of bacterial and ureaplasma tic infections by culture and POR. RESULTS: The presence of any infection during the pregnancy a fter PP ROM was con firmed in 22 patients (Ureaplasma spp. in 12 patients, coin fection in 10 women). The cure rate for Ureaplasma species and other infections was 17% (2/12 patients) and 23% (5/22 patients), respectively There was no correlation between Ureaplasma species infection, coin fection, and cure status with the infection in the newborn. The PPROM to delivery duration also did not affect the newborn infection status. A negative relationship with leukocyte level was detected in patient with newborn infection. CONCLUSIONS: The presence of colonization with Ureaplasma species is not attributable to neonatal short-term morbidity The evaluation of maternal biochemical and microbiological data, regardless of the duration of the pregnancy after PPROM or the cure status, does not add any insight into the newborn infection status.

Correlation of the expression of heparanase and heparin-binding EGF-like growth factor in the implantation window of nonconceptual cycle endometrium.

Although it was suggested that heparanase (HPSE) may affect implantation and pregnancy, so far there have been no wide-ranging studies on the expression of and possible disturbances in the interactions between HPSE, heparan sulfate (HS) and related growth factors, such as heparin-binding EGF-like growth factor (HB-EGF). The aim of this study was to evaluate whether the expression profile of both HPSE and HB-EGF can be associated with impaired reproduction in the endometrial implantation window, in the non-conception cycle. The study group consisted of 32 women with two or more unexplained, consecutive miscarriages, and 61 idiopathic infertility patients, while the control comprised of 22 women with normal reproductive potential. We compared the expression of HB-EGF and HPSE at the transcript (qPCR) and protein (Western Blot) levels in eutopic endometrium. Also assessed were correlations between both factors in the studied groups. In women with consecutive miscarriages we observed lower HPSE relative transcript (p = 0.003) and lower protein (p = 0.002) level compared with the control group. Level of the HB-EGF protein was decreased (p = 0.017). HPSE mRNA level was higher in idiopathic infertility (p = 0.003) compared with women with miscarriages. We found statistically significant correlations in both transcript and protein levels in all groups (p < 0.05). Our results allow the assumption of the existence of a process by which, in normal human endometrium, HB-EGF expression coincides with the synthesis of HPSE. As a result, the HB-EGF molecule can bind to the HS on the cell surface, enhancing its affinity to the receptor. Then, the release of growth factors associated with HS oligomers occurs that is catalyzed by HPSE. We suggest that one of the causes of unexplained miscarriages may result from the impaired expression of HPSE and HB-EGF.

Complement inhibitory proteins expression in placentas of thrombophilic women.

Factors controlling complement activation appear to exert a protective effect on pregnancy. This is particularly important in women with thrombophilia. The aim of this study was to determine the transcript and protein levels of complement decay-accelerating factor (DAF) and membrane cofactor protein (MCP) in the placentas of women with acquired and inherited thrombophilia. Also, we assessed immunohistochemistry staining of inhibitors of the complement cascade, DAF and MCP proteins, in the placentas of thrombophilic women.Placentas were collected from eight women with inherited thrombophilia and ten with acquired thrombophilia.The levels of DAF and MCP transcripts were evaluated by qPCR, the protein level was evaluated by Western blot. We observed a higher transcript (p < 0.05) and protein (p < 0.001) levels of DAF and MCP in the placentas of thrombophilic women than in the control group. DAF and MCP were localized on villous syncytiotrophoblast membranes, but the assessment of staining in all groups did not differ. The observed higher expression level of proteins that control activation of complement control proteins is only seemingly contradictory to the changes observed for example in the antiphospholipid syndrome. However, given the hitherto known biochemical changes associated with thrombophilia, a mechanism in which increased expression of DAF and MCP in the placentas is an effect of proinflammatory cytokines, which accompanies thrombophilia, is probable.