45 research outputs found

    Continuous subcutaneous insulin infusion reduces neonatal risk in pregnant women with type 1 diabetes mellitus

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    Objectives: An attempt was made to demonstrate the superiority of the treatment model using continuous subcutaneous insulin infusion (CSII) over multiple daily injections (MDI) of insulin in achieving a successful pregnancy outcome and good newborn’s condition in patients with type 1 diabetes.  Material and methods: The study included 297 infants born to type 1 diabetic patients; 175 patients were treated with MDI and 122 with CSII.  Maternal metabolic control during pregnancy, gestational weight gain, insulin requirements, pregnancy outcome and neonatal status were compared between MDI and CSII arm.  The composite adverse neonatal outcome was diagnosed if at least one of the following was found: abnormal birth weight (LGA or SGA), congenital malformation, miscarriage, intrauterine fetal death, emergency CS due to fetal risk, iatrogenic prematurity, RDS, hypoglycemia, hyperbilirubinemia, and the postpartum pH in the umbilical artery ≤ 7.1.  Results: The studied groups did not differ regarding gestational week at delivery, a proportion of births at full term, preterm births, miscarriages, or late pregnancy losses (intrauterine fetal death > 22 weeks). Newborns of mothers treated with CSII showed lower incidence of neonatal complications (composite adverse neonatal outcome) compared to those of mothers treated with MDI (60% vs 74%, respectively; p = 0.01). We did not find any association between the mode of treatment and composite adverse maternal outcome.  Conclusions: The use of CSII in the treatment of pregnant women with type 1 diabetes was associated with reduced number of neonatal complications presented as neonatal composite outcome but had no influence on maternal outcome

    Is abnormal vaginal microflora a risk factor for intrauterine fetal growth restriction?

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    Publisher Copyright: © 2015 The Authors.Objective: To conduct a literature review in search of possible preventable causes for fetal growth restriction. Methods: We performed a systematic literature search regarding abnormal vaginal microflora and fetal growth encompassing the last 27-year (starting from 1986) in PubMed, Embase, and Cochrane Central to study the evidence that abnormal vaginal microflora is may be related to diminished fetal growth or small for date birth. Results: Most of the 14 studies suggested a significant role of vaginal organisms in impaired fetal growth, unrelated to preterm birth. The neonatal outcome has shown to be largely linked to the preventable or foreseeable fetal factors, such as genetic abnormalities, but also ascending intrauterine infections. Our previous work suggested a role of vaginal organisms in adverse pregnancy outcome, not only preterm birth, but also impaired fetal growth. Conclusions: There is a need for cohort studies designed to unravel this link between abnormal microflora and FGR, in order to enable preventive actions to protect these small babies from severe damage and death by early screening and treatment.publishersversionPeer reviewe

    Hearing impairment in premature newborns-Analysis based on the national hearing screening database in Poland.

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    OBJECTIVES:The incidence of sensorineural hearing loss is between 1 and 3 per 1000 in healthy neonates and 2-4 per 100 in high-risk infants. The national universal neonatal hearing screening carried out in Poland since 2002 enables selection of infants with suspicion and/or risk factors of hearing loss. In this study, we assessed the incidence and risk factors of hearing impairment in infants ≤33 weeks' gestational age (wga). METHODS:We analyzed the database of the Polish Universal Newborns Hearing Screening Program from 2010 to 2013. The study group involved 11438 infants born before 33 wga, the control group-1487730 infants. Screening was performed by means of transient evoked otoacoustic emissions. The risk factors of hearing loss were recorded. Infants who failed the screening test and/or had risk factors were referred for further audiological evaluation. RESULTS:Hearing deficit was diagnosed in 11% of infants ≤25 wga, 5% at 26-27 wga, 3.46% at 28 wga and 2-3% at 29-32 wga. In the control group the incidence of hearing deficit was 0.2% (2.87% with risk factors). The most important risk factors were craniofacial malformations, very low birth weight, low Apgar score and mechanical ventilation. Hearing screening was positive in 22.42% newborns ≤28 wga and 10% at 29-32 wga and in the control group. CONCLUSIONS:Hearing impairment is a severe consequence of prematurity. Its prevalence is inversely related to the maturity of the baby. Premature infants have many concomitant risk factors which influence the occurrence of hearing deficit

    The association between the positive result of the hearing screening and the final diagnosis of hearing deficit in the study subgroups.

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    <p>The association between the positive result of the hearing screening and the final diagnosis of hearing deficit in the study subgroups.</p

    The contribution of risk factors to hearing loss in infants of the study subgroups and the control group (multivariate logistic regression analysis—odds ratios (OR) and 95% confidence intervals).

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    <p>The contribution of risk factors to hearing loss in infants of the study subgroups and the control group (multivariate logistic regression analysis—odds ratios (OR) and 95% confidence intervals).</p

    Dra/AfaE Adhesin of Uropathogenic Dr/Afa(+) Escherichia coli Mediates Mortality in Pregnant Rats

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    Escherichia coli bearing adhesins of the Dr/Afa family frequently causes urogenital infections during pregnancy in humans and has been associated with mortality in pregnant rats. Two components of the adhesin, Dra/AfaE and Dra/AfaD, considered virulence factors, are responsible for bacterial binding and internalization. We hypothesize that gestational mortality caused by Dr/Afa(+) E. coli is mediated by one of these two proteins, Dra/AfaE or Dra/AfaD. In this study, using afaE and/or afaD mutants, we investigated the role of the afaE and afaD genes in the mortality of pregnant rats from intrauterine infection. Sprague-Dawley rats, on the 17th day of pregnancy, were infected with the E. coli afaE(+) afaD and afaE afaD(+) mutants. The clinical E. coli strain (afaE(+) afaD(+)) and the afaE afaD double mutant were used as positive and negative controls, respectively. The mortality rate was evaluated 24 h after infection. The highest maternal mortality was observed in the group infected with the afaE(+) afaD(+) strain, followed by the group infected with the afaE(+) afaD strain. The mortality was dose dependent. The afaE afaD double mutant did not cause maternal mortality, even with the highest infection dose. The in vivo studies corresponded with the invasion assay, where the afaE(+) strains were the most invasive (afaE(+) afaD strain > afaE(+) afaD(+) strain), while the afaE mutant strains (afaE afaD(+) and afaE afaD strains) seemed to be noninvasive. This study shows for the first time that the afaE gene coding for the AfaE subunit of Dr/Afa adhesin is involved in the lethal outcome of gestational infection in rats. This lethal effect associated with AfaE correlates with the invasiveness of afaE(+) E. coli strains in vitro
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