<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Di Lorenzo, G</style></author><author><style face="normal" font="default" size="100%">Ceccarello, M</style></author><author><style face="normal" font="default" size="100%">Cecotti, V</style></author><author><style face="normal" font="default" size="100%">Ronfani, L</style></author><author><style face="normal" font="default" size="100%">Monasta, L</style></author><author><style face="normal" font="default" size="100%">Vecchi Brumatti, L</style></author><author><style face="normal" font="default" size="100%">Montico, M</style></author><author><style face="normal" font="default" size="100%">D'Ottavio, G</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">First trimester maternal serum PIGF, free β-hCG, PAPP-A, PP-13, uterine artery Doppler and maternal history for the prediction of preeclampsia.</style></title><secondary-title><style face="normal" font="default" size="100%">Placenta</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Placenta</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">Chorionic Gonadotropin, beta Subunit, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Cohort Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Galectins</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypertension, Pregnancy-Induced</style></keyword><keyword><style  face="normal" font="default" size="100%">Pre-Eclampsia</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Complications</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Trimester, First</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy-Associated Plasma Protein-A</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Ultrasonography, Prenatal</style></keyword><keyword><style  face="normal" font="default" size="100%">Uterine Artery</style></keyword><keyword><style  face="normal" font="default" size="100%">Uterus</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">33</style></volume><pages><style face="normal" font="default" size="100%">495-501</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To evaluate the detection of pregnancy hypertensive disorders by integrating maternal history, serum biomarkers and uterine artery Doppler in the first trimester.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We prospectively recruited 2118 women that underwent an 11-13 weeks aneuploidy screening. We gathered information on maternal history, uterine artery Doppler and serum biomarkers (PAPP-A, PlGF, PP-13 and free β-hCG). Models were developed for the prediction of overall preeclampsia (PE), early-onset PE, late-onset PE and gestational hypertension (GH). For each outcome, we performed a multivariate logistic regression starting from the saturated model: adopting a step-down procedure we excluded all factors not statistically significant (p &gt; 0.05). Sensitivity models only for statistically significant parameters were calculated from the ROC curves for fixed false-positive rates (FPR).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Among 2118 women, 46 (2.17%) developed GH and 25 (1.18%) were diagnosed with PE, including 12 (0.57%) early-onset PE and 13 (0.61%) late-onset PE. For a fixed FPR of 10 and 5%, serum PlGF, free β-hCG and chronic hypertension identified respectively 67 and 75% of women who developed early-onset PE. In the model for the prediction of overall PE the combination of the uterine artery Doppler pulsatility index (UtA PI) with PlGF and chronic hypertension reached a sensitivity of 60% for a 20% of FPR.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;An integration of maternal characteristics and first trimester maternal serum biomarkers (free β-hCG and PlGF) provided a possible screening for early-onset PE. In the overall PE model, UtA PI turned out to be statistically significant but did not improve the detection rate.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22459245?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">De Seta, F</style></author><author><style face="normal" font="default" size="100%">Banco, R</style></author><author><style face="normal" font="default" size="100%">Turrisi, A</style></author><author><style face="normal" font="default" size="100%">Airoud, M</style></author><author><style face="normal" font="default" size="100%">De Leo, R</style></author><author><style face="normal" font="default" size="100%">Stabile, G</style></author><author><style face="normal" font="default" size="100%">Ceccarello, M</style></author><author><style face="normal" font="default" size="100%">Restaino, S</style></author><author><style face="normal" font="default" size="100%">De Santo, D</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pelvic inflammatory disease (PID) from Chlamydia trachomatis versus PID from Neisseria gonorrhea: from clinical suspicion to therapy.</style></title><secondary-title><style face="normal" font="default" size="100%">G Ital Dermatol Venereol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">G Ital Dermatol Venereol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chlamydia Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Chlamydia trachomatis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gonorrhea</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Neisseria gonorrhoeae</style></keyword><keyword><style  face="normal" font="default" size="100%">Pelvic Inflammatory Disease</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">147</style></volume><pages><style face="normal" font="default" size="100%">423-30</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Pelvic inflammatory disease (PID) is the most significant complication of sexually transmitted infections in childbearing-age women and it represents an important public health problem because of its long-term sequelae (chronic pelvic pain, tubal infertility, ectopic pregnancy). Prior to the mid 1970s PID was considered a monoetiologic infection, due primarily to Neisseria gonorrhea. Now it is well documented as a polymicrobial process, with a great number of microrganisms involved. In addition to Neisseria gonorrhea and Chlamydia trachomatis, other vaginal microrganisms (anaerobes, Gardnerella vaginalis, Haemophilus influenzae, enteric Gram negative rods, Streptococco agalactie, Mycoplasma genitalium) also have been associated with PID. There is a wide variation in PID clinical features; the type and severity of symptoms vary by microbiologic etiology. Women who have chlamydial PID seem more likely than women who have gonococcal PID to be asymptomatic. Since clinical diagnosis is imprecise, the suspicion of PID should be confirmed by genital assessment for signs of inflammation or infection, blood test and imaging evaluation. Laparoscopic approach is considered the gold standard. According to the polymicrobial etiology of PID, antibiotic treatment must provide broad spectrum coverage of likely pathogens. Early administration of antibiotics is necessary to reduce the risk of long-term sequelae.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23007248?dopt=Abstract</style></custom1></record></records></xml>