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Objective: In the last few decades, attention has been focused on morbidity and mortality associated with late preterm delivery (34-36 + 6/7 weeks), accounting for 60-70% of all preterm births. This study is aimed to determine (1) the prevalence of late preterm deliveries (spontaneous and medically indicated) in our population; and (2) the rate of neonatal morbidity and mortality as well as maternal complications associated with the different phenotypes of late preterm deliveries. Study design: This retrospective population-based cohort study, included 96,176 women who had 257,182 deliveries, occurred between 1988 and 2011, allocated into three groups: term (n = 242,286), spontaneous (n = 10,063), and medically indicated (n = 4833) late preterm deliveries. Results: (1) Medically indicated late preterm deliveries were associated with increased maternal morbidity, as well as neonatal morbidity and mortality, in comparison with other study groups (p < .01 for all comparisons); (2) medically indicated late preterm delivery was an independent risk factor for composite neonatal morbidity (low Apgar score at 5', seizures, asphyxia, acidosis) after adjustment for confounding factors (maternal age and ethnicity and neonatal gender) and stratification according to gestational age at delivery; and (3) the proportion of medically indicated late preterm deliveries affected the neonatal mortality rate. Below 35% of all late preterm deliveries, indicated late preterm birth were associated with a reduction in neonatal mortality; however, above this threshold medically indicated late preterm deliveries were associated with an increased risk for neonatal death. Conclusions: (1) Medically indicated late preterm deliveries were independently associated with adverse composite neonatal outcome; and (2) to benefit in term of neonatal outcome from the tool of medically indicated late preterm birth, their proportion should be kept below 35% of all late preterm deliveries, while exceeding this threshold increases the risk of neonatal mortality. [ABSTRACT FROM AUTHOR]

Objectives: To investigate mechanisms of in utero death in normally formed fetuses by measuring amniotic fluid (AF) biomarkers for hypoxia (erythropoietin [EPO]), myocardial damage (cardiac troponin I [cTnI]) and brain injury (glial fibrillary acidic protein [GFAP]), correlated with risk factors for fetal death and placental histopathology. Methods: This retrospective, observational cohort study included intrauterine deaths with transabdominal amniocentesis prior to induction of labor. Women with a normal pregnancy and an indicated amniocentesis at term were randomly selected as controls. AF was assayed for EPO, cTnI and GFAP using commercial immunoassays. Placental histopathology was reviewed, and CD15-immunohistochemistry was used. Analyte concentrations >90th centile for controls were considered "raised". Raised AF EPO, AF cTnI and AF GFAP concentrations were considered evidence of hypoxia, myocardial and brain injury, respectively. Results: There were 60 cases and 60 controls. Hypoxia was present in 88% (53/60), myocardial damage in 70% (42/60) and brain injury in 45% (27/60) of fetal deaths. Hypoxic fetuses had evidence of myocardial injury, brain injury or both in 77% (41/53), 49% (26/53) and 13% (7/53) of cases, respectively. Histopathological evidence for placental dysfunction was found in 74% (43/58) of these cases. Conclusion: Hypoxia, secondary to placental dysfunction, was found to be the mechanism of death in the majority of fetal deaths among structurally normal fetuses. Ninety-one percent of hypoxic fetal deaths sustained brain, myocardial or both brain and myocardial injuries in utero. Hypoxic myocardial injury was an attributable mechanism of death in 70% of the cases. Non-hypoxic cases may be caused by cardiac arrhythmia secondary to a cardiac conduction defect. [ABSTRACT FROM AUTHOR]

Objective: To determine the frequency and type of histopathologic lesions in placentas delivered by women with a normal pregnancy outcome. Methods: This retrospective cohort study included placental samples from 944 women with a singleton gestation who delivered at term without obstetrical complications. Placental lesions were classified into the following four categories as defined by the Society for Pediatric Pathology and by our unit: (1) acute placental inflammation, (2) chronic placental inflammation, (3) maternal vascular malperfusion and (4) fetal vascular malperfusion. Results: (1) Seventy-eight percent of the placentas had lesions consistent with inflammatory or vascular lesions; (2) acute inflammatory lesions were the most prevalent, observed in 42.3% of the placentas, but only 1.0% of the lesions were severe; (3) acute inflammatory lesions were more common in the placentas of women with labor than in those without labor; (4) chronic inflammatory lesions of the placenta were present in 29.9%; and (5) maternal and fetal vascular lesions of malperfusion were detected in 35.7% and 19.7%, respectively. Two or more lesions with maternal or fetal vascular features consistent with malperfusion (high-burden lesions) were present in 7.4% and 0.7%, respectively. Conclusion: Most placentas had lesions consistent with inflammatory or vascular lesions, but severe and/or high-burden lesions were infrequent. Mild placental lesions may be interpreted either as acute changes associated with parturition or as representative of a subclinical pathological process (intra-amniotic infection or sterile intra-amniotic inflammation) that did not affect the clinical course of pregnancy. [ABSTRACT FROM AUTHOR]

Objective: Recent studies suggest an association between Human Papilloma Virus (HPV) infection, cervical inflammation and obstetric complications (i.e. spontaneous preterm parturition and cervical insufficiency). It has been proposed that viral inflammation of the placenta causes changes in the mother's immune reaction to bacterial pathogens, which leads to enhanced inflammatory reaction and preterm delivery. Therefore, the aim of this population-based study was to determine the association between abnormal cervical cytology prior to pregnancy and obstetric outcomes.Study Design: A Retrospective population-based cohort study was designed, including all women who had a Pap smear up to two years prior to delivery or during first trimester of pregnancy (n = 15,357). Women were divided into the following groups, according to Pap smear results: group 1 - Normal PAP smear (n = 11,261); group 2 - Pap smear with evidence of an inflammatory process (n = 3895); and group 3 - Pap smear with evidence of HPV infection (n = 201). Obstetrical outcomes, gestational age at delivery, and pregnancy complications were compared among the groups.Results: The rate of HPV infection in our study population was 1.3%. The rate of preterm delivery (group 1 - 8.5%, group 2 - 8.5%, group 3 - 7%, p = 0.7), preterm PROM (group 1 - 1.7%, group 2-1.6%, group 3 - 2%, p = 0.66) and cervical insufficiency (group 1 - 0.5%, group 2 - 0.7%, group 3 - 1.5%, p = 0.11) did not differ significantly among the study groups. There was no statistical difference in the rate of premature rapture of membranes, newborn small-for-gestational-age, preeclampsia or placental abruption. Women with abnormal cervical cytology, either due to inflammation or HPV infection, had similar obstetric outcome in comparison to those with a normal cervical cytology.Conclusion: This population-based retrospective cohort study indicates no association between positive HPV testing with Pap smear and obstetric complications such as preterm delivery, cervical insufficiency, placental abruption, PROM, Preterm PROM, neonatal SGA and preeclampsia, in a population with low prevalence HPV infection. [ABSTRACT FROM AUTHOR]