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NSIDRC Journal Article Alert — September 25, 2009Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University. These articles have been selected from PubMed, a service of the National Library of Medicine that includes over 19 million citations from MEDLINE and other life science journals for biomedical articles back to 1948. PubMed includes links to full text articles and other related resources. Availability of full-text journal articles is often limited to subscribers or through inter-library loan. Please see your local library for copies of these articles, or view PubMed's How to Get the Journal Article for more details. Sudden Infant Death 1. Walsh SL, Kryscio R, Holsinger JW, Krous HF Department of Epidemiology, College of Public Health, University of Kentucky, 333 Waller Ave., Suite 200, Lexington, KY, 40504, USA, sabrina.walsh@uky.edu. The Centers for Disease Control and Prevention funded seven states, including Kentucky, to clarify statewide death certification practices in sudden, unexpected infant death and compare state performances with national expectations. Accurate assignment of the cause and manner of death in cases of sudden, unexpected infant death is critical for accurate vital statistics data to direct limited resources to appropriate targets, and to implement optimal and safe risk reduction strategies. The primary objectives are to (1) Compare SUID death certifications recommended by the KY medical examiners with the stated cause of death text field on the hard copy death electronic death certificates and (2) Compare KY and national SUID rates. Causes of death for SUID cases recommended by the medical examiners and those appearing on the hard copy and electronic death certificates in KY were collected retrospectively for 2004 and 2005. Medical examiner recommendations were based upon a classification scheme devised by them in 2003. Coroners hard copy death certificates and the cause of death rates in KY were compared to those occurring nationally. Eleven percent of infants dying suddenly and unexpectedly did not undergo autopsy during the study interval. The KY 2003 classification scheme for SIDS is at variance with the NICHD and San Diego SIDS definitions. Significant differences in causes of death recommended by medical examiners and those appearing on the hard copy and electronic death certificates were identified. SIDS rates increased in KY in contrast to decreasing rates nationally. Nationwide adoption of a widely used SIDS definition, such as that proposed in San Diego in 2004 as well as legislation by states to ensure autopsy in all cases of sudden unexpected infant death are recommended. Medical examiners' recommendations for cause of death should appear on death certificates. Multidisciplinary pediatric death review teams prospectively evaluating cases before death certification is recommended. Research into other jurisdictions death certification process is encouraged. 2. Jenik AG, Vain N Hospital Italiano de Buenos Aires, Argentina. A variety of studies have indicated that pacifier use lowers the risk of SIDS. Many observational studies have demonstrated a negative association between pacifier use and breastfeeding duration. However, observational studies cannot be used to determine whether the pacifier is the real cause of breastfeeding cessation. Evidence for causation can be better supplied by randomised controlled trials (RCTs). Three RCTs have been conducted on the relationship between pacifiers and breastfeeding, but each study has limitations, implying that the evidence of not causal effect can be questionated. We have recently presented the results of a large RCT which demonstrated that in mothers who are successfully breastfeeding at 2 weeks, the recommendation to offer a pacifier does not modify the prevalence of exclusive and any breastfeeding at different ages or the duration of lactation. It is therefore important that lactation consultants and international agencies reexamine their staunch position to discourage the use of pacifiers on the basis of a supposed adverse effect on the success and duration of breastfeeding. 3. Krous HF, Langlois NE Rady Children's Hospital-San Diego, 3020 Children's Way, M5007, San Diego, CA, 92123, USA, hkrous@rchsd.org. Miscarriage/Stillbirth/Prenatal Issues 1. Sarfraz AA, Samuelsen SO, Bruu AL, Jenum PA, Eskild A Department of Gynecology and Obstetrics and Medical Faculty Division, Akershus University Hospital, Lørenskog, Norway. ashi@broadpark.no OBJECTIVES: To assess the association between maternal parvovirus B19 infection and fetal death, birthweight and length of gestation. DESIGN: Case-control study. SETTING: Population based. POPULATION: Cases were all 281 women with fetal death within a cohort of 35 940 pregnant woxmen in Norway. The control group consisted of a random sample of 957 women with a live born child. METHOD: Information on pregnancy outcome was obtained from the Medical Birth Registry of Norway. First trimester serum samples were tested for antibodies against parvovirus B19 (IgM and IgG). In seronegative women, further serum was analysed to detect seroconversion during pregnancy. MAIN OUTCOME MEASURES: Fetal death, length of gestation and birthweight. RESULTS: Two of 281 (0.7%) of the women who experienced fetal death and nine of 957 (0.9%) of the controls had presence of IgM antibodies, crude odds ratio 0.8; 95% CI (0.2-3.5). In initially, seronegative women, 3.1% (2/65) with fetal death and 2.6% (8/307) with a live birth seroconverted, crude odds ratio 1.2; 95% CI (0.2-5.7). Presence of maternal parvovirus-specific IgG or IgM antibodies in the first trimester, or seroconversion during pregnancy were not associated with lower birthweight or reduced length of gestation in live born children, but was associated with low birthweight in stillborn offspring. CONCLUSION: Maternal parvovirus B19 infection was not associated with fetal death in our study. Very few cases of fetal death may be attributed to maternal parvovirus B19 infection. 2. Jin LP, Chen QY, Zhang T, Guo PF, Li DJ Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200011, China. The present study was undertaken to analyze the changes in the proportion of CD4(+)CD25(bright) regulatory T (Treg) cells and the expression of costimulatory molecules, CTLA-4 and CD28, in the peripheral blood and deciduas in the setting of non-pregnancy, normal early pregnancy and miscarriage. In this study, we showed that CD4(+)CD25(bright) T cells significantly increased in the peripheral of normal pregnancy compared to that of non-pregnancy. The proportions of CD4(+)CD25(bright) T cells in both peripheral blood and deciduas were significantly lower in miscarriage than that of normal pregnancy. CD4(+)CD25(bright) T cells were characterized by high-level FoxP3 expression and low-level CD69 expression. An increase in the CD28 mRNA expression was accompanied by a decrease in the CTLA-4 mRNA expression in decidual tissues from human miscarriage. The ratios of CTLA-4(+)/CD28(+) in miscarriage were significantly lower than that of the normal pregnancy both in the peripheral and in deciduas. The ratio of CTLA-4(+)/CD28(+) in CD4(+)CD25(bright) T cells was significantly higher than that of the CD4(+)CD25(dim) T cells both in normal pregnancy and in miscarriage. The decidual T cells in the miscarriage appeared higher in responsiveness and IL-2 and IFN-gamma production in comparison with the decidual T cells in the early pregnancy. These results above suggest that CD4(+)CD25(bright) Treg cells might play a role in the maintenance of pregnancy via up-regulation of CTLA-4 expression. The down-regulation of Treg cells and their functions, and the imbalance of positive and negative regulators of costimulatory signals might lead to an abnormal immune milieu, which confer susceptibility to pregnancy loss. 3. Willinger M, Ko CW, Reddy UM Pregnancy and Perinatology Branch, Center for Developmental Biology and Perinatal Medicine, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD. OBJECTIVE: We sought to determine factors associated with racial disparities in stillbirth risk. STUDY DESIGN: Stillbirth hazard was analyzed using 5,138,122 singleton gestations from the National Center of Health Statistics perinatal mortality and birth files, 2001-2002. RESULTS: Black women have a 2.3-fold increased risk of stillbirth compared with white women. The black/white disparity in stillbirth hazard at 20-23 weeks is 2.75, decreasing to 1.57 at 39-40 weeks. Higher education reduced the hazard for whites more than for blacks and Hispanics. Medical, pregnancy, and labor complications accounted for 30% of the hazard in blacks and 20% in whites and Hispanics. Congenital anomalies and small for gestational age contributed more to preterm stillbirth risk among whites than blacks. Pregnancy and labor conditions contributed more to preterm stillbirth risk among blacks than whites. CONCLUSION: The excess stillbirth risk for blacks was greatest at preterm gestations, and factors contributing to stillbirth risk vary by race and gestational age. 4. Duke CW, Correa A, Romitti PA, Martin J, Kirby RS Division of Birth Defects and Developmental Disabilities, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, 1600 Clifton Rd. NE, MS E-86, Atlanta, GA 30333, USA. cduke@cdc.gov Stillbirths, those with and without birth defects, are an important public health topic. The National Center on Birth Defects and Developmental Disabilities at the Centers for Disease Control and Prevention conducted two workshops during April and July 2005. Both workshops explored the challenges of conducting surveillance of stillbirths. Workshop participants considered an approach that added the surveillance of stillbirths, those with and without birth defects, as part of existing population-based birth defects surveillance programs in Iowa and Atlanta. The workshops addressed three key aspects for expanding birth defects programs to conduct active, population-based surveillance on stillbirths: (1) case identification and ascertainment, (2) data collection, and (3) data use and project evaluation. Participants included experts in pediatrics, obstetrics, epidemiology, maternal-fetal medicine, perinatology and pediatric pathology, midwifery, as well as practicing clinicians and pathologists. Expanding existing birth defects surveillance programs to include information of stillbirths could potentially enhance the data available on fetal death reports and also could benefit such programs by improving the ascertainment of birth defects. Prepared by the
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