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NSIDRC Journal Article Alert — April 10, 2009Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University. Past issues of Resource Center journal alerts are
available at http://www.sidscenter.org. Sudden Infant Death 1. Dwyer T, Ponsonby AL Sudden infant death syndrome and prone sleeping position Ann Epidemiol. 2009 Apr;19(4):245-9 Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, Australia. terry.dwyer@mcri.edu.au In this review, we describe the epidemiological work conducted by ourselves and others on prone sleep position and sudden infant death. What we have learned since 1990 is that the prone sleep position was a major component of a casual pathway that was operating in over half of the SIDS deaths that were occurring in developed countries at the end of the 1980. It has been estimated that advice to place infants supine to sleep may have saved in the order of 850 infants annually in Australia and other countries. The story of the SIDS epidemic is an example of the contribution that epidemiology can make to the understanding and prevention of an important public health problem. 2. Lavezzi AM, Casale V, Oneda R, Weese-Mayer DE, Matturri L Sudden Infant Death Syndrome and Sudden Intrauterine Unexplained Death: Correlation Between Hypoplasia of Raphé Nuclei and Serotonin Transporter Gene Promoter Polymorphism Pediatr Res. 2009 Apr 1. [Epub ahead of print] Department of Surgical, Reconstructive and Diagnostic Sciences [A.M.L., V.C., R.O., L.M.], University of Milan, Milan 20122, Italy; Center for Autonomic Medicine in Pediatrics [D.E.W.-M.], Northwestern University Feinberg School of Medicine, Chicago, IL 60614. The present study, besides to delineate the cytoarchitecture and the localization in the brainstem of the human raphé nuclei, aims to evaluate the correlation between neuropathological raphé defects and serotonin transporter gene (5-HTT) promoter region polymorphisms in a cohort of 28 sudden infant death syndrome (SIDS) victims, 12 sudden intrauterine unexplained deaths (SIUD) and 17 controls. Hypoplasia of one or more nuclei of both the rostral and caudal raphé groups was found in 57% of SIDS, in 67% of SIUD and only in 12% of controls. Furthermore, a significant correlation between 5-HTT Long (L) allele, hypoplasia of the raphé nuclei and maternal smoking in pregnancy was observed in sudden fetal and infant deaths. The presence of the L allele represents a predisposing factor for sudden fetal and infant death in association with morphological developmental defects of the raphé nuclei and prenatal smoke exposure. A further consideration of the authors is that SIUD should not be regarded as a separate entity from SIDS, given the potentially shared neuropathological and genetic bases. 3. Sakai J, Takahashi S, Funayama M Gas dispersal potential of infant bedding of sudden death cases (II): Mathematical simulation of O(2) deprivation around the face of infant mannequin model Leg Med (Tokyo). 2009 Mar 31. [Epub ahead of print] Division of Forensic Medicine, Tohoku University School of Medicine, 2-1 Seiryou-chou, Aoba-ku, Sendai, Japan. We assessed O(2) gas deprivation potential of bedding that had actually been used by 26 infants diagnosed with sudden unexpected infant death using FiCO(2) time course of baby mannequin model. All cases were the same ones in our poster paper (I). Mathematically, time-FiCO(2) (t) graphs were given as FiCO(2) (t)=C(1-e(Dt)). Here, "C" approximates the maximum FiCO(2) value, while "D" is the velocity to reach maximum FiCO(2). FiO(2) in a potential space around the mannequin's nares was estimated using a formula: FiO(2)=0.21-FiCO(2)/RQ. RQ is the respiratory quotient, and the normal human value is 0.8. The graph pattern of FiO(2) is roughly the inverse of the FiCO(2) time course. Four cases showed the bottom of estimated FiO(2) to be more than 15%, 15 were 15-6%, and the other seven were 6% or less. Considering the minimal tissue stores of O(2), changes in FiO(2) may be affected by both CO(2) production and gas movement around the infant's face. Especially, the latter seven cases may suggest the participation of the role not only of CO(2) accumulation but also of the decrease of O(2) around the face. 4. Vennemann MM, Bajanowski T, Brinkmann B, Jorch G, Sauerland C, Mitchell EA; GeSID Study Group.Collaborators (26) Sleep environment risk factors for sudden infant death syndrome: the German sudden infant death syndrome study Pediatrics. 2009 Apr;123(4):1162-70 Bach P, Bockholt B, Bohnert M, Cremer U, Deml U, Freislederer A, Heide S, Huckenbeck W, Jachau K, Kaatsch HJ, Klein A, Kleemann WJ, Larsch KP, Fiegut A, Fischer D, Leukel W, Rauch E, Paulus W, Penning R, Rublack F, Sauerland C, Schlaud M, Schmidt B, Sperhake J, Zimmer G, Zweihoff R. Institute of Legal Medicine, University of Münster, Röntgenstrasse 23, D-48149 Münster, Germany. mechtild.vennemann@ukmuenster.de OBJECTIVE: Our goal was to investigate the risk factors for sudden infant death syndrome in the infants' sleep environment for a population in which few infants sleep prone as a result of education campaigns. METHODS: This was a population-based sudden infant death syndrome case-control study over 3 years (1998-2001) in Germany. RESULTS: There were 333 sudden infant death syndrome cases and 998 matched controls. Although only 4.1% of the infants were placed prone to sleep, those infants were at a high risk of sudden infant death syndrome. Those who were unaccustomed to sleeping prone were at very high risk, as were those who turned to prone. Bed sharing (especially for infants younger than 13 weeks); duvets; sleeping prone on a sheepskin; sleeping in the house of a friend or a relative (compared with sleeping in the parental home); and sleeping in the living room (compared with sleeping in the parental bedroom) increased the risk for sudden infant death syndrome; pacifier use during the last sleep was associated with a significantly reduced risk of sudden infant death syndrome. CONCLUSIONS: This study has clarified the risk factors for sudden infant death syndrome in a population where few infants sleep prone. This study supports the current recommendations of the American Academy of Pediatrics. This study has identified several novel risk factors for sudden infant death syndrome: an increased risk if the infants sleeps outside the parental home, death in the living room, and the high risk when sleeping prone on a sheepskin; however, because the numbers of cases in these groups are small, additional studies are needed to confirm these findings.
Miscarriage/Stillbirth/Prenatal Issues 1. Joó JG, Beke A, Berkes E, Papp Z, Rigó Jr J, Papp C Fetal Pathology in Second-Trimester Miscarriages Fetal Diagn Ther. 2009 Apr 7;25(2):186-191. [Epub ahead of print] First Department of Obstetrics and Gynaecology, Faculty of General Medicine, Semmelweis University, Budapest, Hungary. Objective: We aimed to analyze, based upon autopsy, the main characteristics of miscarriages in the second trimester. Methods: We have processed the results of fetopathological investigations of 544 aborted fetuses resulting from 486 second-trimester miscarriages. Results: Malformation could be identified in 13.05% of all cases. In almost one third of the patients there was a positive history. In the cases having a malformation, expressed dominance of male fetuses could be observed. Among the fetopathologically identified malformations, 49 were isolated. The most common was the single umbilical artery (22.4%). In 1.3% of the cases a chromosome aberration was verified. Conclusion: Miscarriage in pregnancies complicated by a malformation occurs approximately 3 weeks earlier than in cases without a confirmed malformation. There is practically no difference between affected and unaffected miscarriages as far as the cumulative ratio of positive history is concerned. A single umbilical artery alone predisposes to miscarriage, while in association with other malformations it may result from chromosome aberration. Copyright © 2009 S. Karger AG, Basel. 2. Jamshidi M, Jahromi AS, Davoodian P, Amirian M, Zangeneh M, Jadcareh F Seropositivity for Listeria monocytogenes in women with spontaneous abortion: a case-control study in Iran Taiwan J Obstet Gynecol. 2009 Mar;48(1):46-8 Infectious and Tropical Diseases Research Center, Hormozgan University of Medical Sciences, Banddar Abbas, Iran. OBJECTIVE: There are many studies supporting the role of certain asymptomatic infections such as Listeria monocytogenes (L. monocytogenes) in spontaneous abortion. In some cases, latent listeriosis may complicate the pregnancy, and serologic tests can, therefore, be used to detect the disease. This study was designed to assess the relationship between seropositivity for L. monocytogenes and spontaneous abortion. MATERIALS AND METHODS: A total of 250 women with previous spontaneous abortion and a control group of 200 women with normal full-term deliveries entered the study as case and control groups, respectively. Demographic characteristics were recorded for each subject, and serum samples were obtained from all participants. All serum samples were examined using the indirect immunofluorescence antibody test for L. monocytogenes antibody. Data was analyzed using Chi-squared and t tests. RESULTS: The average age of participants was 25.6 +/- 7.6 years in cases and 25.3 +/- 6.5 years in controls. Eighty-nine (35.6%) of the cases with abortion and 35 (17.5%) of the control group were positive for L. monocytogenes antibody (p = 0.001). No relationship was observed between the number of pregnancies and infection with L. monocytogenes (p = 0.4), or between the number of previous abortions and L. monocytogenes seropositivity (p = 0.2). CONCLUSION: We suggest monitoring L. monocytogenes seroprevalence in pregnant women at high risk of threatened abortion, and further microbiological assessment of symptomatic women for detection of L. monocytogenes and insidious infection. 3. Hasegawa J, Matsuoka R, Ichizuka K, Sekizawa A, Okai T Ultrasound diagnosis and management of umbilical cord abnormalities Taiwan J Obstet Gynecol. 2009 Mar;48(1):23-7 Department of Obstetrics and Gynecology, Showa University School of Medicine, Tokyo, Japan. hasejun@oak.dti.ne.jp The incidence of placenta and umbilical cord abnormalities is high in abnormal course of the delivery. Although the detection rate of umbilical cord abnormalities is steadily increasing with the improvement of ultrasound technology, and the fact that ultrasound scanning can distinguish umbilical cord conditions, this information has not exerted much impact on the management of labor to date. We believe prenatal detection of umbilical cord abnormalities must reduce the number of emergent cesarean sections and intrauterine fetal death. In this review, we describe the ultrasound diagnosis and management of major umbilical cord abnormalities, including abnormalities of cord insertion site (velamentous and marginal cord insertion), hypercoiled cord and nuchal cord, considering the current knowledge on physiologic and pathologic aspects of each umbilical cord abnormality. 4. Toth B, Bastug M, Mylonas I, Scholz C, Makovitzky J, Kunze S, Thaler C, Friese K, Jeschke U Peroxisome proliferator-activated receptor-gamma in normal human pregnancy and miscarriage Acta Histochem. 2009 Mar 31. [Epub ahead of print] Department of Obstetrics and Gynecology, Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany. Peroxisome proliferator-activated receptors (PPAR) belong to the superfamily of nuclear hormone receptors. Recent investigations emphasize a possible involvement of PPAR in obstetric and gynaecologic disorders like polycystic ovarian syndrome, endometriosis and preeclampsia. The aim of this study was to determine the frequency and distribution of peroxisome proliferator-activated receptor-gamma (PPARgamma) in normal human pregnancy and miscarriage. Placental tissue was obtained from normal human pregnancy and miscarriage during the first trimester of pregnancy. PPARgamma localisation was investigated by immunohistochemical methods. Immediate immunoreactivity of PPARgamma was observed in villous and extravillous trophoblast nuclei in normal first trimester pregnancy. A significantly enhanced labelling of PPARgamma was identified in extravillous trophoblast of miscarriage patients. This enhanced immunopositivity was also found in nuclei of villous trophoblast cells of miscarriage patients but without statistical significance. Because trophoblast invasion is negatively correlated to PPARgamma stimulation and blocking of PPARgamma leads to increased trophoblast invasion, our findings may suggest that enhanced expression of PPARgamma in abortive extravillous trophoblasts may be one factor linked to miscarriage. Prepared by the
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