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NSIDRC Journal Article Alert — February 12, 2010

Prepared 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 or Partners in Information Access for the Public Health Workforce's How to Access Journal Articles for more details.


Sudden Infant Death

1. Ostfeld BM, Esposito L, Perl H, Hegyi T
Concurrent Risks in Sudden Infant Death Syndrome
Pediatrics. 2010 Feb 15. [Epub ahead of print]

SIDS Center of New Jersey, Department of Pediatrics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, New Jersey; and.

Background: Despite improved education on safe sleep, infants are still exposed to multiple risks for sudden infant death syndrome (SIDS). Variability among health care providers continues to exist regarding knowledge of risk factors and the provision of education to caregivers. Objective: To enhance the content and delivery of SIDS risk-reduction initiatives by physicians and other health care providers and to provide them with a context for evaluating their discussions of risks and compensatory strategies, we sought to raise awareness of the frequency of risk factors in SIDS cases, patterns of co-occurrence, associations between modifiable and nonmodifiable risks, and the rarity of cases without risk. Design and Methods: In a population-based retrospective review of 244 (97%) New Jersey SIDS cases (1996-2000), we assessed the frequencies and co-occurrences of modifiable (maternal and paternal smoking, nonsupine sleep or prone status at discovery, bed-sharing, or scene risks) and nonmodifiable (upper respiratory infection or <37 weeks' gestational age) risks. Results: Nonsupine sleep occurred in 70.4% of cases with data on position (159 of 226). Thirteen cases were of infants who were discovered prone, with an increased positional risk to 76.1%, in which 87% contained additional risks. Maternal smoking occurred in 42.6% (92 of 216) of the cases with data on this risk, and 98% among those cases had additional risks. At least 1 risk was found in 96% of the cases, and 78% had 2 to 7 risks. Of the 9 of 244 risk-free cases (3.7%), 7 lacked data on 2 to 5 risks per case. On the basis of the complete data, only 2 (0.8%) of all 244 cases were risk free. When nonmodifiable risks were excluded, 5.3% of the cases met this definition. Conclusions: Risk-free and single-risk SIDS cases are rare, and most contain multiple risks. Parent education should be comprehensive and address compensatory strategies for nonmodifiable risks.

Miscarriage/Stillbirth/Prenatal Issues

1. Chaiworapongsa T, Kusanovic JP, Savasan ZA, Mazaki-Tovi S, Kim SK, Vaisbuch E, Tarca AL, Mittal P, Ogge G, Madan I, Dong Z, Yeo L, Hassan SS, Romero R
Fetal death: A condition with a dissociation in the concentrations of soluble vascular endothelial growth factor receptor-2 between the maternal and fetal compartments
J Matern Fetal Neonatal Med. 2010 Feb 16. [Epub ahead of print]

Perinatology Research Branch, NICHD, NIH, DHHS, Bethesda, Maryland, USA and Detroit, Michigan, USA.

Objective. An anti-angiogenic state has been implicated in the pathophysiology of preeclampsia, fetal growth restriction and fetal death. Vascular endothelial growth factor (VEGF), an indispensible angiogenic factor for embryonic and placental development exerts its angiogenic properties through the VEGF receptor (VEGFR)-2. A soluble form of this protein (sVEGFR-2) has been recently detected in maternal blood. The aim of this study was to determine if fetal death was associated with changes in the concentrations of sVEGFR-2 in maternal plasma and amniotic fluid. Study Design. Maternal plasma was obtained from patients with fetal death (n = 59) and normal pregnant women (n = 134). Amniotic fluid was collected from 36 patients with fetal death and the control group consisting of patients who had an amniocentesis and delivered at term (n = 160). Patients with fetal death were classified according to the clinical circumstances into the following groups: (1) unexplained; (2) preeclampsia and/or placental abruption; (3) chromosomal and/or congenital anomalies. Plasma and amniotic fluid concentrations of sVEGFR-2 were determined by ELISA. Non-parametric statistics and logistic regression analysis were applied. Results. (1) Patients with a fetal death had a significantly lower median plasma concentration of sVEGFR-2 than normal pregnant women (p < 0.001). The median plasma concentration of sVEGFR-2 in patients with unexplained fetal death and in those with preeclampsia/abruption, but not that of those with congenital anomalies, was lower than that of normal pregnant women (p = 0.006, p < 0.001 and p = 0.2, respectively); (2) the association between plasma sVEGFR-2 concentrations and preterm unexplained fetal death remained significant after adjusting for potential confounders (OR: 3.2; 95% CI: 1.4-7.3 per each quartile decrease in plasma sVEGFR-2 concentrations); (3) each subgroup of fetal death had a higher median amniotic fluid concentration of sVEGFR-2 than the control group (p < 0.001 for each); (4) the association between amniotic fluid sVEGFR-2 concentrations and preterm unexplained fetal death remained significant after adjusting for potential confounders (OR: 15.6; 95% CI: 1.5-164.2 per each quartile increase in amniotic fluid sVEGFR-2 concentrations); (5) among women with fetal death, there was no relationship between maternal plasma and amniotic fluid concentrations of sVEGFR-2 (Spearman Rho: 0.02; p = 0.9). Conclusion. Pregnancies with a fetal death, at the time of diagnosis, are characterized by a decrease in the maternal plasma concentration of sVEGFR-2, but an increase in the amniotic fluid concentration of this protein. Although a decrease in sVEGFR-2 concentration in maternal circulation depends upon the clinical circumstances of fetal death, an increase in sVEGFR-2 concentration in amniotic fluid seems to be a common feature of fetal death. It remains to be determined if the perturbation in sVEGFR-2 concentrations in maternal and fetal compartments observed herein preceded the death of a fetus.

2. Musizzano Y, Fulcheri E
Decidual vascular patterns in first-trimester abortions
Virchows Arch. 2010 Feb 16. [Epub ahead of print]

Anatomic Pathology, University of Genoa, Genoa, Italy

In many cases of early spontaneous abortion (ESA), no reasonable etiology can be documented. However, some of these cases show abnormal decidual vessels that could be overlooked when examined on hematoxylin and eosin (H&E) slides alone. Diagnostic accuracy could be improved by the use of a limited histochemical (HC) and immunohistochemical (IHC) panel. We reviewed 1,095 ESAs, selecting 176 cases with abnormal decidual vessels and subclassifying them into three groups on the basis of decidual vascular pattern. Various HC and IHC stainings were performed in order to assess their use in improving diagnostic sensitivity. Histological findings on H&E were recorded and compared to the results obtained with HC and IHC. A variable role in the improvement of morphologic details was demonstrated for all three tested HC stainings (periodic acid-Schiff, Masson's trichrome, Weigert's stain for fibrin) and for two of the IHC markers (smooth muscle actin, human placental lactogen). In many cases of ESA, only compatibility diagnoses can be formulated. However, using a limited panel of HC and IHC stainings, some significant findings can be more reliably reported, allowing the pathologist to acquire confidence in his routine diagnostic work.


Prepared by the
National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center
Georgetown University
2115 Wisconsin Avenue, N.W., Suite 601
Washington, DC  20007
(866) 866-7437 toll free
(202) 687-7466 local
(202) 784-9777 fax
info@sidscenter.org
http://www.sidscenter.org


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