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NSIDRC Journal Article Alert — May 21, 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. Highet AR, Gibson CS, Goldwater PN
CD14 (C-260T) polymorphism is not associated with sudden infant death syndrome (SIDS) in a large South Australian cohort
Innate Immun. 2010 May 14. [Epub ahead of print]

SA Pathology at the Women's & Children's Hospital and University of Adelaide Discipline of Paediatrics, Adelaide, Australia.

Similarities have been drawn between models of endotoxic shock and gross and microscopic pathology observed in sudden infant death syndrome (SIDS) cases. Polymorphisms in genes that influence the expression of endotoxin receptors could affect the outcome of toxaemia, and could, therefore, play a role in SIDS. The CD14 gene promoter contains a single nucleotide polymorphism that affects the level of CD14 gene expression. The TT genotype of the CD14 (C-260T) polymorphism causes a significantly higher density of CD14 receptor expression on monocytes which makes the individual more sensitive to endotoxin than those with the wild-type (CC). This investigation was designed to determine whether SIDS infants have a higher frequency of the CD14 (C-260T) polymorphism compared with non-SIDS controls. One hundred and sixteen SIDS and 228 control infants were genotyped using PCR followed by restriction fragment length analysis of amplified product. Carriage of the TT or CT genotypes did not significantly differ between SIDS and control infants (P = 0.218 and 0.081, respectively). The frequencies observed in the control group were consistent with Hardy-Weinberg equilibrium and did not differ significantly from the published frequencies in Caucasian Australians. These results suggest that CD14 (C-260T) polymorphism is unlikely to be implicated in SIDS.

2. Dempers J, Wadee SA, Boyd T, Wright C, Odendaal H, Sens MA
Hepatic Hemangioendothelioma Presenting as Sudden Unexpected Death in Infancy: A Case Report
Pediatr Dev Pathol. 2010 May 13. [Epub ahead of print]

1 Stellenbosch University.

Abstract The classification of an unexpected infant death as the sudden infant death syndrome (SIDS) depends upon a complete autopsy, death scene investigation and review of medical history to exclude known causes of death. Death from occult neoplastic disease in infancy is extremely rare but is within the broad differential of SIDS. We report the sudden and unexpected death of a one-month-old infant from a hepatic (infantile) hemangioendothelioma. The physiologic mechanism of death was likely cardiac failure induced by the circulatory demands of this large vascular tumor and respiratory compromise from diaphragmatic thoracic incursion. The clinical progression and pathology of these relatively common tumors of infant livers are extremely variable. This case dramatically illustrates the potential for fatal outcome of this tumor, as well as the need for the autopsy to determine the cause of sudden and unexpected death in an infant.

Miscarriage/Stillbirth/Prenatal Issues

1. Tveit JV, Saastad E, Stray-Pedersen B, Børdahl PE, Frøen JF
Concerns for decreased foetal movements in uncomplicated pregnancies - Increased risk of foetal growth restriction and stillbirth among women being overweight, advanced age or smoking
J Matern Fetal Neonatal Med. 2010 May 17. [Epub ahead of print]

Division of Obstetrics and Gynecology and Center for Perinatal Research, Medical Faculty, Rikshospitalet University Hospital, University of Oslo, Norway.

Introduction. We aimed to determine whether the clinical characteristics of women in uncomplicated pregnancies presenting with decreased foetal movements (DFMs) would help target subgroups of women at the highest risk. Furthermore, we also aimed whether DFMs in complicated pregnancies identified the additional needs for intensified management. Methods. Singleton third trimester pregnancies (n = 2374) presenting with DFMs from June 2004 through October 2005 were prospectively registered in 14 delivery units in Norway. Among pregnancies that were uncomplicated until registration for DFMs, cases with good outcomes (birth weight between 10th and 90th percentile, term delivery and live-born child) were compared with cases with adverse outcomes. Results. In uncomplicated pregnancies, maternal overweight, advanced age and smoking identified subgroups of cases at increased risk of foetal growth restriction and stillbirth. DFMs of longer duration, in particular the perceived absence of movements, identified cases at increased risk of stillbirth, irrespective of other maternal characteristics. When women with complicated pregnancies reported DFMs, additional indications for follow-up were found in 1/3 of cases. Conclusions. Maternal overweight, advanced age, smoking and the duration of DFMs are the characteristics that help in identifying pregnancies that should be targeted for intensified management. Time matters and knowledge-based information are needed to improve foetal health.

2. De Vivo A, Mancuso A, Giacobbe A, Moleti M, Savasta LM, De Dominici R, Priolo AM, Vermiglio F
Thyroid Function in Women Found to Have Early Pregnancy Loss
Thyroid. 2010 May 16. [Epub ahead of print]

1 Department of Gynecological, Obstetrical Sciences, and Reproductive Medicine, University Hospital "G. Martino," Messina, Italy .

Background: Pregnancy influences thyroid function and may bring to light mild and latent disorders. Thyroid dysfunction has been related to obstetrical complications such as premature delivery, gestational hypertension, preeclampsia, and placental abruption. The aim of our study was to evaluate whether the occurrence and timing of pregnancy loss could be related to thyroid autoimmunity or subclinical hypothyroidism (SH) per se. Methods: Two hundred sixteen apparently healthy pregnant women with no previous history of thyroid disease and with diagnosis of early miscarriage (before the 12th week of gestation) were enrolled. Miscarriages were classified as very early pregnancy loss (EPL) or embryo loss (crown rump length </=10 mm) and EPL or fetal loss (crown rump length > 10 mm). Women were subdivided into four groups: euthyroid (ET), SH, overt hypothyroidism, and thyroid autoimmunity group. Results: One hundred seventy-six women had a normal thyroid function (84.6%), 24 patients were found to have positive thyroid antibodies (11.5%), 8 women (3.8%) an SH, and 8 cases were excluded. Thyroid-stimulating hormone levels were found to be higher in the very early (1.4 +/- 1.0 mU/L) than in the EPL group (1.1 +/- 0.7 mU/L) (p = 0.04), and in patients affected by SH (3.9 +/- 0.1 mU/L) compared to ET (1.0 +/- 0.5 mU/L) (p < 0.001) and autoimmune women (1.0 +/- 0.4 mU/L) (p < 0.001). Although the multivariate logistic regression analysis revealed that both autoimmunity and SH were independently correlated with the onset of very EPL, abortion was more precocious in the SH group (6.5 +/- 0.9 weeks), followed by the autoimmune (8.2 +/- 2.1 weeks) and ET groups (8.2 +/- 1.6 weeks) (p = 0.02). Conclusions: Both thyroid diseases SH and autoimmune disorder are independently associated with very early embryo loss, but women suffering from SH have a lower gestational age at abortion.


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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