NSIDRC Journal Article Alert — February 27, 2009
Prepared 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.
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. Kinney HC
Brainstem mechanisms underlying the sudden infant death syndrome: Evidence from human pathologic studies
Dev Psychobiol. 2009 Feb 23. [Epub ahead of print]
Department of Pathology, Children's Hospital Boston and Harvard Medical School, Enders Building Room 1112, 300 Longwood Avenue, Boston, MA 02115.
The brainstem hypothesis is one of the leading hypotheses concerning the sudden infant death syndrome (SIDS). It states that SIDS, or an important subset of SIDS, is due to abnormal brainstem mechanisms in the control of respiration, chemosensitivity, autonomic regulation, and/or arousal which impairs the infant's response to life-threatening, but often occurring, stressors during sleep (e.g., hypoxia, hypercarbia, asphyxia, hyperthermia) and leads to sudden death in a vulnerable developmental period. In this review, we summarize neuropathologic evidence from SIDS cases that support this hypothesis, beginning with the seminal report of subtle brainstem gliosis three decades ago. We focus upon recent neurochemical studies in our laboratory concerning the neurotransmitter serotonin (5-HT) and its key role in mediating protective responses to homeostatic stressors via medullary circuits. The possible fetal origin of brainstem defects in SIDS is reviewed, including evidence for adverse effects of prenatal exposure to maternal cigarette smoking and alcohol upon the postnatal development of human brainstem 5-HT pathways. (c) 2009 Wiley Periodicals, Inc.
2. Mitchell EA
What Is the mechanism of SIDS? Clues from epidemiology
Dev Psychobiol. 2009 Feb 17. [Epub ahead of print]
Professor of Child Health Research, Department of Paediatrics, University of Auckland, Private Bag 92019, Auckland, New Zealand.
The cause of sudden infant death syndrome (SIDS) is unknown. Many mechanisms have been postulated, although thermal stress, rebreathing of expired gases and infection/inflammation seem the most viable hypotheses for the causation of SIDS. Deaths from SIDS have reduced dramatically following the recommendation not to place infants to sleep prone. Epidemiological data have shown that prone sleeping position is more risky in winter, colder latitudes, higher altitudes, if the infant is unwell or has excessive bedding or clothing. This suggests prone sleeping position involves either directly or indirectly a thermal mechanism. SIDS caused by an infective/inflammatory mechanism might be associated with deaths occurring during the night. Rebreathing of expired gases, airway obstruction, long QT syndrome and other genetic conditions may explain a small number of sudden unexpected deaths in infancy. (c) 2009 Wiley Periodicals, Inc.
Miscarriage/Stillbirth/Prenatal Issues
1. Marchetti D, Belviso M, Fulcheri E
A case of stillbirth: the importance of placental investigation in medico-legal practice
Am J Forensic Med Pathol. 2009 Mar;30(1):64-8
Istituto di Medicina Legale, Università Cattolica del Sacro Cuore, Roma, Italy. d.marchetti@rm.unicatt.it
The authors present a case of stillbirth in which histologic examination of the placenta provides the opportunity to make a definitive diagnosis of a death due to fetal thrombotic vasculopathy (FTV). Establishing the etiology in cases of stillbirth may avoid medical malpractice litigation. The better knowledge of the cause of stillbirths also helped obstetricians to recognize factors that could have prejudiced future pregnancies.
2. Nielsen HS, Steffensen R, Varming K, Van Halteren AG, Spierings E, Ryder LP, Goulmy E, Christiansen OB
Association of Hy-Restricting Hla Class Ii Alleles with Pregnancy Outcome in Patients with Recurrent Miscarriage Subsequent to a Firstborn Boy
Hum Mol Genet. 2009 Feb 17. [Epub ahead of print]
The Fertility Clinic 4071, University Hospital Copenhagen, Rigshospitalet, DK-2100 Copenhagen Ø, Denmark.
Background Healthy females, pregnant with a boy, generate immune responses against male specific minor histocompatibility (HY-) antigens. The clinical importance of these responses is evident in Stem Cell Transplantation. Birth of a boy prior to a series of miscarriages reduces the chance of a subsequent live birth. This study explores the putative impact of known HY-presenting HLA alleles on future pregnancy outcome in women with at least three consecutive miscarriages following a birth (secondary recurrent miscarriages (SRM)). Methods HLA-A, -B, -DRB1, DRB3-5, DQB1 genotyping was performed in 358 SRM patients and in 203 of their children born prior to the miscarriages. Results The subsequent live birth in women with boys prior to the miscarriages compared to girls is lower in women with HY-restricting HLA class II alleles (OR: 0.17 (0.1-0.4), p = 0.0001). One HY-restricting HLA class II allele in women with firstborn boys significantly reduces the chances of a live birth (OR: 0.46 (0.2-0.9), p = 0.02). Two HY-restricting HLA class II alleles further reduced this chance (OR: 0.21 (0.1-0.7), p = 0.02). HY-restricting HLA class II did not reduce the chances of a live birth in SRM women with firstborn girls. Conclusion HY-restricting HLA class II alleles are associated with a decreased chance of a live birth in SRM women with firstborn boys. These findings strongly indicate an aberrant maternal immune reactions against fetal HY-antigens in SRM. The results may shed light on the as yet unknown immunological causes of SRM and may help to understand the successful maternal acceptance of the fetal semi-allograft.
3. James AH
Venous thromboembolism in pregnancy
Arterioscler Thromb Vasc Biol. 2009 Mar;29(3):326-31
Division of Maternal-Fetal Medicine Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC 27710, USA. andra.james@duke.edu
The purpose of this review is to summarize the epidemiology of venous thromboembolism (VTE) in pregnancy and describe strategies used to prevent and treat it. The main reason for the increased risk of VTE in pregnancy is hypercoagulability. The hypercoagulability of pregnancy, which has likely evolved to protect women from the bleeding challenges of miscarriage and childbirth, is present as early as the first trimester and so is the increased risk of VTE. Other risk factors include a history of thrombosis, inherited and acquired thrombophilia, certain medical conditions, and complications of pregnancy and childbirth. Candidates for anticoagulation are women with a current thrombosis, a history of thrombosis, thrombophilia, and a history of poor pregnancy outcome, or postpartum risk factors for VTE. For fetal reasons, the preferred agents for anticoagulation in pregnancy are heparins. There are no large trials of anticoagulants in pregnancy and recommendations are based on case series and the opinion of experts. Nonetheless, anticoagulants are believed to improve the outcome of pregnancy for women who have or have had VTE.
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
