NSIDRC Journal Article Alert — December
21, 2007
Prepared by the National Sudden Infant Death Resource Center
at Georgetown University.
This journal article alert provides selected items added to
the National Library of Medicine’s PubMed database in
the last week.
Past issues of NSIDRC journal alerts are available at http://www.sidscenter.org.
Availability of full-text journal articles is often limited to
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Sudden Infant Death
1. Stray-Pedersen A, Vege A, Stray-Pedersen A, Holmskov U,
Rognum TO.
Post-Neonatal drop in alveolar SP-A expression: Biological significance for increased
vulnerability to SIDS?
Pediatr Pulmonol. 2007 Dec 17
Institute of Forensic Medicine, University ofOslo, Rikshospitalet,
Oslo, Norway.
BACKGROUND: Surfactant protein A (SP-A) is synthesized in
the lung and is a part of the innate immune system. The aim
of this study was to evaluate the expression of SP-A in lung
tissue from fetuses, infants, children and adults with special
regard to sudden infant death syndrome (SIDS). METHODS: A total
of 160 cases were studied; 19 fetuses and neonates, 59 SIDS
and 49 explained infant deaths below 1 year of age, 19 toddlers
and 14 adults. Immunohistochemical detection of SP-A using
monoclonal antibodies was performed by microscopy of lung tissue
specimens collected at autopsy. A scoring system was developed
enabling semi-quantitative estimation of staining intensity
and distribution. RESULTS: SP-A was detected in the terminal
bronchioles and alveolar spaces of fetuses >35 weeks gestation.
The intra-alveolar SP-A expression increased in the perinatal
period followed by a marked drop in infants aged between 1
week and 5 months. Infants aged >5 months had abundant SP-A
expression corresponding to older children and adults. There
was no difference in the age distribution between cases of
SIDS and explained deaths. CONCLUSIONS: The apparent drop in
SP-A expression takes place in the first months after birth,
corresponding with the classical age peak of SIDS. We therefore
hypothesize that low expression of SP-A may be related in some
as-yet undetermined way to the increased risk of SIDS at that
age. Pediatr
2. Wiemann M, Frede S, Tschentscher F, Kiwull-Schöne
H, Kiwull P, Bingmann D, Brinkmann
B, Bajanowski T.
NHE3 in the human brainstem: implication for the pathogenesis
of the sudden infant death syndrome
(SIDS)?
Adv Exp Med Biol. 2008;605:508-13.
University of Duisburg-Essen, Department of Physiology. martin.wiemann@uni-due.de
Previous studies have demonstrated an inverse correlation
between the degree of respiratory drive and NHE3 mRNA expression
in the brainstem of awake rabbits. Here we show that the levels
of NHE3 mRNA extractable from kryo-conserved tissue are highly
variable also in the human brainstem. As an insufficient drive
to breath may be a final event causing sudden infant death,
we compared the expression of NHE3 mRNA in a collective of
children who died from non-natural causes to an equal number
of SIDS victims. Evaluation of signals from NHE3 RT-PCR showed
higher values for the SIDS collective than for the control
group. We suggest that the level of NHE3 expression in brainstem
tissue may contribute to the vulnerability of infants for SIDS.
3. Machaalani R, Waters KA.
Neuronal cell death in the Sudden Infant Death Syndrome brainstem
and associations with risk factors.
Brain. 2008 Jan;131(Pt 1):218-28.
Department of Medicine, Room 206, Blackburn Building, D06,
The University of Sydney, NSW 2006,
Australia.
Immunoreactive expression of three cell death markers was
quantitatively analysed in the human infant brainstem medulla.
We assessed active caspase-3, TUNEL and single-stranded DNA
(ssDNA) in a cohort of 92 infants, and analysed for: (i) variations
in the immunoreactive expression with development; (ii) comparison
of infants diagnosed with the Sudden Infant Death Syndrome
(SIDS, n = 67) to infants who died suddenly with another diagnosis
(non-SIDS, n = 25); and (iii) correlations with known clinical
risk factors for SIDS. Five nuclei from the brainstem medulla
(caudal and rostral levels) were studied, including the hypoglossal
(XII), dorsal motor nucleus of the vagus (DMNV), the dorsal
column nuclei (gracile and cuneate) and the arcuate nucleus.
Our main hypothesis was that neuronal cell death would be increased
in SIDS compared to non-SIDS infants, and the increase would
correlate with risk factors such as prone sleeping and cigarette
smoke exposure. Comparing SIDS to non-SIDS, there was an increase
in caspase-3 in the rostral DMNV (P = 0.01), and a trend to
increased TUNEL in the arcuate nucleus (P = 0.1), which was
statistically significant when comparing the male SIDS to male
non-SIDS cohort (P = 0.04). No major changes for ssDNA immunoreactivity
were found. Moreover, TUNEL expression was affected by post-conceptional
age, by sleep-related risk factors (predominantly affecting
the dorsal column nuclei), and by cigarette smoke exposure
in the rostral DMNV and arcuate nucleus. Active caspase-3 was
affected by post-conceptional age but only in the XII, while
gender-related differences were seen in the arcuate nucleus.
This study provides further evidence of increased apoptosis
in the brainstem of SIDS infants, but shows for the first time
that these changes are also affected by age and gender, and
by clinical risk factors such as the sleep position and cigarette
smoke exposure.
4. Price SK.
Social work, siblings, and SIDS: conceptual and case-based
guidance for family system intervention.
J Soc Work End Life Palliat Care. 2007;3(3):81-101.
Virginia Commonwealth University School of Social Work, Richmond,
VA 23227, USA. skprice@vcu.edu
Sudden Infant Death Syndrome (SIDS) is a tragic loss event
within the family, impacting adults as well as children. This
article uses three case illustrations to discuss the role of
a SIDS event on the family system with a special focus on the
emergent challenges for surviving siblings of various ages.
Practice application examples are woven throughout the review
to illustrate the age-specific grief responses which may occur
following a SIDS event. The article also presents a theoretically
supported intervention matrix that integrates models of bereavement
support and family system responses, taking into account children's
varying developmental needs and tasks based on sibling age.
5. Román R, López P, Johnson MC, Boric
MA, Gallo M, Ponce C, Vargas S, Codner E, Cassorla F.
Sudden infant death syndrome and activating gnas1 gene mutations.
Fetal Pediatr Pathol. 2007 Jul-Aug;26(4):199-205.
Institute of Maternal and Child Research, San Borja Arriarán
Clinical Hospital, School of
Medicine, University of Chile, Santiago, Chile.
GNAS1 gene mutations cause the McCune-Albright syndrome. Some
patients may develop unusual, severe, nonendocrine manifestations
that may lead to death. We postulate that some cases of sudden
infant death syndrome (SIDS) might be caused by GNAS1 gene
mutations affecting vital organs. We studied two GNAS1 gene
mutations (R201H and R201C) by allele specific PCR and enzymatic
digestion in pulmonary, pancreas, liver, kidney, and heart
tissue from 29 infants who suffered SIDS. The infants died
at age 96 ± 78 days. At the time of death, children
had a height Z score of -0,04 ± 0,95, a weight Z score
of 0,04 ± 0,91, and a weight for length Z score of 0,1 ± 0,83.
The molecular study by both techniques did not reveal any GNAS1
mutations in the tissues examined. We conclude that GNAS1 gene
mutations do not appear to be present in tissues of infants
with SIDS.
Miscarriage/Stillbirth/Prenatal Issues
1. Black M, Shetty A, Bhattacharya S
Obstetric outcomes subsequent to intrauterine death in the first pregnancy.
BJOG. 2008 Feb;115(2):269-74.
Department of Obstetrics and Gynaecology, Aberdeen Maternity
Hospital, Aberdeen, UK.
OBJECTIVE: To compare obstetric outcomes in the pregnancy
subsequent to intrauterine death with that following live birth
in first pregnancy. DESIGN: Retrospective cohort study. SETTING:
Grampian region of Scotland, UK. POPULATION: All women who
had their first and second deliveries in Grampian between 1976
and 2006. METHODS: All women delivering for the first time
between 1976 and 2002 had follow up until 2006 to study their
next pregnancy. Those women who had an intrauterine death in
their first pregnancy formed the exposed cohort, while those
who had a live birth formed the unexposed cohort. MAIN OUTCOME
MEASURES: Maternal and neonatal outcomes in the second pregnancy,
including pre-eclampsia, placental abruption, induction of
labour, instrumental delivery, caesarean delivery, malpresentation,
prematurity, low birthweight and stillbirth. RESULTS: The exposed
cohort (n = 364) was at increased risk of pre-eclampsia (OR
3.1, 95% CI 1.7-5.7); placental abruption (OR 9.4, 95% CI 4.5-19.7);
induction of labour (OR 3.2, 95% CI 2.4-4.2); instrumental
delivery (OR 2.0, 95% CI 1.4-3.0); elective (OR 3.1, 95% CI
2-4.8) and emergency caesarean deliveries (OR 2.1, 95% CI 1.5-3.0);
and prematurity (OR 2.8, 95% CI 1.9-4.2), low birthweight (OR
2.8, 95% CI 1.7-4.5) and malpresentation (OR 2.8, 95% CI 2.0-3.9)
of the infant as compared with the unexposed cohort (n = 33,715).
The adjusted odds ratio for stillbirth was 1.2 and 95% CI 0.4-3.4.
CONCLUSION: While the majority of women with a previous stillbirth
have a live birth in the subsequent pregnancy, they are a high-risk
group with an increased incidence of adverse maternal and neonatal
outcomes.
2. Cacciatore J, Bushfield S.
Stillbirth: the mother's experience and implications for improving
care.
J Soc Work End Life Palliat Care. 2007;3(3):59-79.
Social Work Department, Arizona State University, Phoenix,
AZ 85069-7100, USA. joanne.cacciatore@asu.edu
More children die as a result of stillbirth than all other
causes of infant deaths combined (Ananth, Shiliang, Kinzler,
and Kramer, 2005; Goldenberg, Kirby, and Culhane, 2004; Froen,
2005; National Institute of Health, 2004); yet, mothers experiencing
stillbirth are often left without support afterwards (Kubler-Ross,
2004; Fahey-McCarthy, 2003; Fletcher 2002; Saddler, 1987; DeFrain,
1986; Kirkley-Best & Kellner, 1982). Despite social work's
growing involvement in care at the end of life, parents of
stillborn children have not experienced consistent, relevant,
and competent professional care in coping with the tragedy
of death. Forty-seven women between the ages of 19 and 51 were
recruited through nonprofit agencies that provide bereavement
care to grieving families. Results of this qualitative study
suggest that stillbirth is emotionally complex with long-lasting
symptoms of grief and significant struggles to find meaning.
The findings also support the need for perceived psychosocial
and spiritual support from professional caregivers, family,
and friends. The women's own experiences argue for comprehensive
approaches to support the grief and loss of stillbirth, and
for the importance of social work involvement in both immediate
and longer term interventions.
Prepared by the
National Sudden Infant Death 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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