NSIDRC Journal Article Alert — December
7, 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
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: Yang Z, Lantz PE, Ibdah JA
Post-mortem analysis for two prevalent beta-oxidation mutations
in sudden infant death.
.Pediatr Int. 2007 Dec;49(6):883-7.
Department of Internal Medicine, Wake Forest University School
of Medicine, Winston-Salem, North Carolina,
USA.
Background: Fatty acid oxidation disorders may cause sudden
and unexpected infant death and are associated
with the histological hallmark of hepatic steatosis. The goal
of the present study was to assess the value of
post-mortem molecular analysis for medium-chain acyl-coenzyme
A dehydrogenase (MCAD) and mitochondrial trifunctional protein (MTP) defects in unexplained sudden infant
death (SID) associated with fatty infiltration of
the liver. MCAD catalyzes the first step of medium-chain fatty
acid oxidation while MTP catalyzes the last three
steps of long-chain fatty acid oxidation. Methods: In a retrospective
study, 220 consecutive cases of sudden
and unexplained infant death certified by medical examiners
at Wake Forest University Medical Center were
assessed for hepatic steatosis. Subjects with evidence of hepatic
steatosis were screened for mutations in
MCAD and MTPalpha-subunit using DNA isolated from paraffin-embedded
liver tissue, single-strand
conformation variance, and nucleotide sequence analyses. Results:
Sixteen cases (7.3%) were associated with
diffuse micro-vesicular or mixed micro- and macro-vesicular
hepatic steatosis. Two of these 16 cases (12.5%)
had disease-causing mutations. One was homozygous for the prevalent
MCAD A985G mutation. The second
was a compound heterozygous for the prevalent MTP G1528C mutation
and a novel 1 bp deletion in exon 18 of
the MTPalpha-subunit gene. Conclusions: A significant proportion
(7.3%) of SID is associated with hepatic
steatosis. The present data support post-mortem molecular analysis
for the MCAD A985G and MTP G1528C
prevalent mutations in cases of sudden and unexplained infant
death associated with hepatic steatosis.
2: McKenna JJ, Ball HL, Gettler LT.
Mother-infant cosleeping, breastfeeding and sudden infant death
syndrome: What biological anthropology has
discovered about normal infant sleep and pediatric sleep medicine.
Am J Phys Anthropol. 2007 Nov 28;134(S45):133-161 [Epub ahead
of print]
Department of Anthropology and Mother-Baby Behavioral Sleep
Laboratory, University of Notre Dame, Notre
Dame, IN 46556.
Twenty years ago a new area of inquiry was launched when anthropologists
proposed that an evolutionary
perspective on infancy could contribute to our understanding
of unexplained infant deaths. Here we review two
decades of research examining parent-infant sleep practices
and the variability of maternal and infant sleep
physiology and behavior in social and solitary sleeping environments.
The results challenge clinical wisdom
regarding "normal" infant sleep, and over the past
two decades the perspective of evolutionary pediatrics has
challenged the supremacy of pediatric sleep medicine in defining
what are appropriate sleep environments and
behaviors for healthy human infants. In this review, we employ
a biocultural approach that integrates diverse
lines of evidence in order to illustrate the limitations of
pediatric sleep medicine in adopting a view of infants
that prioritizes recent western social values over the human
infant's biological heritage. We review what is
known regarding infant sleeping arrangements among nonhuman
primates and briefly explore the possible
paleoecological context within which early human sleep patterns
and parent-infant sleeping arrangements
might have evolved. The first challenges made by anthropologists
to the pediatric and SIDS research
communities are traced, and two decades of studies into the
behavior and physiology of mothers and infants
sleeping together are presented up to the present. Laboratory,
hospital and home studies are used to assess
the biological functions of shared mother-infant sleep, especially
with regard to breastfeeding promotion and
SIDS reduction. Finally, we encourage other anthropologists
to participate in pediatric sleep research using the
unique skills and insights anthropological data provide. By
employing comparative, evolutionary and cross-cultural perspectives an anthropological approach stimulates
new research insights that influence the
traditional medical paradigm and help to make it more inclusive.
That this review will potentially stimulate
similar research by other anthropologists is one obvious goal.
That this article might do so makes it ever more
possible that anthropologically inspired work on infant sleep
will ultimately lead to infant sleep scientists,
pediatricians, and parents becoming more informed about the
consequences of caring for human infants in
ways that are not congruent with their evolutionary biology.
Yrbk Phys Anthropol 50:133-161, 2007. (c) 2007
Wiley-Liss, Inc.
Miscarriage/Stillbirth/Prenatal Issues
1: Molokhia M, Maconochie N, Patrick AL, Doyle P.
Cross-sectional analysis of adverse outcomes in 1029 pregnancies
of Afro-Caribbean women in Trinidad with
and without systemic lupus erythematosus.
Arthritis Res Ther. 2007 Nov 27;9(6):R124 [Epub ahead of print]
ABSTRACT: The objective of the study was to examine pregnancy
outcomes in patients with systemic lupus
erythematosus (SLE) and population controls in Trinidad. We
performed a cross-sectional analysis of adverse
outcomes in pregnancies of Afro-Caribbean women with, and without,
SLE. 122 female adult cases of SLE and
203 neighbourhood age matched women without SLE were interviewed
concerning details of reproductive
history, and anticardiolipin antibody (ACL) status was established
for women with SLE. 1029 pregnancies were
reported (356 by SLE cases; 673 by women without SLE). In women
with [greater than or equal to] 1 pregnancy
the total number of pregnancies were similar in women with
a diagnosis of SLE and women without, however a
lower proportion of women with SLE had ever been pregnant compared
to women without SLE. (80% vs. 91%,
p=0.002). In multivariate logistic regression analyses adjusted
for maternal age, district of residence,
pregnancy order and smoking, SLE pregnancies were more than
twice as likely to end in fetal death than non-
SLE pregnancies (OR 2.4, 95% CI 1.2-4.7). This effect was driven
by a large increase in odds of stillbirth (OR 8.5,
95% CI 2.5-28.8). Odds of early miscarriage (OR 1.4, 95% CI
0.6-3.1) and mid-trimester miscarriage (OR 1.9,
95% CI 0.4-9.5) were higher, but not statistically significantly
different, in SLE pregnancies than in non- SLE
pregnancies. Odds of ectopic pregnancy (OR 7.5, 95% CI 0.9-62.5),
and preterm birth (OR 3.4, 95% CI 1.2-10.0)
were higher in SLE pregnancies conceived after diagnosis than
in non-SLE pregnancies. There was no evidence
of raised levels of IgG or IgM ACL among the majority 93/97
(96%) of SLE cases who reported sporadic mid
trimester miscarriage or stillbirth, though there was evidence
of high levels of IgM and IgG ACL among women
reporting 3 or more miscarriages and 3 consecutive miscarriages,
and raised IgG ACL among those
experiencing ectopic pregnancy. In conclusion we found evidence
for a large increase in risk of stillbirth in the
pregnancies of Afro-Caribbean Trinidadian women with SLE (not
accounted for by high ACL antibody status).
There was some evidence of an increased risk of preterm delivery
and ectopic pregnancy in pregnancies
conceived after a diagnosis of maternal SLE.
2: Balen AH, Anderson RA.
Impact of Obesity on female reproductive health: British Fertility
Society, Policy and Practice Guidelines.
Hum Fertil (Camb). 2007 Dec;10(4):195-206.
Reproductive Medicine & Surgery, Leeds Teaching Hospitals,
Leeds, UK.
Obesity has a significant adverse impact on reproductive outcome.
It influences not only the chance of
conception but also the response to fertility treatment, and
increases the risk of miscarriage, congenital
anomalies and pregnancy complications in addition to potential
adverse effects on long term health of both
mother and infant. Women should aim for a normal BMI before
starting any form of fertility treatment.
Treatment should be deferred until the BMI is less than 35
kg/m(2), although in those with more time (e.g., less
than 37 years; normal serum FSH concentration) a weight reduction
to a BMI of less than 30 kg/m(2) is
preferable. Clinicians should consider deferring treatment
to women outside these guidelines. Women should
be provided with assistance to lose weight, including psychological
support, dietary advice, exercise classes
and where appropriate, weight reducing agents or bariatric
surgery. Even a moderate weight loss of 5 - 10% of
body weight can be sufficient to restore fertility and improve
metabolic markers.
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
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info@sidscenter.org
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