NSIDRC Journal Article Alert — May 30, 2008
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.
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Sudden Infant Death
1. Verbeek MM, Richardson HL, Parslow PM, Walker AM, Harding
R, Horne RS
Arousal and ventilatory responses to mild hypoxia in sleeping
preterm infants
J Sleep Res. 2008 May 21. [Epub ahead of print]
Ritchie Centre for Baby Health Research, Monash Institute
for Medical Research, Melbourne, Victoria, Australia.
A failure to adequately respond to hypoxia has been implicated
in the Sudden Infant Death Syndrome (SIDS). Preterm infants
are at increased risk for SIDS, thus we compared ventilatory
and arousal responses to mild hypoxia [15% oxygen (O(2))] in
preterm and term infants. Eight preterm and 15 term infants
were serially studied with daytime polysomnography during which
nasal airflow was monitored by pneumotachograph at 2-5 weeks,
2-3 and 5-6 months. At each age, in both groups, hypoxia induced
a significant decrease in oxygen saturation (SpO(2)) during
both active sleep (AS) and quiet sleep (QS). Infants invariably
aroused in AS; and in QS either aroused or failed to arouse.
In preterm infants arousal latency in AS was longer than in
term infants (P < 0.05) at 2-5 weeks. Compared with term
infants, preterm infants reached significantly lower SpO(2)
levels at 2-5 weeks in both AS and QS non-arousing tests and
at 2-3 months in QS. A biphasic hypoxic ventilatory response
was observed in QS non-arousing tests in both groups of infants
at all three ages. We conclude that the greater desaturation
during a hypoxic challenge combined with the longer arousal
latency in preterm infants could contribute to greater risk
for SIDS.
2. Campbell MJ, Hall DM, Stephenson T, Bacon CJ, Madan J
Recurrence rates for SIDS - the importance of risk stratification
Arch Dis Child. 2008 May 22. [Epub ahead of print]
University of Sheffield, United Kingdom.
OBJECTIVE: To investigate the importance of stratification
by risk factors in computing the probability of a second SIDS
in a family. DESIGN: Simulation Study BACKGROUND: The fact
that a baby dies suddenly and unexpectedly means that there
is a raised probability that the baby's family have risk factors
associated with Sudden Infant Death Syndrome (SIDS). Thus one
cannot consider the risk of a subsequent death to be that of
the general population. The Confidential Enquiry into Stillbirths
and Deaths in Infancy (CESDI)6 identified three major social
risk factors: smoking, age<27 and parity>1, and unemployed/unwaged
as major risk factors. It gave estimates of risk for families
with different numbers of these risk factors. We investigate
whether it is reasonable to assume that, conditional on these
risk factors, the risk of a second event is independent of
the risk of the first and as a consequence one can square the
risks to get the risk of two SIDS in a family. We have used
CESDI data to estimate the probability of a second SID in a
family under different plausible scenarios of the prevalence
of the risk factors. We have applied the model to make predictions
in the Care of Next Infant (CONI) study7. RESULTS: The model
gave plausible predictions. The CONI study observed 18 second
SIDS. Our model predicted 14 (95% prediction interval 1 to
21). CONCLUSION: When considering the risk of a subsequent
SIDS in a family one should always take into account the known
risk factors. If all risks have been identified, then conditional
on these risks, the risk of two events is the product of the
individual risks However for a given family we cannot quantify
the magnitude of the increased risk because of other possible
risk factors not accounted for in the model.
3. Waldhoer T, Wald M, Heinzl H
Analysis of the spatial distribution of infant mortality by
cause of death in Austria in 1984 to 2006
Int J Health Geogr. 2008 May 21;7(1):21. [Epub ahead of print]
ABSTRACT: BACKGROUND: In Austria, over the last 20 years infant
mortality declined from 11.2 per 1,000 life births (1985) to
4.7 per 1,000 in1997 but remained rather constant since then.
In addition to this time trend we already reported a non-random
spatial distribution of infant mortality rates in a recent
study covering the time period 1984 to 2002. This present study
includes four additional years and now covers about 1.9 million
individual birth certificates. It aimes to elucidate the observed
non-random spatial distribution in more detail. We split up
infant mortality into six groups according to the underlying
cause of death. The underlying spatial distribution of standardized
mortality ratios (SMR) is estimated by univariate models as
well as by two models incorporating all six groups simultaneously.
RESULTS: We observe strong correlations between the individual
spatial patterns of SMR's except for "Sudden Infant Death
Syndrome" and to some extent for "Peripartal Problems".
The spatial distribution of SMR's is non-random with an area
of decreased risk in the South-East of Austria. The group "Sudden
Infant Death Syndrome" clearly and the group "Peripartal
Problems" slightly show deviations from the common pattern.
When comparing univariate and multivariate SMR estimates we
observe that the resulting spatial distributions are very similar.
CONCLUSIONS: We observe different non-random spatial distributions
of infant mortality rates when grouped by cause of death. The
models applied were based on individual data thereby avoiding
ecological regression bias. The estimated spatial distributions
do not substantially depend on the employed estimation method.
The observed non-random spatial patterns of Austrian infant
mortality remain to appear ambiguous.
Other Infant Death
1. Johnson PJ, Oakes JM, Anderton DL
Neighborhood Poverty and American Indian Infant Death: Are
The Effects Identifiable?
Ann Epidemiol. 2008 May 24. [Epub ahead of print]
Divisions of Health Policy & Management (P.J.J.) and Epidemiology & Community
Health (J.M.O.), School of Public Health, University of Minnesota,
Minneapolis; and Social and Demographic Research Institute
and Department of Sociology, University of Massachusetts-Amherst
(D.L.A.).
PURPOSE: Poor living conditions are posited as an underlying
cause of American Indian (AI) infant mortality, which is unusually
high in the postneonatal period. We explore whether the effects
of neighborhood poverty on AI infant death are identifiable
by using observational data. METHODS: Vital records for infants
born between 1990 and 1999 to AI women in a metropolitan area
(n = 4751) are linked with tract-level poverty data. A counterfactual
framework, an explicit causal contrast study design, and propensity
score matching methods were used. For each comparison, we created
exchangeable groups by matching infants with the same probability
of exposure to poverty when one was exposed and the other was
not. RESULTS: Our results suggest that neighborhood poverty
has little effect on AI infant death outcomes. Importantly,
the study design makes transparent the challenge of identifying
appropriate analytic comparison groups in studies of neighborhood
poverty and health. CONCLUSIONS: Collecting additional data
will likely not overcome the fact that AIs with a high probability
of living in poverty rarely reside in low-poverty neighborhoods.
Yet, some of them must if a meaningful counterfactual comparison
is to be made and the effects of neighborhood poverty on AI
infant death are to be identified.
Miscarriage/Stillbirth/Prenatal Issues
1. Bersinger NA, Wunder DM, Nicolas M, Birkhauser MH, Porquet
D, Guibourdenche J
Serum Hyperglycosylated Human Chorionic Gonadotropin to Predict
the Gestational Outcome in in vitro Fertilization/Intracytoplasmic
Sperm Injection Pregnancies
Fetal Diagn Ther. 2008 May 27;24(1):74-78. [Epub ahead of print]
Department of Obstetrics and Gynaecology, University of Berne,
Berne, Switzerland.
Hyperglycosylated human chorionic gonadotropin (H-hCG) is
secreted by the placenta in early pregnancy. Decreased H-hCG
levels have been associated with abortion in spontaneous pregnancy.
We retrospectively measured H-hCG and dimeric hCG in the sera
of 87 in vitro fertilization patients obtained in the 3 weeks
following embryo transfer and set the results in relation to
pregnancy outcome. H-hCG and dimeric hCG were correlated (r(2)
= 0.89), and were significantly decreased in biochemical pregnancy
(2 mug/l and 18 IU/l, respectively) compared to early pregnancy
loss (22 mug/l and 331 IU/l) and ongoing pregnancy (32 mug/l
and 353 IU/l). Only H-hCG tended to discriminate between these
last two groups. Copyright © 2008 S. Karger AG, Basel.
2. Clin Hemorheol Microcirc. 2008;39(1-4):329-32
Schenk JF, Stephan B, Zewinger S, Speer T, Pindur G
Comparison of the plasminogen activator inhibitor-1 4G/5G gene
polymorphism in females with venous thromboembolism during
pregnancy or spontaneous abortion
Genetic polymorphisms in plasminogen activator inhibitor-1
gene-675 4G/5G (PAI-1 4G/5G) are claimed to contribute to an
increased risk of venous thromboembolism. Inherited thrombophilia,
on the other hand, is associated with the occurrence of spontaneous
abortions. The objective of this study was, to explore the
significance of genetic polymorphisms of PAI-1 4G/5G with particular
emphasis on 4G alleles in pregnant women suffering from venous
thromboembolism or early spontaneous abortion, respectively.
Therefore genetic PAI-1 4G/5G polymorphisms were studied in
108 pregnant females suffering from venous thromboembolism
(n=69) or from spontaneous abortion (<20 week, n=39), respectively.
Healthy volunteers (n=238) were taken as controls. The frequencies
of 4G alleles (4G/4G or 4G/5G genotypes) of PAI-1 were significantly
higher in venous thromboembolism (OR: 3.40, p=0.0088) and slightly
higher, but not significantly, in abortions (RR: 2.33; p=0.1162)
compared to controls. The incidence of 4G-carriers in females
with abortion was 0.68 (-32%) compared to women suffering from
venous thromboembolism alone. We conclude from these data,
that the occurrence of PAI-1 4G/4G or 4G/5G genotypes, respectively,
is clinically significant for the pathogenesis of venous thromboembolism
in pregnancy but not for early abortion.
3. Cervera R, Balasch J
Bidirectional effects on autoimmunity and reproduction
Hum Reprod Update. 2008 May 22. [Epub ahead of print]
Department of Autoimmune Diseases, Institut Clínic
of Medicine and Dermatology, Faculty of Medicine, University
of Barcelona, Hospital Clínic-Institut d'Investigacions
Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona,
Catalonia, Spain.
Autoimmune diseases may selectively affect women in their
reproductive years, and conversely, pregnancy may affect the
expression of autoimmune disease. This review addresses the
impact of abnormal autoimmunity on female fertility, premature
ovarian failure (POF) and recurrent pregnancy loss, as well
as the influence of pregnancy in systemic lupus erythematosus
(SLE). METHODS From a PubMed search, citations were selected
for their immunological and gynecological relevance. RESULTS
The presence of antiphospholipid antibody (aPL) does neither
correlate with the type of female infertility diagnosis nor
affect outcomes, and treatment is not indicated. Autoimmunity
as a cause of POF is probably limited to the cases associated
with the autoimmune thyroid diseases. With respect to recurrent
spontaneous abortion, there is no consensus on the mechanisms
of an autoimmune effect, although vasculopathy of the terminal
spiral arteries may be implicated, but there is a general consensus
to screen for aPL when recurrent spontaneous abortion is unexplained.
Well-designed diagnostic studies are needed to estimate the
true association between specific autoantibodies and recurrent
spontaneous abortion. With respect to SLE, pregnancy should
be avoided when the disease is active, and the potentially
harmful impact of pregnancy can be minimized by multi-disciplinary
care. CONCLUSIONS Autoimmunity may impair female fertility
and, in particular, the antiphospholipid syndrome is associated
with recurrent spontaneous abortion. Integration of mechanistic
and clinical information by multi-disciplinary teams is needed
to manage reproductive issues in women with autoimmune diseases.
4. Maintz L, Schwarzer V, Bieber T, van der Ven K, Novak N
Effects of histamine and diamine oxidase activities on pregnancy:
a critical review
Hum Reprod Update. 2008 May 22. [Epub ahead of print]
Department of Dermatology and Allergology, University of Bonn,
Sigmund-Freud-Str. 25, 53105 Bonn, Germany.
BACKGROUND Histamine has been assumed to contribute to embryo-uterine
interactions due to its vasoactive, differentiation and growth-promoting
properties. However, its exact functions in pregnancy are unclear.
The histamine-degrading enzyme diamine oxidase (DAO) is produced
in high amounts by the placenta and has been supposed to act
as a metabolic barrier to prevent excessive entry of bioactive
histamine from the placenta into the maternal or fetal circulation.
METHODS The literature available on PubMed published in English
between 1910 and 2008 has been searched using the isolated
and combined key words histamine, diamine oxidase, pregnancy,
placenta, endometrium, miscarriage, implantation, pre-eclampsia,
intrauterine growth retardation, diabetes and embryonic histamine-releasing
factor (EHRF). RESULTS High expression of the histamine-producing
enzyme histidine decarboxylase in the placenta, histamine receptors
at the feto-maternal interface and the existence of an EHRF
suggest a physiological role of histamine during gestation.
The balance between histamine and DAO seems to be crucial for
an uncomplicated course of pregnancy. Reduced DAO activities
have been found in multiple heterogeneous complications of
pregnancy such as diabetes, threatened and missed abortion
and trophoblastic disorders. Whether women with histamine intolerance
suffer from more complicated pregnancies and higher abortion
rates due to impaired DAO activities and if low DAO levels
or genetic modifications in the DAO gene might therefore represent
a prognostic factor for a higher risk of abortion, has not
been investigated yet. CONCLUSIONS Low activities of the histamine-degrading
enzyme DAO might indicate high-risk pregnancies, although high
intra- and interindividual variations limit its value as a
screening tool.
5. Goodman C, Jeyendran RS, Coulam CB
Vascular endothelial growth factor gene polymorphism and implantation
failure
Reprod Biomed Online. 2008 May;16(5):720-3
Department of Obstetrics and Gynecology, University of Southern
California, Los Angeles, California, USA.
Implantation failure is the most frequent cause of lack of
pregnancy after IVF and embryo transfer. Successful implantation
requires the invading blastocyst to stimulate its own blood
supply through angiogenesis. Vascular endothelial growth factor
(VEGF) is the best-characterized regulator of angiogenesis.
Since one polymorphism of the VEGF gene, -1154 G/A, has been
previously suggested to be associated with recurrent spontaneous
abortion, the present study was undertaken to determine whether
VEGF -1154 G/A genotype is also related to recurrent implantation
failure. Buccal swabs were obtained from 70 women with a history
of recurrent implantation failure after IVF-embryo transfer
and from 73 control women. DNA was extracted from the buccal
swabs and analysed for the presence of the VEGF -1154 A/A gene.
The frequency of homozygosity of the VEGF -1154 A/A gene was
significantly higher among women experiencing recurrent implantation
failure compared with fertile control women (19% versus 5%,
P = 0.02). It is concluded that homozygosity of the VEGF -1154
A/A gene may serve as a susceptibility factor affecting the
chances of recurrent implantation failure.
Prepared by the
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