NSIDRC Journal Article Alert — May 9, 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.
Availability of full-text journal articles is often limited to
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Sudden Infant Death
1. Yiallourou SR, Walker AM, Horne RS
Effects of sleeping position on development of infant cardiovascular
control
Arch Dis Child. 2008 May 2 [Epub ahead of print]
Monash University, Australia
OBJECTIVE: Sudden Infant Death Syndrome (SIDS) is associated
with prone
sleeping and circulatory failure has been hypothesised as a
factor in
the fatal event. We aimed to determine the effect of prone
sleeping on
heart rate (HR) and blood pressure (BP) control over the first
6 mo of
life. SUBJECTS: Term infants (N=20) were studied longitudinally
at 2-4
wk, 2-3 mo and 5-6 mo with daytime polysomnography. MAIN OUTCOME
MEASURES: A photoplethysmographic cuff (FinometerTM) on the
infant's
wrist measured (MAP), systolic (SAP), diastolic (DAP) arterial
pressure
and HR during quiet sleep (QS) and active sleep (AS) in both
the supine
and prone positions. RESULTS: BP in QS was lower compared to
AS (by 3-9
mmHg) in both positions and at all three ages (p<0.05).
At 2-3 mo a
change from supine to prone in QS induced a fall in SAP (6
mmHg, p<0.05)
and a rise in HR (4 bpm, p<0.05). An overall effect of PNA
on BP was
identified (ANOVA) with MAP and DAP consistently averaging
less (by 1-9
mmHg) at 2-3 mo in both sleep states and sleeping positions
compared
with both other ages. CONCLUSIONS: Infant BP is modified by
sleep state
and sleeping position. A tendency for BP to fall in the prone
position
appears to be prevented by elevated HR, except at 2-3 mo in
QS. An
uncompensated fall in BP in the prone position at 2-3 mo (when
SIDS risk
is greatest) could increase the possibility of circulatory
failure and
SIDS in vulnerable infants.
2. Van Norstrand DW, Tester DJ, Ackerman MJ
Overrepresentation of the proarrhythmic, sudden death predisposing
sodium channel polymorphism S1103Y in a population-based cohort
of
African-American sudden infant death syndrome
Heart Rhythm.
2008 May;5(5):712-5. Epub 2008 Feb 16
Department of Molecular Pharmacology and Experimental Therapeutics,
Mayo
Clinic, Rochester, Minnesota 55905, USA
BACKGROUND: The S1103Y-SCN5A polymorphism has been implicated
as a
proarrhythmic, sudden death predisposing risk factor in African
Americans, including one postmortem investigation of African-American
infants with sudden infant death syndrome (SIDS). OBJECTIVE:
The purpose
of this study was to assess whether the relatively
African-American-specific common polymorphism S1103Y in the
SCN5A-encoded cardiac sodium channel is overrepresented in
SIDS among
African Americans. METHODS: Seventy-one cases from a population-based
cohort of unexplained infant deaths among African Americans
(37 females
and 34 males, average age 3 +/- 2 months, age range birth to
11 months)
were submitted to the Mayo Clinic Windland Smith Rice Sudden
Death
Genomics Laboratory for postmortem genetic testing. Polymerase
chain
reaction and a restriction digest assay were performed to genotype
this
cohort for S1103Y. RESULTS: Targeted mutational analysis of
exon 18 in
SCN5A of the African-American SIDS cohort (n = 71) revealed
the S1103Y
polymorphism in 16 (22.5%) of 71 African-American cases of
SIDS compared
to 135 (11.6%) of 1,161 ostensibly healthy adult African Americans
(P =
.01). CONCLUSION: This study provides an independent assessment
of the
prevalence of S1103Y-SCN5A among African-American infants with
sudden,
unexpected, unexplained death prior to their first birthday.
Further
scrutiny and quantification of the risk apparently associated
with
S1103Y appear warranted.
3. Blair PS, Mitchell EA, Heckstall-Smith EM, Fleming PJ
Head Covering - A major modifiable risk factor for Sudden Infant
Death
Syndrome: A systematic review
Arch Dis Child. 2008 May 1 [Epub ahead of print]
University of Bristol, United Kingdom
BACKGROUND: Some victims of sudden infant death syndrome (SIDS)
are
found with their heads covered with bedclothes but the significance
is
uncertain. The aim of this review is to describe the prevalence
of head
covering, the magnitude of the risk and how the suggested causal
mechanisms fit with current epidemiological evidence. METHODS:
Systematic review of population-based age-matched controlled
studies.
RESULTS: Controlled observations of head covering for the final
sleep
were found in ten studies. The pooled prevalence in SIDS victims
was
24.6% [95% CI: 22.3-27.1%] compared to 3.2% [95% CI: 2.7-3.8%]
amongst
the controls. The pooled univariate odds ratio (OR) was 9.6
[95% CI:
7.9-11.7] and the pooled adjusted OR from studies mainly conducted
after
the fall in SIDS rate was 16.9 [95% CI: 12.6-22.7]. The risk
varied in
strength but was significant across all studies. In a quarter
of cases
and controls head covering had occurred at least once previously
(pooled
adjusted OR=1.1 [95% CI: 0.9-1.4]). The population attributable
risk
(27.1% [95% CI: 24.7%-29.4%]) suggests avoiding head covering
might
reduce SIDS deaths by more than a quarter. CONCLUSIONS: The
epidemiological evidence does not fully support postulated
causal
mechanisms such as hypoxia, hypercapnoea and thermal stress,
but neither
does it support the idea that head covering is part of some
terminal
struggle. Head covering is a major modifiable risk factor associated
with SIDS deaths and parental advice to avoid these circumstances
should
be emphasised.
4. Moore BM, Fernbach KL, Finkelstein MJ, Carolan PL
Impact of Changes in Infant Death Classification on the Diagnosis
of
Sudden Infant Death Syndrome
Clin Pediatr (Phila). 2008 Apr 30 [Epub ahead of print]
This study evaluates the hypothesis that a decline in sudden
infant
death syndrome in Minnesota is associated with increases in
other
categories of sudden unexpected infant death. Matched birth
and death
certificates, autopsy reports, and home visit questionnaires
were
reviewed for 722 sudden unexpected infant deaths that occurred
from
January 1, 1996 through December 31, 2002. Descriptive data
and cause of
death were recorded. Cause of death was compared for 2 periods:
early
(1996-1998) and late (2000-2002). The age of the infant at
death, sex,
race, and infant death rates were similar between the 2 periods
(P =
.637). Sudden infant death syndrome declined by 50.1% (P < .001).
Overlay deaths increased 235.5% (P < .01). Asphyxia related
deaths
increased 259.6% (P < .001). Injury-related deaths increased
840.0% (P <
.001). A decline in sudden infant death syndrome in Minnesota
was
associated with increased deaths in categories that are asphyxial
in
nature and are potentially preventable.
5. Edston E, Perskvist N
Histiocytoid cardiomyopathy and ventricular non-compaction
in a case of
sudden death in a female infant
Int J Legal Med. 2008 Apr 30 [Epub ahead of print]
Department of Forensic Medicine, Artillerigatan 12, 581 33,
Linköping,
Sweden, eried@imk.liu.se
A case of sudden infant death with histiocytoid cardiomyopathy
and
ventricular non-compaction was investigated with immunohistochemical
methods. Histiocytoid cardiomyopathy is thought to be a developmental
defect of the cardiomyocytes of the conduction system. In contrast
to
mature cardiomyocytes, the histiocytoid cells showed only weak
reactions
to desmin and myosin antibodies. They lacked cross-striation
but reacted
strongly to enolase and myoglobin antibodies. The protein Pax-7,
seen
only in cells undergoing differentiation, and the proliferation
marker
Ki-67 were not expressed in the histiocytoid cells. In areas
of altered
myocardium, clusters of CD4-, CD8-, and CD68-positive inflammatory
cells
were seen as well an abundance of mast cells. With the TUNEL
method, it
was found that many of the histiocytoid cells were undergoing
apoptosis.
Our results confirm that the histiocytoid cells are defective
cardiomyocytes. The apoptotic and inflammatory changes point
to a
degenerative process rather than defective maturation of cardiomyocytes
as has been suggested in some earlier studies. Ventricular
non-compaction is a developmental defect of the subendocardial
tissue
with hypertrabeculation and weak development of the papillary
muscles.
Only one case combined with histiocytoid cardiomyopathy has
been
described previously. A causal connection between the two conditions
cannot be established until more cases have been analyzed.
Other Infant Death
1. Sloan NL, Ahmed S, Mitra SN, Choudhury N, Chowdhury M,
Rob U, Winikoff B
Community-based kangaroo mother care to prevent neonatal and
infant
mortality: a randomized, controlled cluster trial
Pediatrics
Department of Epidemiology, Columbia University, Mailman School
of
Public Health, 722 West 168th St, New York, NY 10032, USA.
nlsloan@gmail.com
OBJECTIVE: We adapted kangaroo mother care for immediate postnatal
community-based application in rural Bangladesh, where the
incidence of
home delivery, low birth weight, and neonatal and infant mortality
is
high and neonatal intensive care is unavailable. This trial
tested
whether community-based kangaroo mother care reduces the overall
neonatal mortality rate by 27.5%, infant mortality rate by
25%, and low
birth weight neonatal mortality rate by 30%. METHODS: Half
of 42 unions
in 2 Bangladesh divisions with the highest infant mortality
rates were
randomly assigned to community-based kangaroo mother care,
and half were
not. One village per union was randomly selected proportionate
to union
population size. A baseline survey of 39,888 eligible consenting
women
collected sociodemographic information. Community-based workers
were
taught to teach community-based kangaroo mother care to all
expectant
and postpartum women in the intervention villages. A total
of 4165 live
births were identified and enrolled. Newborns were followed
for 30 to 45
days and infants were followed quarterly through their first
birthday to
record infant care, feeding, growth, health, and vital status.
RESULTS:
Forty percent overall and approximately 65% of newborns who
died were
not weighed at birth, and missing birth weight was differential
by study
group. There was no difference in overall neonatal mortality
rate or
infant mortality rate. Except for care seeking, community-based
kangaroo
mother care behaviors were more common in the intervention
than control
group, but implementation was weak compared with the pilot
study.
CONCLUSIONS: The extensive missing birth weight and its potential
bias
render the evidence insufficient to justify implementing community-based
kangaroo mother care. Additional experimental research ensuring
baseline
comparability of mortality, adequate kangaroo mother care
implementation, and birth weight assessment is necessary to
clarify the
effect of community-based kangaroo mother care on survival.
Miscarriage/Stillbirth/Prenatal Issues
1. Zhang X, Decker A, Platt RW, Kramer MS
How big is too big? The perinatal consequences of fetal macrosomia
Am J Obstet Gynecol. 2008 May;198(5):517.e1-6
Department of Pediatrics, McGill University Faculty of Medicine,
Montreal, QC, Canada
OBJECTIVE: The objective of the study was to examine the birthweight
at
which risks of perinatal death, neonatal morbidity, and cesarean
delivery begin to rise and the causes and timing (antenatal,
early or
late neonatal, or postneonatal) of these risks. STUDY DESIGN:
This was a
cohort study based on 1999-2001 US-linked stillbirth, live
birth, and
infant death records. Singletons weighing 2500 g or larger
born to white
non-Hispanic mothers at 37-44 weeks of gestation were selected
(n =
5,983,409). RESULTS: Infants with birthweights from 4000 to
4499 g were
not at increased risk of mortality or morbidity vs those at
3500-3999 g,
whereas those 4500-4999 g had significantly increased risks
of
stillbirth, neonatal mortality (especially because of birth
asphyxia),
birth injury, neonatal asphyxia, meconium aspiration, and cesarean
delivery. Births at 5000 g or larger had even higher risks,
including
risk of sudden infant death syndrome. CONCLUSION: Birthweight
greater
than 4500 g, and especially greater than 5000 g, is associated
with
increased risks of perinatal and infant mortality and morbidity.
2. Mobeen N, Jehan I, Banday N, Moore J, McClure EM, Pasha
O, Wright LL,
Goldenberg RL
Periodontal disease and adverse birth outcomes: a study from
Pakistan
Am J Obstet Gynecol. 2008 May;198(5):514.e1-8
Department of Community Health Sciences, Aga Khan University,
Karachi,
Pakistan
OBJECTIVE: Periodontal disease may increase the risk of adverse
birth
outcomes; however, results have been mixed. Few studies have
examined
periodontal disease in developing countries. We describe the
relationship between periodontal disease and birth outcomes
in a
community setting in Pakistan. STUDY DESIGN: This was a prospective
cohort study. Enrollment occurred at 20-26 weeks of gestation.
A study
dentist performed the periodontal examination to assess probing
depth,
clinical attachment level, gingival index, and plaque index.
Outcomes
included stillbirth, neonatal death, perinatal death, < 32
weeks preterm
birth, 32-36 weeks preterm birth, and low birthweight and are
presented
for increasing periodontal disease severity by quartiles. RESULTS:
Dental examinations and outcome data were completed for 1152
women: 81%
of the women were multiparous, with a mean age of 27 years;
33% of the
women had no education. Forty-seven percent of the women had
dental
caries; 27% of the women had missing teeth, and 91% of the
women had had
no dental care in the last year. Periodontal disease was common:
76% of
the women had > or = 3 teeth with a probing depth of > or
= 3 mm; 87% of
the women had > or = 4 teeth with a clinical attachment
level of > or =
3 mm; 56% of the women had > or = 4 teeth with a plaque
index of 3; and
60% of the women had > or = 4 teeth with a gingival index
of 3. As the
measures of periodontal disease increased from the 1st to 4th
quartile,
stillbirth and neonatal and perinatal death also increased,
with
relative risks of approximately 1.3. Early preterm birth increased,
but
the results were not significant. Late preterm birth and low
birthweight
were not related to measures of periodontal disease. CONCLUSION:
Pregnant Pakistani women have high levels of moderate-to-severe
dental
disease. Stillbirth and neonatal and perinatal deaths increased
with the
severity of periodontal disease.
3. Lagerberg RE
Malaria in pregnancy: a literature review
J Midwifery Womens Health. 2008 May-Jun;53(3):209-15
Center for Community Health and Education, New York-Presbyterian
Hospital, NewYork, NY, USA. rl2392@columbia.edu
Pregnant women are more likely than nonpregnant women to become
infected
with malaria and to have severe infection. The effects of malaria
during
pregnancy include spontaneous abortion, preterm delivery, low
birth
weight, stillbirth, congenital infection, and maternal death.
Malaria is
caused by the four species of the protozoa of the genus Plasmodium,
which is transmitted by the bite of the female Anopheline mosquito,
congenitally, or through exposure to infected blood products.
This
article reviews the epidemiology, pathology, clinical symptoms,
diagnosis, and treatment of malaria in pregnant women. Interventions
to
prevent malaria include intermittent preventive treatment,
insecticide-treated nets, and case management of malaria infection
and
anemia.
4. Henley A, Schott J
The death of a baby before, during or shortly after birth:
Good practice
from the parents' perspective
Semin Fetal Neonatal Med. 2008 Apr 29 [Epub ahead of print]
Sonneggstrasse 9, 4125 Riehen, Switzerland
This chapter is adapted from Pregnancy Loss and the Death
of a Baby:
Guidelines for Professionals (3rd edition) by Judith Schott,
Alix Henley
and Nancy Kohner, published by Sands (the UK Stillbirth and
Neonatal
Death charity) in 2007. The article highlights those aspects
of care
given to families facing perinatal loss that parents value
and those
that add, often inadvertently, to their distress. It is based
on
research findings and on views expressed by parents.
5. Ma S
Paternal Race/Ethnicity and Birth Outcomes
Am J Public Health. 2008 Apr 29 [Epub ahead of print]
Johns Hopkins University.
Objectives. I sought to identify whether there were associations
between
paternal race/ethnicity and birth outcomes among infants with
parents of
different races/ethnicities. Methods. Using the National Center
for
Health Statistics 2001 linked birth and infant death file,
I compared
birth outcomes of infants of White mothers and fathers of different
races/ethnicities by matching and weighting racial/ethnic groups
following a propensity scoring approach so other characteristics
were
distributed identically. I applied the same analysis to infants
of Black
parents and infants with a Black mother and White father. Results.
Variation in risk factors and outcomes was found in infants
of White
mothers by paternal race/ethnicity. After propensity score
weighting,
the disparities in outcomes by paternal or parental race/ethnicity
could
be largely attributed to nonracial parental characteristics.
Infants
whose paternal race/ethnicity was unreported on their birth
certificates
had the worst outcomes. Conclusions. The estimated effect of
maternal
race/ethnicity on birth outcomes was more than 3 times as large
as that
of paternal race/ethnicity after I controlled for all covariates.
Unreported paternal race/ethnicity had a strong association
with
outcomes, which might be a source of bias in existing data
and a marker
for identifying infants at risk.
6. Díaz JM, Canal C, Giménez I, Guirado L, Facundo
C, Solà R, Ballarín J
Pregnancy in recipients of kidney transplantation: effects
on the mother
and the child
Nefrologia. 2008;28(2):174-177.
When the field of transplantation was first developing, physicians
worried about the teratogenicity of immunosuppressive medications
and
considered pregnancy ill-advised. The purpose of this study
is to
analyze pregnancy after kidney transplantation and their consequences
on
mother, graft and child. We rewiew ten pregnant women with
kidney
transplantation, average of 29 years old and 44 months post-kidney
transplantation. The mean glomerular filtration rate was 64
ml/min and
the immunosuppression was with prednisone and tacrolimus. We
analyze
outcomes of differents variables before and during pregnancy,
and after
labour. Pregnancy finished in nine of ten patients. Three patients
needed cesarean section and only one patient had a miscarriage
on the
first term. Blood arterial pressure increased at the end of
pregnancy
and the creatinine level was stable with a few increase of
proteinuria
at the third term. We increased the tacrolimus dose to obtain
the
correct blood levels and any rejection was detected. We had
only one
patient with preeclampsia that we solved with a cesarean section.
Labours were a mean of 37.2 weeks and the mean birth weight
of infant
was 2809 grams. Two newborns had prematurity without structural
malformations. Pregnancy after kidney transplantation is safe
with
prednisone and tacrolimus when the renal function is good,
proteinuria
doesn't exist and blood pressure is controlled.
7. Pãunescu MM, Feier V, Pãunescu M, Dorneanu
F, Sisak A, Ambros-Rudolph CM
Dermatoses of pregnancy
Acta Dermatovenerol Alp Panonica Adriat. 2008 Mar;17(1):4-11
Department of Dermatology, Victor Babes University of Medicine
and
Pharmacy, Str Mãrã e ti 5, Timisoara, Romania.
magdalenapaunescu@yahoo.com
The dermatoses of pregnancy represent a heterogeneous group
of pruritic
inflammatory skin diseases related to pregnancy and/or the
postpartum
period. Whereas some dermatoses are distressing only to the
mother
because of severe pruritus, others are associated with fetal
risks
including fetal distress, prematurity, and stillbirth. Early
diagnosis
and prompt treatment are essential for improving maternal and
fetal
prognosis. This review discusses the various pregnancy dermatoses
in
detail and offers an algorithmic approach to their diagnosis
and management.
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
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