NSIDRC Journal Article Alert — February 1, 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
subscribers or through inter-library loan. Please see
your local library for copies of these articles, or view PubMed's
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more details.
Sudden Infant Death
1. Rhodes TE, Abraham RA, Welch RC, Vanoye CG, Crotti L, Arnestad
M, Insolia R,
Pedrazzini M, Ferrandi C, Vege A, Rognum T, Roden DM, Schwartz
PJ, George AL Jr J Cardiac potassium channel dysfunction in
sudden infant death syndrome. Mol Cell Cardiol. 2007 Dec 7
Department of Medicine, Vanderbilt University, Nashville,
TN
Life-threatening arrhythmias have been suspected as one cause
of the sudden infant death syndrome (SIDS), and this hypothesis
is supported by the observation that mutations in arrhythmia
susceptibility genes occur in 5-10% of cases. However, the
functional consequences of cardiac potassium channel gene mutations
associated with SIDS and how these alleles might mechanistically
predispose to sudden death are unknown. To address these questions,
we studied four missense KCNH2 (encoding HERG) variants, one
compound KCNH2 genotype, and a missense KCNQ1 mutation all
previously identified in Norwegian SIDS cases. Three of the
six variants exhibited functional impairments while three were
biophysically similar to wild-type channels (KCNH2 variants
V279M, R885C, and S1040G). When co-expressed with WT-HERG,
R273Q and K897T/R954C generated currents resembling the rapid
component of the cardiac delayed rectifier current (I(Kr))
but with significantly diminished amplitude. Action potential
modeling demonstrated that this level of functional impairment
was sufficient to evoke increased action potential duration
and pause-dependent early afterdepolarizations. By contrast,
KCNQ1-I274V causes a gain-of-function in I(Ks) characterized
by increased current density, faster activation, and slower
deactivation leading to accumulation of instantaneous current
upon repeated stimulation. Action potential simulations using
a Markov model of heterozygous I274V-I(Ks) incorporated into
the Luo-Rudy (LRd) ventricular cell model demonstrated marked
rate-dependent shortening of action potential duration predicting
a short QT phenotype. Our results indicate that certain potassium
channel mutations associated with SIDS confer overt functional
defects consistent with either LQTS or SQTS, and further emphasize
the role of congenital arrhythmia susceptibility in this syndrome.
Other Infant Death
1. Turlington A, Hodgman JE, Barton L. Decreasing trend in
postneonatal mortality.
J Perinatol. 2008 Jan 24
1USC Division of Newborn Medicine, Department of Pediatrics,
Women's and Children's Hospital, LAC+USC Medical Center and
Children's Hospital of Los Angeles, Keck School of Medicine,
University of Southern California, Los Angeles, CA
Objective: The objective was to evaluate the postneonatal
mortality rate at our institution from 1999 to 2006 as a follow-up
to a previous report from our hospital covering 1993 to 1998
and to investigate the causes of death in infants dying in
the postneonatal period.Study Design: We identified all infant
deaths before discharge from the nursery aged >/=28 days.
Clinical data for all cases and autopsy records where available
were reviewed and the cause of death was determined for each
infant.Result: Total nursery deaths for the 7 years were 211,
of which 14 (6.6%) occurred after the neonatal period. This
represents a decreasing trend from the 12% reported in 1993
to 1998. Causes of death were the complications of prematurity
and congenital defects. The five infants whose cause of death
was the complications of prematurity had chronic lung disease,
four had abdominal surgery for perforation and resection and
two had intraventricular hemorrhage (IVH) Gr IV. All infants
had multiple organ failure by the time of
death and the final event was infection and/or renal failure.
The nine congenital defects included two trisomy 21 with complications,
one CHARGE association with heart defects, one hypertrophic
cardiomyopathy and two others with multiple congenital heart
defects. Of the three remaining infants, the anomalies included
one with hydranencephaly, one with caudal regression and one
with multiple vascular liver tumors.Conclusion:Along with the
general decrease in infant mortality, postneonatal mortality
is decreasing as a percentage of nursery deaths. The causes
of death include complications of prematurity and congenital
defects.Journal of Perinatology advance online publication,
24 January 2008, doi:10.1038/sj.jp.7211910.
Bereavement
1. Ajdacic-Gross V, Ring M, Gadola E, Lauber C, Bopp M, Gutzwiller
F, Rössler W.
Suicide after bereavement: an overlooked problem. Psychol Med.
2008 Jan 29;:1-4
Institute of Social and Preventive Medicine, University of
Zurich, Zurich,
Switzerland.
BACKGROUND: To examine the effect of time on suicide after
bereavement among widowed persons. METHOD: The data were extracted
from Swiss mortality statistics for the period 1987-2005. The
time between bereavement and subsequent death, specifically
by suicide, was determined by linkage of individual records
of married persons. The suicide rates and the standardized
mortality ratios in the first week/month/year of widowhood
were calculated based on person-year calculations. RESULTS:
The annualized suicide rates in widowed persons were
highest in the first week after bereavement: 941 males and
207 females per 100 000. The corresponding standardized mortality
ratios were approximately 34 and 19 respectively. In the first
month(s) after bereavement, the rates and the ratios decreased,
first rapidly, then gradually. Except in older widows, they
did not reach the baseline levels during the first year after
bereavement. CONCLUSIONS: The suicide risk of widowed persons
is increased in the days, weeks and months after bereavement.
Widowed persons are a clear-cut risk group under the aegis
of undertakers, priests and general practitioners.
Miscarriage/Stillbirth/Prenatal Issues
1. Wilson RE, Alio AP, Kirby RS, Salihu HM. Young maternal
age and risk of intrapartum stillbirth. Arch Gynecol Obstet.
2008 Jan 24
Department of Epidemiology and Biostatistics, University of
South Florida, Tampa, FL
OBJECTIVES: To determine the risk of intrapartum stillbirth
among teen mothers.
METHODS: The Missouri maternally linked data containing births
from 1978 to 1997 were analyzed. The study group (teen mothers)
was sub-divided into younger (<15 years) and older (15-19
years) teenagers. Women aged 20-24 were the referent category.
We used Kaplan-Meier product-limit estimator to calculate the
cumulative probability of death for each group and the Cox
Proportional Hazards Regression models to obtain adjusted hazards
ratios. RESULTS: The rate of antepartum and intrapartum stillbirth
among teenagers was 3.8 per 1,000 and 1.0 per 1,000, respectively,
compared to 3.5 per 1,000 and 0.8 per 1,000 among the reference
group. The adjusted risk of intrapartum stillbirth was more
than 4 times as high among younger teens (adjusted hazard ratio
[AHR] 4.3 [95% CI 4.0-4.7]) and 50% higher among older teens
(AHR 1.5 [95% CI 1.2-1.8]). The risk of intrapartum stillbirth
occurred in a dose-dependent fashion, with risk increasing
as maternal age decreased (P < 0.01). CONCLUSION: Teenagers
are at an increased risk of stillbirth, with the greatest risk
disparity occurring intrapartum, especially among younger teens.
This new information is potentially useful for targeting intervention
measures aimed at improving in utero fetal survival among pregnant
women at the lower extreme of the maternal age spectrum.
2. Weng X, Odouli R, Li DK. Maternal caffeine consumption
during pregnancy and the risk of miscarriage: a prospective
cohort study. Am J Obstet Gynecol. 2008 Jan 24
Division of Research, Kaiser Permanente, Oakland, CA
OBJECTIVE: The objective of the study was to examine whether
the risk of miscarriage is associated with caffeine consumption
during pregnancy after controlling for pregnancy-related symptoms.
STUDY DESIGN: This was a population-based prospective cohort
study. RESULTS: An increasing dose of daily caffeine intake
during pregnancy was associated with an increased risk of miscarriage,
compared with no caffeine intake, with an adjusted hazard ratio
(aHR) of 1.42 (95% confidence interval 0.93 to 2.15) for caffeine
intake of less than 200 mg/day, and aHR of 2.23 (1.34 to 3.69)
for intake of 200 or more mg/day, respectively. Nausea or vomiting
during pregnancy did not materially affect this observed association,
nor did the change in intake pattern of caffeine during pregnancy.
In addition, the magnitude of the association appeared to be
stronger among women without a history of miscarriage (aHR
2.33, 1.48 to 3.67) than that among women with such a history
(aHR 0.81, 0.34 to 1.94). CONCLUSION: Our results demonstrated
that high doses of caffeine intake during pregnancy increase
the risk of miscarriage, independent of pregnancy-related symptoms.
Prepared by the
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