Maternal alcohol-use disorder is associated with increased risk of sudden infant death syndrome and infant death from other causes

2013 ◽  
Vol 17 (2) ◽  
pp. 46-47
Author(s):  
Katrine Strandberg-Larsen
Keyword(s):  
Alcohol Use ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Alcohol Use Disorder ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Maternal Alcohol ◽  
Increased Risk

Maternal Alcohol Use and Sudden Infant Death Syndrome and Infant Mortality Excluding SIDS

PEDIATRICS ◽  
2013 ◽  
Vol 131 (3) ◽  
pp. e770-e778 ◽  
Author(s):  
C. M. O'Leary ◽  
P. J. Jacoby ◽  
A. Bartu ◽  
H. D'Antoine ◽  
C. Bower
Keyword(s):  
Alcohol Use ◽  
Infant Mortality ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Maternal Alcohol

scholarly journals Association between monoamine oxidase A promoter polymorphism and the risk of sudden infant death syndrome: a meta-analysis

2021 ◽  
Author(s):  
Qiaoxia Zhou ◽  
Daoyin Gong ◽  
Yu Zhang ◽  
Feijun Huang
Keyword(s):  
Monoamine Oxidase ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Protective Factor ◽  
Meta Analysis ◽  
Variable Number Tandem Repeat ◽  
Sudden Infant Death ◽  
Monoamine Oxidase A ◽  
Sudden Infant ◽  
Increased Risk

Abstract Introduction The etiology of sudden infant death syndrome (SIDS) remains an unsolved problem. The aim of this meta-analysis is to investigate the potential association between monoamine oxidase A (MAOA) promoter variable number tandem repeat (VNTR) polymorphism and SIDS risk. Methods A systematic review and meta-analysis were conducted on studies from accessible electronic databases. Each VNTR variant was examined in each gender independently by comparing with the pooled results of other alleles. Results A total of six independent case–control studies including 1022 SIDS cases and 1839 controls were enrolled in this meta-analysis. In both of the whole populations and Caucasian populations, male infants with the low-MAOA-expression alleles (2R+3R) were found to exhibit a statistically significant increased risk of SIDS, whereas those with a 4R allele exhibited a reduced risk of SIDS. Besides, an increased risk of SIDS was detected in male Caucasian infants with 2R or 3R alleles. However, none of the allele or genotype variants was associated with SIDS in female victims. Conclusion In male Caucasian infants, the low expression of MAOA promoter VNTR alleles (2R and 3R) is associated with an increased risk of SIDS, and the existence of the 4R allele could be regarded as a protective factor.

Smoking and the Sudden Infant Death Syndrome

PEDIATRICS ◽  
1993 ◽  
Vol 91 (5) ◽  
pp. 893-896 ◽  
Author(s):  
E. A. Mitchell ◽  
R. P. K. Ford ◽  
A. W. Stewart ◽  
B. J. Taylor ◽  
D. M. O. Becroft ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Maternal Smoking ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Risk Of Death ◽  
Increased Risk ◽  
Wide Range ◽  
Household Members ◽  
Control Study

Objective. Maternal smoking has been shown to be a risk factor for sudden infant death syndrome (SIDS). The effect of smoking by the father and other household members has not previously been examined. Methods. A large nationwide case-control study. Four hundred eighty-five SIDS deaths in the postneonatal age group were compared with 1800 control infants. Results. Infants of mothers who smoked during pregnancy had a 4.09 (95% confidence interval [CI] = 3.28, 5.11) greater risk of death than infants of mothers who did not smoke. Infants of mothers who smoked postnatally also had an increased risk of SIDS compared with infants of nonsmokers and, furthermore, the risk increased with increasing levels of maternal smoking. Smoking by the father and other household members increased the risk (odds ratio [OR] = 2.41, 95% CI = 1.92, 3.02 and OR = 1.54, 95% CI = 1.20, 1.99, respectively). Smoking by the father increased the risk of SIDS if the mother smoked, but had no effect if she did not smoke. In analyses controlled for a wide range of potential confounders, smoking by the mother and father was still significantly associated with an increased risk of SIDS. Conclusion. Passive tobacco smoking is causally related to SIDS.

Sudden Infant Death Syndrome in Twins and Singletons

2007 ◽  
Vol 10 (4) ◽  
pp. 644-648 ◽  
Author(s):  
Peter O. D. Pharoah ◽  
Mary J. Platt
Keyword(s):  
Risk Factor ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Low Birthweight ◽  
Sudden Infant Death ◽  
Multiple Births ◽  
Sudden Infant ◽  
Microscopical Examination ◽  
Increased Risk ◽  
Opposite Sex

AbstractTwins compared with singletons and monozygous (MZ) compared with dizygous (DZ) twins are at increased risk of fetal and infant death, cerebral palsy and many congenital anomalies. The aim of this study is to investigate whether zygosity is a risk factor for the sudden infant death syndrome (SIDS). Birth registration data and draft infant death certificates for all multiple births in England and Wales 1993 to 2003 were provided by the Office for National Statistics. As a partial proxy for zygosity, same-sex was compared with opposite-sex twins for birthweight-specific mortality and mortality attributed to SIDS. Data on singleton infants were obtained by subtraction of multiple births from routinely published population births and infant deaths. SIDS mortality among low birthweight infants was significantly less in twins than singletons. The twin-singleton relative risk was reversed in infants of normal birthweight. Among infants of normal birthweight, neonatal SIDS was significantly more common in same- compared with opposite-sex pairs. Among infants of low birthweight, postneonatal SIDS was significantly more common in same- compared with opposite-sex pairs. The difference in birthweight distribution of same- compared with opposite-sex twins for neonatal SIDS suggests that zygosity is a risk factor for SIDS. As congenital cerebral anomalies are a feature of many monozygous twin conceptions, a detailed macro- and microscopical examination of the brain in twin SIDS may indicate an otherwise unrecognised pathology.

Incidence of Recurrence of Sudden Infant Death Syndrome

1993 ◽  
Vol 14 (3) ◽  
pp. 94-116
Keyword(s):  
United States ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
South Australia ◽  
Sudden Infant Death ◽  
The United States ◽  
Sudden Infant ◽  
Specific Population ◽  
Live Births ◽  
Increased Risk

Incidence figures for sudden infant death syndrome (SIDS) are affected by the specific population being studied, the method of data collection, the way in which the diagnosis is determined, and other variables. The occurrence of SIDS per 100 live births has been estimated to be 1.3 in Norway, 2.1 in South Australia, and 2 to 3 in the United States. Subsequent siblings are at increased risk of SIDS, with estimates ranging from 3.7 times that of the general population to as high as 10 times. Beal et al found that families in South Australia who lost a child older than 12 months of age to SIDS were 11 times more likely to have a subsequent child with SIDS than were families in which the SIDS victim was younger than 1 year of age.

Sleep Parameters and Respiratory Variables in ‘Near Miss’ Sudden Infant Death Syndrome Infants

PEDIATRICS ◽  
1981 ◽  
Vol 68 (3) ◽  
pp. 354-360
Author(s):  
Christian Guilleminault ◽  
Ronald Ariagno ◽  
Rowena Korobkin ◽  
Susan Coons ◽  
Margaret Owen-Boeddiker ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sleep Onset ◽  
Sudden Infant Death ◽  
Near Miss ◽  
Sudden Infant ◽  
Normal Infant ◽  
Respiratory Events ◽  
Increased Risk ◽  
Sleep Parameters

Twenty-nine near miss for sudden infant death syndrome and thirty normal infants between the ages of 3 weeks and 6 months were monitored polygraphically for 24 hours. The distribution of sleep and abnormal respiratory events were analyzed for both groups. On the basis of mixed and obstructive apnea, 12-hour nocturnal segments (8 pm to 8 am) consistently distinguished near miss from normal infant groups between the ages of 3 weeks and 4.5 months. Daytime naps do not provide statistical differences sufficient to differentiate between the two groups. During sleep, abnormal respiratory events are more likely to occur between 1 am and 6 am, at least 40 minutes after sleep onset. Respiratory pauses show a significant increase just prior to waking (a strong respiratory stimulus). Any impairment of the arousal threshold during sleep will place near miss infants at increased risk.

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