Does β-APP staining of the brain in infant bed-sharing deaths differentiate these cases from sudden infant death syndrome?

AbstractSeveral studies have indicated that a vulnerability in the development and regulation of brain function is involved in sudden infant death syndrome (SIDS). The aim of this study was to investigate the genes encoding the brain aquaporins (AQPs) AQP1 and AQP9 in SIDS. The hypothesis was that specific variants of these genes are part of the genetic vulnerability predisposing infants to sudden unexpected death. The study included 168 SIDS cases with a median age of 15.5 (range 2–52) weeks and 372 adolescent/adult deceased controls with a median age of 44 (range 11–91) years. In the AQP1 gene, the rs17159702 CC/CT genotypes were found to be associated with SIDS (p = 0.02). In the AQP9 gene, the combination of a TT genotype of rs8042354, rs2292711 and rs13329178 was more frequent in SIDS cases than in controls (p = 0.03). In the SIDS group, an association was found between genetic variations in the AQP1 gene and maternal smoking and between the 3xTT combination in the AQP9 gene and being found lifeless in a prone position. In conclusion, this study adds further evidence to the involvement of brain aquaporins in SIDS, suggesting that specific variants of AQP genes constitute a genetic predisposition, making the infant vulnerable to sudden death together with external risk factors and probably other genetic factors.

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Sleep Environment and the Risk of Sudden Infant Death Syndrome in an Urban Population: The Chicago Infant Mortality Study

PEDIATRICS ◽

10.1542/peds.111.s1.1207 ◽

2003 ◽

Vol 111 (Supplement_1) ◽

pp. 1207-1214 ◽

Cited By ~ 25

Author(s):

Fern R. Hauck ◽

Stanislaw M. Herman ◽

Mark Donovan ◽

Solomon Iyasu ◽

Cathryn Merrick Moore ◽

...

Keyword(s):

Sudden Infant Death Syndrome ◽

Infant Death ◽

Sudden Infant Death ◽

Ethnic Composition ◽

Sudden Infant ◽

Bed Sharing ◽

Soft Surface ◽

Sleep Environment ◽

Racial Ethnic ◽

Hispanic White

Objective. To examine risk factors for sudden infant death syndrome (SIDS) with the goal of reducing SIDS mortality among blacks, which continues to affect this group at twice the rate of whites. Methods. We analyzed data from a population-based case-control study of 260 SIDS deaths that occurred in Chicago between 1993 and 1996 and an equal number of matched living controls to determine the association between SIDS and factors in the sleep environment and other variables related to infant care. Results. The racial/ethnic composition of the study groups was 75.0% black; 13.1% Hispanic white; and 11.9% non-Hispanic white. Several factors related to the sleep environment during last sleep were associated with higher risk of SIDS: placement in the prone position (unadjusted odds ratio [OR]: 2.4; 95% confidence interval [CI]: 1.7–3.4), soft surface (OR: 5.1; 95% CI: 3.1–8.3), pillow use (OR: 2.5; 95% CI: 1.5–4.2), face and/or head covered with bedding (OR: 2.5; 95% CI: 1.3–4.6), bed sharing overall (OR: 2.7; 95% CI: 1.8–4.2), bed sharing with parent(s) alone (OR: 1.9; 95% CI: 1.2–3.1), and bed sharing in other combinations (OR: 5.4; 95% CI: 2.8–10.2). Pacifier use was associated with decreased risk (unadjusted OR: 0.3; 95% CI: 0.2–0.5), as was breastfeeding either ever (OR: 0.2; 95% CI: 0.1–0.3) or currently (OR: 0.2; 95% CI: 0.1–0.4). In a multivariate model, several factors remained significant: prone sleep position, soft surface, pillow use, bed sharing other than with parent(s) alone, and not using a pacifier. Conclusions. To lower further the SIDS rate among black and other racial/ethnic groups, prone sleeping, the use of soft bedding and pillows, and some types of bed sharing should be reduced.

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