Dataset Information

The genetic susceptibility to respiratory distress syndrome.

ABSTRACT: Previous studies to identify a genetic component to RDS have shown conflicting results. Our objectives were to evaluate and quantify the genetic contribution to RDS using data that comprehensively includes known environmental factors in a large sample of premature twins. Data from a retrospective chart review of twins born at < or =32 wk GA were obtained from two neonatal units. Mixed effects logistic regression (MELR) analysis was used to assess the influence of several independent covariates on RDS. A zygosity analysis, including the effects of additive genetic, common environmental and residual effects (ACE) factors, was performed to estimate the genetic contribution. Results reveal that the 332 twin pairs had a mean GA of 29.5 wk and birth weight (BW) of 1372 g. An MELR identified significant nongenetic covariates as male gender (p = 0.04), BW (p < 0.001), 5-min Apgar score (p < 0.001), and treating institution (p = 0.001) as significant predictors for RDS. The ACE model was used to estimate the genetic susceptibility to RDS by adjusting for the above factors. We found 49.7% (p = 0.04) of the variance in liability to RDS was the result of genetic factors alone. We conclude that there is a significant genetic susceptibility to RDS in preterm infants.

SUBMITTER: Levit O

PROVIDER: S-EPMC2796284 | biostudies-literature | 2009 Dec

REPOSITORIES: biostudies-literature

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The genetic susceptibility to respiratory distress syndrome.

Levit Orly O Jiang Yuan Y Bizzarro Matthew J MJ Hussain Naveed N Buhimschi Catalin S CS Gruen Jeffrey R JR Zhang Heping H Bhandari Vineet V

Pediatric research 20091201 6

Previous studies to identify a genetic component to RDS have shown conflicting results. Our objectives were to evaluate and quantify the genetic contribution to RDS using data that comprehensively includes known environmental factors in a large sample of premature twins. Data from a retrospective chart review of twins born at < or =32 wk GA were obtained from two neonatal units. Mixed effects logistic regression (MELR) analysis was used to assess the influence of several independent covariates o ...[more]

PMID: 19687775

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Project description:RationaleAdiponectin is an anti-inflammatory adipokine that is the most abundant gene product of adipose tissue. Lower levels have been observed in obesity, insulin resistance, and in critical illness. However, elevated levels early in acute respiratory failure have been associated with mortality. Polymorphisms in adiponectin-related genes (ADIPOQ, ADIPOR1, ADIPOR2) have been examined for relationships with obesity, insulin resistance and diabetes, cardiovascular disease, and to circulating adipokine levels, but many gaps in knowledge remain. The current study aims to assess the association between potentially functional polymorphisms in adiponectin-related genes with acute respiratory distress syndrome (ARDS) risk and mortality.MethodsConsecutive patients with risk factors for ARDS admitted to the ICU were enrolled and followed prospectively for development of ARDS. ARDS cases were followed through day 60 for all-cause mortality. 2067 patients were successfully genotyped using the Illumina CVD BeadChip high-density platform. Of these, 567 patients developed ARDS. Forty-four single nucleotide polymorphisms (SNPs) on ADIPOQ, ADIPOR1 and ADIPOR2 were successfully genotyped. Of these, 9 SNPs were hypothesized to be functional based on their location (promoter, exon, or 3' untranslated region). These 9 SNPs were analyzed for association with ARDS case status and mortality among ARDS cases.ResultsAfter multivariable analysis and adjustment for multiple comparisons, no SNPs were significantly associated with ARDS case status. Among ARDS cases, homozygotes for the minor allele of rs2082940 (ADIPOQ) had increased mortality (hazard ratio 2.61, 95% confidence interval 1.36-5.00, p = 0.0039) after adjustment for significant covariates. The significance of this association persisted after adjustment for multiple comparisons (FDR_q = 0.029).ConclusionsA common and potentially functional polymorphism in ADIPOQ may impact survival in ARDS. Further studies are required to replicate these results and to correlate genotype with circulating adiponectin levels.

Dataset Information

The genetic susceptibility to respiratory distress syndrome.

Publications

The genetic susceptibility to respiratory distress syndrome.

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