Garmany Tami H, Wambach Jennifer A, Heins Hillary B, Watkins-Torry Julie M, Wegner Daniel J, Bennet Kate, An Ping, Land Garland, Saugstad Ola D, Henderson Howard, Nogee Lawrence M, Cole F Sessions, Hamvas Aaron
Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Pediatr Res. 2008 Jun;63(6):645-9. doi: 10.1203/PDR.0b013e31816fdbeb.
The prevalence of the common mutations in the surfactant protein-B (121ins2), surfactant protein-C (I73T), and ATP-binding cassette member A3 (E292V) genes in population-based or case-control cohorts of newborn respiratory distress syndrome (RDS) is unknown. We determined the frequencies of these mutations in ethnically diverse population and disease-based cohorts using restriction enzyme analysis (121ins2 and E292V) and a 5' nuclease assay (I73T) in DNA samples from population-based cohorts in Missouri, Norway, South Korea, and South Africa, and from a case-control cohort of newborns with and without RDS (n = 420). We resequenced the ATP-binding cassette member A3 gene (ABCA3) in E292V carriers and computationally inferred ABCA3 haplotypes. The population-based frequencies of 121ins2, E292V, and I73T were rare (<0.4%). E292V was present in 3.8% of newborns with RDS, a 10-fold greater prevalence than in the Missouri cohort (p < 0.001). We did not identify other loss of function mutations in ABCA3 among patients with E292V that would account for their RDS. E292V occurred on a unique haplotype that was derived from a recombination of two common ABCA3 haplotypes. E292V was over-represented in newborns with RDS suggesting that E292V or its unique haplotype impart increased genetic risk for RDS.
在基于人群或病例对照的新生儿呼吸窘迫综合征(RDS)队列中,表面活性蛋白B(121ins2)、表面活性蛋白C(I73T)和ATP结合盒成员A3(E292V)基因常见突变的患病率尚不清楚。我们使用限制性内切酶分析(121ins2和E292V)和5'核酸酶分析(I73T),对来自密苏里州、挪威、韩国和南非基于人群的队列以及一个有或无RDS的新生儿病例对照队列(n = 420)的DNA样本,测定了不同种族人群和疾病队列中这些突变的频率。我们对E292V携带者的ATP结合盒成员A3基因(ABCA3)进行了重测序,并通过计算推断出ABCA3单倍型。基于人群的121ins2、E292V和I73T频率很低(<0.4%)。E292V在3.8%的RDS新生儿中出现,其患病率比密苏里队列高10倍(p < 0.001)。我们在E292V患者中未发现ABCA3的其他功能丧失突变可以解释他们的RDS。E292V出现在一个独特的单倍型上,该单倍型源自两种常见ABCA3单倍型的重组。E292V在RDS新生儿中过度存在,表明E292V或其独特的单倍型会增加RDS的遗传风险。