No abstract

Preterm birth is the single most important cause of perinatal mortality in North America. Given that American Indians/Alaskan Natives (AI/ANs) in the United States continue to have adverse birth outcomes, the purpose of this study is to compare the risk of preterm birth among AI/AN mothers to Non-Hispanic White mothers living in Washington and Montana from 2003 to 2009. A population-based retrospective cohort study was conducted examining the association between AI/AN mothers (self-reported) and the risk of preterm birth (gestational age <37 weeks) using birth certificate data from Washington and Montana. All AI/AN singleton lives births (n = 26,648) from residents of Washington and Montana from 2003 to 2009 were identified and included in our study. An identical number of Non-Hispanic White singleton infants (n = 26,648) born to residents of Washington and Montana were randomly selected as a comparison group and logistic regression was used to analyze the data. AI/AN mothers living in Washington and Montana between 2003 and 2009 were 1.34 times (95 % CI 1.25-1.44) as likely to have a preterm birth compared to Non-Hispanic Whites after adjusting for maternal and paternal characteristics as well as pregnancy risk factors. AI/AN mothers residing in Washington and Montana from 2003 to 2009 were at a significantly increased risk of having a preterm birth compared to Non-Hispanic Whites. Identifying etiologic differences in preterm birth experienced by AI/ANs is essential in targeting future interventions.

Thrombophilia has been subject to extensive genetic research. This review focuses on the genetic variants that have confirmed associations with venous thrombosis (VT). For incident VT, the early discovery of variants with large-magnitude associations, such as mutations in antithrombin, protein C, and protein S genes, has been followed by genetic variants that are associated with more moderate risk, such as the factor V Leiden, and prothrombin G20210A. More recently, large candidate-gene and genome-wide association studies have discovered multiple genetic variants with generally weak association with VT. For recurrent VT, the evidence for genetic risk factors remains very limited. Although thrombophilia testing is broadly available to clinicians, the impact on the clinical management of patients remains modest and depends on the strength of the association with VT. More promising for clinical practice may be global assessments of risk that combine risk information from multiple genetic variants, or with those from acquired risk factors. These models have yet to be defined and tested in large and diverse populations to demonstrate that this new genetic risk information has clinical applicability and improves health outcomes.