7101 Wisconsin Ave, Suite 1101, Bethesda, MD 20814
301-718-9603
nbstrn@nbstrn.org

Reaching Goals: Continuous Improvement of Newborn Screening and Public Health Systems

Continuous improvement of newborn screening and public health systems is an arduous goal. Though Newborn Screening (NBS) is a national success that evokes a decrease in mortality among newborns and improves developmental outcomes for patients of screened conditions, it is uncertain to what degree it achieves the long-term goals concerning the health of patients identified. Hinton and colleagues (2017), propose a framework for assessing outcomes for the well-being and development of children with conditions discovered through NBS. The proposed structure of assessment is applicable to every screened condition on the Recommended Uniform Screening Panel (RUSP). To provide an example, researchers in this study applied their framework to sickle cell disease and phenylketonuria (PKU). Overall, this framework provides a vision for a comprehensive approach to monitor and continuously improve the NBS system as opportunities arise for better outcomes through new measures and improved treatments in the U.S. The results of this examination will aid in the expansion of consistent and widespread NBS and child health systems in the United States and other countries.

The first author of this article, Cynthia F. Hinton, PhD, is associated with the Division of Laboratory Sciences with the Centers for Disease Control and Prevention (CDC). Her work affects the lives of patients across the United States and is focused on improving the health of children through newborn screening and disability inclusion.

The Newborn Screening Translational Network (NBSTRN) is an international network of clinicians, researchers, and parents advocates who support the research and development of newborn screening programs. 

Read the complete article at:

Hinton CF, Homer CJ, Thompson AA, et al. A framework for assessing outcomes from newborn screening: on the road to measuring its promise. Mol Genet Metab. 2016;118(4):221-229. doi:10.1016/j.ymgme.2016.05.017

https://pubmed.ncbi.nlm.nih.gov/27268406/

Leave a Reply

Your email address will not be published. Required fields are marked *