Opportunities on the road to value-based payment for children with chronic respiratory disease.

The transition from a fee-for-service payment system to value-based payment system gained momentum in the US in 2010 with the passage of the Affordable Care Act and continues to progress rapidly. Market research estimates that value-based payment models will surpass fee-for-service by 2020. This change offers both great opportunity and great risk to the medical care of the heterogeneous populations of children with chronic respiratory disease. The fee-for-service model has driven the emergence of a healthcare delivery infrastructure markedly misaligned with the medical needs of children with chronic respiratory disease. A change to value-based payment models offers the opportunity to create systems better aligned with the complex and varied care needs of these children. However, rapid change without input from the relevant stakeholders could yield an infrastructure even more misaligned with the needs of children with chronic respiratory disease than the current one and threaten access to high quality medical care for these populations. Through the lens offered by three fictional case studies, this review: (1) illustrates current and evolving payment models; (2) describes limitations of these payment models; and (3) suggests a novel way to envision and evaluate value-based payment models for children with chronic respiratory disease.

A role for macrophage migration inhibitory factor in the neonatal respiratory distress syndrome.

Using a mouse model of neonatal respiratory distress syndrome (RDS), we demonstrate a central role for macrophage migration inhibitory factor (MIF) in lung maturation at the developmental stage when human neonates are most susceptible to RDS. We prematurely delivered mouse pups at embryonic day 18, during the early saccular stage of pulmonary development. Only 8% of the prematurely delivered pups genetically deficient in MIF survived 8 h vs 75% of wild-type controls (p<0.001). This phenotype was corrected when pups of all genotypes were bred from dams heterozygote for MIF deficiency. Local production of MIF in the lung increased at embryonic day 18, continued until full-term at embryonic day 19.5, and decreased in adulthood, thus coinciding with this developmental window. The lungs of pups genetically deficient in MIF were less mature upon histological evaluation, and demonstrated lower levels of vascular endothelial growth factor and corticosterone--two factors that promote fetal lung maturation. In vitro studies support a role for MIF in surfactant production by pulmonary epithelial cells. In a cohort of human neonates with RDS, higher intrapulmonary MIF levels were associated with a lower likelihood of developing bronchopulmonary dysplasia, a sequelae of RDS (p<0.03). This study demonstrates for the first time a role for MIF in lung maturation, and supports a protective role for MIF in newborn lung disease.