Preterm deliveries that result from multiple pregnancies associated with assisted reproductive technologies in the USA: a cost analysis.

PURPOSE OF REVIEW: Simultaneous transfer of multiple embryos in an assisted reproductive technology (ART) cycle results in a high rate of multiple pregnancy. Besides the medical complications associated with multiple pregnancy, the financial burden of the resultant preterm infants is also substantial. The current review evaluates the costs associated with the care of preterm infants that are born as a result of ART-associated multiple pregnancies. RECENT FINDINGS: In 2006, 30% of all ART live births were multiple infant deliveries in the USA. This resulted in 48% of all ART neonates being the product of a multiple infant delivery. In the same year, 62% of ART twins and 97% of ART triplets were delivered preterm, corresponding to approximately 17 000 infants. The Board of Health Sciences Policy has estimated the mean cost of each preterm infant to be US$ 51 600. Therefore, the financial burden of ART-associated preterm deliveries is estimated to be approximately US$ 1 billion annually. This figure has remained essentially unchanged between 2001 and 2006, despite decreasing number of embryos transferred, due to increasing total number of ART cycles performed. SUMMARY: Preterm deliveries that result from ART-associated multiple pregnancies add a substantial burden to overall US healthcare expenditure annually. Policies limiting the number of embryos transferred should be considered with a perspective to increase elective single embryo transfers.

A1 adenosine receptors mediate hypoxia-induced ventriculomegaly.

Periventricular leukomalacia is characterized by a reduction in brain matter and secondary ventriculomegaly and is a major cause of developmental delay and cerebral palsy in prematurely born infants. Currently, our understanding of the pathogenesis of this condition is limited. In animal models, features of periventricular leukomalacia can be induced by hypoxia and activation of A1 adenosine receptors (A1ARs). Using mice that are deficient in the A1AR gene (A1AR-/-), we show that A1ARs play a prominent role in the development of hypoxia-induced ventriculomegaly in neonates. Supporting a role for adenosine in the pathogenesis of developmental brain injury, ventriculomegaly was also observed in mice lacking the enzyme adenosine deaminase, which degrades adenosine. Thus, adenosine acting on A1ARs appears to mediate hypoxia-induced brain injury ventriculomegaly during early postnatal development.

Estradiol suppresses vascular monocyte chemotactic protein-1 expression during early atherogenesis.

OBJECTIVE: This study was undertaken to determine whether estrogen down-regulates vascular monocyte chemotactic protein-1 expression during the development of atherosclerosis in vivo and to identify the cellular localization of monocyte chemotactic protein-1 expression under baseline conditions and in response to atherogenic stimuli. STUDY DESIGN: Female, homozygous low-density lipoprotein-receptor-deficient mice (n = 68) in a C57BL/6 background underwent ovariectomy, were implanted subcutaneously with 17beta-estradiol or placebo pellets, and were changed to a high cholesterol (1.25%) diet. Thereafter, four mice from each group were killed weekly for 8 weeks, and their aortae were frozen for immunohistochemical analysis. The lipid deposition was identified by Sudan black B staining. Monocyte chemotactic protein-1 expression was detected with a rabbit anti-mice monocyte chemotactic protein-1 antibody, and semiquantitative analysis was performed. RESULTS: Consistent with previous reports, estradiol resulted in diminished vascular lipid deposition (22% +/- 7% vs 15% +/- 6% at 8 weeks of gestation, P <.05). We found that the inhibition of lipid deposition in aortae of animals that were treated with estrogen is associated with a concomitant down-regulation of monocyte chemotactic protein-1 immunoreactivity in aortic endothelial and smooth muscle cells (P <.05). Serum total cholesterol concentrations did not differ between the two treatment groups, which suggests a direct effect of estradiol on the aorta. CONCLUSION: Our findings suggest that one of the mechanisms by which estrogen down-regulates atherogenesis is by the suppression of vascular monocyte chemotactic protein-1 expression, which leads to decreased macrophage recruitment to the arterial wall early in the process.