9%, 84.8%, 81.7%, and 68.5%, respectively, for the no treatment, medical therapy only, surgical treatment only, and medical plus surgical therapy groups. Recurrent fracture-free rates were significantly different for patients who received surgical or medical or surgical plus medical therapy (P = .0007), with patients in the medical
plus surgical group having the shortest time to refracture, although these patients may have been sicker and more frail than the other groups.
Conclusion: We found that surgical treatment with vertebroplasty or kyphoplasty did not decrease recurrent vertebral fractures in patients presenting with an initial vertebral fracture. Medical and surgical therapies together may shorten the time to refracture, but the observed elevated risk may be due to other confounding factors. We found no difference in survival in patients undergoing MLN2238 solubility dmso kyphoplasty or vertebroplasty PX-478 Angiogenesis inhibitor in comparison with medical or no treatment groups. The relationship between surgical and medical therapy and vertebral refracture rates should be further evaluated with use of a prospective cohort design. (Endocr Pract. 2012;18:499-507)”
“The obesity epidemic, including a marked increase in the prevalence of obesity among pregnant women, represents a critical public health problem in the United States
and throughout the world. Over the past two decades, it has been increasingly recognized that the risk of adult health disorders, XMU-MP-1 particularly metabolic syndrome, can be markedly influenced by prenatal and infant environmental exposures (ie, developmental programming). Low birth weight, together with infant catch-up growth, is associated with a significant risk of adult obesity and cardiovascular disease, as well as adverse effects on pulmonary, renal, and cerebral function. Conversely, exposure to maternal obesity or high birth weight also represents an increased risk for childhood and adult obesity. In addition, fetal exposure to select chemicals (eg, phytoestrogens) or environmental pollutants (eg, tobacco smoke) may
affect the predisposition to adult disease. Animal models have confirmed human epidemiologic findings and provided insight into putative programming mechanisms, including altered organ development, cellular signaling responses, and epigenetic modifications (ie, control of gene expression without modification of DNA sequence). Prenatal care is transitioning to incorporate goals of optimizing maternal, fetal, and neonatal health to prevent or reduce adult-onset diseases. Guidelines regarding optimal pregnancy nutrition and weight gain, management of low-and high-fetal-weight pregnancies, use of maternal glucocorticoids, and newborn feeding strategies, among others, have yet to fully integrate long-term consequences on adult health. (Obstet Gynecol 2011;117:978-85) DOI: 10.1097/AOG.
No related posts.