Uterine rupture: what family physicians need to know.

Vaginal birth after cesarean section is common in this country. Physicians providing obstetric care should be aware of the potential complications. Uterine rupture occurs in approximately one of every 67 to 500 women (with one prior low-transverse incision) undergoing a trial of labor for vaginal birth after cesarean section. Rupture poses serious risks to mother and infant. There are no reliable predictors or unequivocal clinical manifestations of rupture, so physicians must maintain a high index of suspicion for possible rupture, especially in the presence of fetal bradycardia or other evidence of fetal distress. Management is surgery for prompt delivery of the infant and control of maternal hemorrhage. Newborns often require admission to an intensive care nursery. Prevention of poor outcomes depends on thorough anticipation and preparation. The physicians and the delivery institution should be prepared to provide emergency surgical and neonatal care in the event of uterine rupture.

Regulation of eosinophil-active cytokine production from human cord blood-derived mast cells.

Human mast cells are multifunctional tissue-dwelling cells that play a crucial role in eosinophil-dependent disorders, such as asthma and parasitic diseases, by the secretion of eosinophil-active mediators. Mast cell-derived cytokines, generated in response to cross-linking of the high-affinity IgE receptor, can regulate eosinophil activation, survival, and chemotaxis. In this study, mast cells generated from human cord blood progenitors (stem cells) were studied for eosinophil-active inflammatory cytokine expression. Cord blood-derived mast cells (CBDMC) expressed typical intracellular scroll granules and microvilli-like structures on their cell surfaces, demonstrated the presence of tryptase, and elaborated prostaglandin D2 (PGD2) after cross-linkage of the high-affinity receptor for IgE (FcepsilonRI). CBDMC expressed tumor necrosis factor-alpha (TNF-alpha) and the eosinophil-active growth factors, interleukin-5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF) after activation. (IL-1beta greatly enhanced IgE-dependent production of these cytokines in response to FcepsilonRI cross-linkage, suggesting a role for bystander/phagocytic cells in modulating mast cell function. In contrast, interferon-alpha (IFN-alpha) inhibited IL-5 and GM-CSF generation, and the glucocorticoid, dexamethasone (Dex), inhibited production of IL-5 and GM-CSF from CBDMC. A macrophage-mast cell-eosinophil axis may exist in vivo that may be susceptible to pharmacologic manipulation.