Epidural analgesia complicated by dural ectasia in the Marfan syndrome.

Patients with the Marfan syndrome are considered to be high risk during pregnancy and warrant a complete multidisciplinary evaluation. One goal is to minimize hemodynamic fluctuations during labor since hypertensive episodes may result in aortic dissection or rupture. Although they may prevent these complications, neuraxial techniques may be complicated by dural ectasia. The case of a parturient with the Marfan syndrome and mild dural ectasia is presented. During attempted labor epidural placement, unintentional dural puncture occurred. A spinal catheter was used for adequate labor analgesia, and a resultant postdural puncture headache was alleviated by an epidural blood patch under fluoroscopic guidance.

A p38 mitogen-activated protein kinase inhibitor attenuates cardiotonic steroids-induced apoptotic and stress signaling in a Sw-71 cytotrophoblast cell line.

INTRODUCTION: Preeclampsia (preE) is characterized by abnormal placentation. Marinobufagenin (MBG), a cardiotonic steroid (CTS), inhibits the function of cytotrophoblast cells (CTBs). We demonstrated that CTSs induce anti-angiogenic and anti-proliferative effects in Sw-71 CTBs. This study tests that CTSs induce apoptotic and stress signaling. METHODS: Human extravillous Sw-71 CTBs were incubated with 0, 0.1, 1, 10, and 100 nM of each of three CTSs (MBG, cinobufatalin (CINO) and ouabain (OUB)) for 48 h. Some cells were pretreated with 10 µM p38 mitogen-activated protein kinase (p38 MAPK) inhibitor (SB203580) for 2 h prior to CTSs treatment. We analyzed p38 MAPK phosphorylation, expression of pro-inflammatory protein cyclooxygenase-2 (Cox-2) and ratio of pro-apoptotic Bcl-2-associated X protein (Bax) to anti-apoptotic Bcl-2 protein by western blot in CTSs-treated CTBs lysates. Levels of vascular endothelial growth factor (VEGF), placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng) were measured in culture media using ELISA kits. Statistical comparisons were performed using analysis of variance with Duncan's post hoc test. RESULTS: p38 MAPK phosphorylation, expression of Cox-2 and Bax/Bcl-2 was upregulated (*p < 0.05) in CTBs exposed to ≥ 0.1 nM CTSs. Secretion of sFlt-1 and sEng were increased while VEGF and PIGF were decreased in Sw-71 CTBs treated ≥1 nM of each CTSs (*p < 0.01 for each). The SB203580 pretreatment of CTBs significantly attenuated CTS-induced effects. DISCUSSION: Exposure of Sw-71 CTBs to CTSs induced apoptotic and stress signaling and causing anti-angiongenic effect. The observed diminution of CTS-induced signaling by SB203580 pretreatment implicates p38 MAPK as a regulator of these pathways.