Abruptio placentae in the setting of an atypical presentation of acute appendicitis: a case report.

BACKGROUND: Causes of placental abruption include traumatic events, cocaine use, hypertension, cigarette smoking and advanced maternal age. Recent studies also implicate inflammatory precursors, such as preterm premature rupture of membranes and chorioamnionitis. Clear precipitating events are often not identified, and precise etiologic determinants are still being determined. CASE: A 25-year-old woman, grayida 4, para 2012, presented with acute onset of severe abdominal pain; frequent, low-amplitude contractions; and a nonreassuring fetal heart tracing. While performing an urgent cesarean section for acute placental abruption, a ruptured appendicitis was identified. CONCLUSION: This case suggests that appendicitis in the third trimester may be a risk factor for placental abruption.

The activity of PPAR gamma in primary human trophoblasts is enhanced by oxidized lipids.

The ligand-dependent nuclear receptor PPAR gamma plays an important role in murine and human trophoblast differentiation. Oxidized lipids, which are implicated in the pathophysiology of placental dysfunction, have recently been identified as ligands for PPAR gamma. We therefore hypothesized that oxidized lipids activate PPAR gamma in human trophoblasts and influence placental function. To test our hypothesis, we examined the effect of 9S-hydroxy-10E,12Z-octadecadienoic acid (9-HODE), 13S-hydroxy-9Z,11E-octadecadienoic acid (13-HODE), and 15S-hydroxy-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-HETE) on PPAR gamma activity in cultured term human trophoblasts. Our results demonstrate that these lipids stimulate PPAR gamma activity and that the AF-2 fragment, which harbors the ligand-binding domain of PPAR gamma, mediates this effect. Furthermore, we assessed the consequences of PPAR gamma activation by the oxidized lipids, and we found that these lipids stimulate human CG production, a measure of trophoblast differentiation. In contrast, the expression of syncytin, a marker for syncytium formation as well as the expression of the cell cycle modulators cyclin E and p27 are unchanged by the oxidized lipids. We concluded that 9-HODE, 13-HODE, and 15-HETE activate PPAR gamma in primary human trophoblasts. These PPAR gamma ligands may play a role in placental differentiation, yet they are unlikely to contribute to trophoblast dysfunction.