RESUMEN
Studies suggest that preeclampsia (PE) originates in the placenta and is associated with deficient trophoblast invasion of spiral arteries. The direct cause remains unknown, but preeclampsia is often associated with circulating factors that can induce generalized endothelial dysfunction. Antiphospholipid antibodies (APA) in circulation are also associated with vascular diseases. Although the quantification of APA is not currently used as a prognostic of the risk of PE, studies suggest that thrombophilias play a role in PE pathogenesis. In fact, the pathology of placentae from PE and Antiphospholipid syndrome patients is similar; atherosis, thrombosis and infarction, and endothelium activation represent the pathological mechanisms. We identified a new antibody which recognizes non-bilayer phospholipid arrangements (NPA) in membrane models and in cell membranes in vivo, and which triggered an autoimmune-like disease in mice. We evaluated the presence of NPA in the placentae and in sera, and whether NPA induced NPA antibodies in patients with hypertensive disorders of pregnancy (HDP). Results showed increased levels of NPA in the syncytiotrophoblast, extravillous cytotrophoblast, syncytial knots and the amnion epithelial cell membranes of the placenta, as well as increases in NPA and NPA antibodies in sera from HDP patients, when compared with controls. This suggests that NPA derived from placenta could be one of multiple factors associated with pregnancy pathologies.
Asunto(s)
Anticuerpos Antifosfolípidos/análisis , Lípidos de la Membrana/análisis , Fosfolípidos/análisis , Placenta/química , Preeclampsia/etiología , Anticuerpos Antifosfolípidos/sangre , Femenino , Retardo del Crecimiento Fetal/etiología , Humanos , Lípidos de la Membrana/sangre , Fosfolípidos/sangre , EmbarazoRESUMEN
The purpose of this study was to evaluate the accuracy of clinical diagnosis of acute pelvic inflammatory disease (PID). Data were obtained on 176 consecutive women admitted to St. Elizabeth Hospital Medical Center with a clinical diagnosis of PID. All underwent diagnostic laparoscopy. PID was established laparoscopically in 134 (76.1%) of the patients. Statistical tests for significant associations between PID and each of 21 clinical indicators of the disease were conducted using the chi 2 and Mann-Whitney tests. Stepwise logistic regression was performed on those variables whose univariate tests of significant association with PID resulted in P values < 0.20. An optimal set of PID indicators consisted of adnexal tenderness, lower abdominal pain of < one week's duration and an elevated white blood cell count. Use of these indicators resulted in a test with an estimated sensitivity and specificity of 86.6% and 45.7%, respectively. Estimated predictive values for positive and negative test results were 0.84 and 0.52, respectively. These results confirm the fact that laparoscopy is the definitive diagnostic modality in PID.