| Autor: |
Baptista LC; 1 Center for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas - UNICAMP, Campinas, SP 13083-875, Brazil.; Shared first and last authorship., Figueira CO; 2 Department of Obstetrics and Gynecology, University of Campinas - UNICAMP, Campinas, SP 13083-880, Brazil.; Shared first and last authorship., Souza BB; 1 Center for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas - UNICAMP, Campinas, SP 13083-875, Brazil., Fertrin KY; 3 Division of Hematology, University of Washington, Seattle, WA 98195-7230, USA., Antolini A; 4 Department of Pathology, University of Campinas - UNICAMP, Campinas, SP 13083-887, Brazil., Costa FF; 5 Hematology and Hemotherapy Center, University of Campinas - UNICAMP, Campinas, SP 13083-878., de Melo MB; 1 Center for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas - UNICAMP, Campinas, SP 13083-875, Brazil.; Shared first and last authorship., Costa ML; 2 Department of Obstetrics and Gynecology, University of Campinas - UNICAMP, Campinas, SP 13083-880, Brazil.; Shared first and last authorship. |
| Abstrakt: |
Impact Statement: Environmentally induced changes in placental morphological and molecular phenotypes may provide relevant insight towards pathophysiology of diseases. The rare opportunity to evaluate the same patient, with sickle cell anemia (SCA), in two different pregnancies, of opposite outcomes (one early onset severe preeclampsia (PE) and the other mostly non-complicated) can prove such concept. In addition, the comparison to other conditions of known placental and vascular/inflammatory involvement strengthens such findings. Our results suggest that the clinical association between SCA and PE can be supported by common pathophysiological mechanisms, but that pathways involving response to copper and triglyceride metabolism may be important drivers of the pathophysiology of PE. Future studies using in a larger number of samples should confirm these findings and explore pathways involved in the pathophysiology of PE and its relationship with SCA. |
