title: Hypertension and maternal-fetal conflict during placental malaria.
abstract: BACKGROUND
  Malaria and hypertension are major causes of maternal mortality in tropical countries, especially during first pregnancies, but evidence for a relationship between these syndromes is contradictory.
  
  
  RESULTS
  In a cross-sectional survey of Tanzanian parturients, the rate of hypertension was similar in placental malaria (PM)-positive (11/85 = 13%) and PM-negative (73/602 = 12%) individuals. However, we found that PM was associated with hypertension in first-time mothers aged 18-20 y but not other mothers. Hypertension was also associated with histologic features of chronic malaria, which is common in first-time mothers. Levels of soluble vascular endothelial growth factor receptor 1 (sVEGFR1), a preeclampsia biomarker, were elevated in first-time mothers with either PM, hypertension, or both, but levels were not elevated in other mothers with these conditions. In first-time mothers with PM, the inflammatory mediator vascular endothelial growth factor (VEGF) was localized to maternal macrophages in the placenta, while sVEGFR1, its soluble inhibitor, was localized to the fetal trophoblast.
  
  
  CONCLUSIONS
  The data suggest that maternal-fetal conflict involving the VEGF pathway occurs during PM, and that sVEGFR1 may be involved in the relationship between chronic PM and hypertension in first-time mothers. Because placental inflammation causes poor fetal outcomes, we hypothesize that fetal mechanisms that promote sVEGFR1 expression may be under selective pressure during first pregnancies in malaria-endemic areas.
authors.affiliation: MOMS Project, Seattle Biomedical Research Institute, Seattle, Washington, United States of America.
authors.forename: Atis
authors.initials: A
authors.lastname: Muehlenbachs
authors.forename: Theonest K
authors.initials: TK
authors.lastname: Mutabingwa
authors.forename: Sally
authors.initials: S
authors.lastname: Edmonds
authors.forename: Michal
authors.initials: M
authors.lastname: Fried
authors.forename: Patrick E
authors.initials: PE
authors.lastname: Duffy
mesh_terms: D000328:Adult; D003430:Cross-Sectional Studies; D005260:Female; D005333:Fetus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications*; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008288:Malaria / Q000097:blood / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D010298:Parity; D010920:Placenta / Q000378:metabolism / Q000473:pathology; D010922:Placenta Diseases / Q000097:blood / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000097:blood; D015597:Pregnancy Complications, Parasitic / Q000097:blood / Q000378:metabolism / Q000473:pathology; D014327:Trophoblasts / Q000378:metabolism / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood
chemical_list: D042461:Vascular Endothelial Growth Factor A; D040281:Vascular Endothelial Growth Factor Receptor-1