Genetic contributors to preeclampsia found

Certain genetic errors appear to increase a pregnant woman’s risk for developing preeclampsia, according to a new study published in PloS Medicine (2011;8[3]:e1001013). Identification of the errors could point to new ways to recognize and treat women at risk, the authors say.

Researchers from the Washington University School of Medicine, St. Louis, Missouri, analyzed DNA from more than 300 pregnant women: 250 with systemic lupus erythmatosis (SLE) or antiphospholipid antibodies (APL Ab)-which are linked to increased risk for preeclampsia (40 of these women later developed the condition)-and 40 otherwise healthy women who were hospitalized with severe preeclampsia. DNA analysis revealed genetic errors shared by 7 of the 40 women with autoimmune disease who developed preeclampsia and 5 of the controls.

The genes on which the errors were identified encode 3 complement regulatory proteins-membrane cofactor protein, complement factor I, and complement factor H-that play a role in regulating immune response. “The presence of risk variants in complement regulatory proteins in patients with SLE and/or APL Ab who develop preeclampsia, as well as in preeclampsia patients lacking autoimmune disease, links complement activation to disease pathogenesis,” the authors write.

Many cases of preeclampsia are thought to arise from immune dysfunction because of the increased risk for the disorder in women with SLE and APL Ab. The researchers suggest that faulty regulation of the complement system causes excessive complement activation, which damages the placenta and leads to abnormal placental development and a series of events culminating in clinical preeclampsia.