Mirroring preeclampsia: the molecular basis of Ballantyne syndrome.

The purpose of this article was to further elucidate the pathophysiology of Mirror (Ballantyne) syndrome within the context of known biomarkers for preeclampsia. This novel insight from clinical practice involved a case of post-twin-to-twin transfusion syndrome-laser hydrops in an ex-donor twin, corroborated by histopathologic placental territory edema and maternal sequelae of Mirror syndrome. We serially measured the levels of activin A, follistatin, endothelin-1 (ET-1), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), soluble fms-like tyrosine kinase 1 (sFlt), and von Willebrand factor (vWF) in the maternal serum from disease evolution through to recovery. The paired finding of hydropic ex-donor twin and placenta, supports the theory of placental injury as the source of potential molecular mediators, leading to local placental edema, associated fetal hydrops and the maternal preeclamptic picture. Notably, we elucidated a temporal spectrum of maternal serum mediators (soluble Flt-1, endothelin-1, 8-isoprostane, activin-A, ICAM-1, and vWF) involved in the pathogenesis of Mirror syndrome. Better understanding of the pathogenesis of Mirror syndrome has important implications for clinical management.