Sebastian Rupert Hobson1,2,3, Euan Morrison Wallace1,3, Yuen Fu Chan4, Andrew Grant Edwards1,2, Mark Wui Tee Teoh1,2, Andrea Phaik-Leng Khaw5. 1. a Department of Obstetrics and Gynaecology , Monash University , Melbourne , Australia. 2. b Women'S Health Program , Monash Health , Melbourne , Australia. 3. c Ritchie Centre, Hudson Institute of Medical Research , Monash University , Melbourne , Australia. 4. d Department of Anatomical Pathology , Monash Health , Melbourne , Australia. 5. e Perinatal Research Centre , The Royal Women's Hospital , Melbourne , Australia.
Abstract
OBJECTIVES: The purpose of this article was to further elucidate the pathophysiology of Mirror (Ballantyne) syndrome within the context of known biomarkers for preeclampsia. METHODS: 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. RESULTS: 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. CONCLUSION: Better understanding of the pathogenesis of Mirror syndrome has important implications for clinical management.
OBJECTIVES: The purpose of this article was to further elucidate the pathophysiology of Mirror (Ballantyne) syndrome within the context of known biomarkers for preeclampsia. METHODS: 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. RESULTS: 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. CONCLUSION: Better understanding of the pathogenesis of Mirror syndrome has important implications for clinical management.
Authors: Jesús Arnulfo Velásquez-Penagos; Ana María Flórez-Ríos; Edison Muñoz-Ortiz; Jairo Alfonso Gándara-Ricardo; Juan Pablo Flórez-Muñoz; Erika Holguín-González Journal: Rev Colomb Obstet Ginecol Date: 2021-09-30