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[Physiopathology of pre-eclampsia: the role of immunology]
D Vinatier1, J F Prolongeau, P Dufour
1Maternité du Pavillon Olivier, Centre Hospitalier Universitaire de Lille.
Preeclampsia complicating 3% of all births is an important cause of maternal death and is associated with an increased risks of neonatal morbidity and mortality. Among the numerous theories proposed to explain this syndrome, the concept of placental ischaemia resulting in a generalized disturbance of endothelial physiology is receiving increasing support. Maternal immunological systems is often solicited during normal pregnancy. Most likely the immunological system is implicated in preeclampsia. Its responsibility is protean. Trophoblastic antigens may not be properly recognized by maternal immunologic system, resulting in a defect of trophoblastic invasion of the myometrial segment of the spiral arteries. Preeclampsia does not seem to be accompanied with trophoblast immunological rejection by the mother. Some cases of preeclampsia are associated with autoimmune phenomena. The autoantibodies could be directed against phospholipids or/and trophoblastic membrane components. Activated neutrophils release a variety of substances, capable of mediating vascular damage. An imbalance between the protective antioxidant activity and aggressive oxidant mechanisms could initiate the endothelial lesions. Preeclampsia could be one presentation of immunodystrophism with local excess of harmful cytokines. The immunologic system is probably not the initiator of preeclampsia, but its role is ambiguous: either the protective immunologic mechanisms usually operating during pregnancy can be surpassed, or immunologic responses are inadequate and directly aggressive. A better understanding of the underlying immunologic anomalies will improve the nosologic classification of preeclampsia syndrome.
Preeclampsia complicating 3% of all births is an important cause of maternal death and is associated with an increased risks of neonatal morbidity and mortality. Among the numerous theories proposed to explain this syndrome, the concept of placental ischaemia resulting in a generalized disturbance of endothelial physiology is receiving increasing support. Maternal immunological systems is often solicited during normal pregnancy. Most likely the immunological system is implicated in preeclampsia. Its responsibility is protean. Trophoblastic antigens may not be properly recognized by maternal immunologic system, resulting in a defect of trophoblastic invasion of the myometrial segment of the spiral arteries. Preeclampsia does not seem to be accompanied with trophoblast immunological rejection by the mother. Some cases of preeclampsia are associated with autoimmune phenomena. The autoantibodies could be directed against phospholipids or/and trophoblastic membrane components. Activated neutrophils release a variety of substances, capable of mediating vascular damage. An imbalance between the protective antioxidant activity and aggressive oxidant mechanisms could initiate the endothelial lesions. Preeclampsia could be one presentation of immunodystrophism with local excess of harmful cytokines. The immunologic system is probably not the initiator of preeclampsia, but its role is ambiguous: either the protective immunologic mechanisms usually operating during pregnancy can be surpassed, or immunologic responses are inadequate and directly aggressive. A better understanding of the underlying immunologic anomalies will improve the nosologic classification of preeclampsia syndrome.