Impact of the Antiphospholipid Syndrome on Complications during Pregnancy

Abstract

The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the appearance of antiphospholipid antibodies (APA) and at least one clinical manifestation like venous and arterial thrombosis or recurrent miscarriages and fetal loss in the second and third trimester. This most common acquired thrombophilia can also cause placental insufficiency, preeclampsia, intrauterine growth retardation, and placental abruption. Several potential pathogenic pathways leading to a procoagulant state by activation of endothelial cells, monocytes or platelets and inhibition of the protein C activation pathway have been identified. These are supposed to be responsible for thrombosis and obstetric complications. Failed trophoblast differentiation and invasiveness, with subsequently hampered uteroplacental development, as well as thrombosis in the placental vessels are further pathogenic pathways for observed complications specific for pregnancy. Tests for anticardiolipin antibodies and lupus anticoagulant are most commonly used in clinical practice although antiphospholipid antibodies are a heterogeneous group. Current criteria for the classification of APS recommend the use of standardized ELISAs that measure ß2- glycoprotein I-dependent IgG and IgM anticardiolipin antibodies and/or lupus anticoagulant. Current recommendations regarding prophylactic and therapeutic strategies in pregnancy are based on a systematic Cochrane review. Although APS is an autoimmune disease, anticoagulant therapy is the favored strategy to prevent thromboembolic events, miscarriages, or other pregnancy complications. The recommended therapy is the combination of heparin and low-dose aspirin reducing pregnancy loss by 54%. Aspirin alone, prednisone, or intravenous immunoglobulin infusion had no significant beneficial effect on pregnancy outcome, but rather a higher rate of side effects. Oral anticoagulants are contraindicated during pregnancy because of substantial embryotoxic side effects. Currently lowmolecular- weight heparin replaces unfractionated heparin as drug of choice because of safe use for mother and fetus as well as fewer side effects as several studies have shown. Our experience has taught us that prophylaxis should be initiated as soon as pregnancy has been recognized in order to prevent the described pathologies in placental development.

Gyn Update: Thrombophilie

“…4-6 h vor der erwartenden Kindsentwicklung das Fenster einer unzureichenden Antikoagulation verkleinern [8]. [17]. [17].…”

Perinatal Transfusion Medicine – Immunological Aspects

“…The most specific clinical features are thrombosis, recurrent miscarriages and fetal loss, and autoimmune thrombocytopenia. As highlighted by a review of Schleussner [2], this heterogeneous group of autoantibodies attracts growing interest and clinical significance in the treatment of recurrent pregnancy loss, placental insufficiency, preeclampsia, placental abruption, and thrombosis. Fetal/neonatal alloimmune thrombocytopenia (FNAITP) is due to transplacental transfer of maternal IgG alloantibodies which react with an alloantigen on fetal platetelets that is inherited from the father and is lacking in the mother.…”