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[Pre-eclampsia. Etiology--physiopathology--treatment]
1Arhus Kommunehospital, gynaekologisk obstetrisk afdeling Y.
Recent observations indicate that pre-eclampsia is a disease, which occurs because of a partially defective maternal immune response against the fetal (paternal) antigen expressed on trophoblast tissue. The resulting defective or insufficient placentation can cause ischaemic changes, which seem to act in a harmful way on the vascular endothelium, initially locally in the utero-placental circulation, but later with universal systemic effects. The resulting endothelial dysfunction and concommitant thrombocyte activation seems to account for an important part of the pathophysiology of pre-eclampsia. Hypertension is presumably a secondary phenomenon. The definitive treatment of pre-eclampsia is delivery, which is always indicated in cases of severe pre-eclampsia after 32 weeks of pregnancy. In milder cases and before 32 weeks it is reasonable to await delivery, if necessary starting anti-hypertensive treatment. Treatment of hypertension has to balance the risks of maternal cerebral complications against the risks of reduced utero-placental bloodflow with resulting intra-uterine growth retardation. Low-dose acetylsalicylic acid treatment could in theory constitute a prophylactic principle, but the results of new, large, well-conducted, randomised trials advise against using such treatment prophylacctically at present. The effect of fish-oil supplements is not yet clarified, whereas mineral supplements such as calcium and magnesium are unlikely to have prophylactic effects on the development of pre-eclampsia, at least not in western industrialized society.
Recent observations indicate that pre-eclampsia is a disease, which occurs because of a partially defective maternal immune response against the fetal (paternal) antigen expressed on trophoblast tissue. The resulting defective or insufficient placentation can cause ischaemic changes, which seem to act in a harmful way on the vascular endothelium, initially locally in the utero-placental circulation, but later with universal systemic effects. The resulting endothelial dysfunction and concommitant thrombocyte activation seems to account for an important part of the pathophysiology of pre-eclampsia. Hypertension is presumably a secondary phenomenon. The definitive treatment of pre-eclampsia is delivery, which is always indicated in cases of severe pre-eclampsia after 32 weeks of pregnancy. In milder cases and before 32 weeks it is reasonable to await delivery, if necessary starting anti-hypertensive treatment. Treatment of hypertension has to balance the risks of maternal cerebral complications against the risks of reduced utero-placental bloodflow with resulting intra-uterine growth retardation. Low-dose acetylsalicylic acid treatment could in theory constitute a prophylactic principle, but the results of new, large, well-conducted, randomised trials advise against using such treatment prophylacctically at present. The effect of fish-oil supplements is not yet clarified, whereas mineral supplements such as calcium and magnesium are unlikely to have prophylactic effects on the development of pre-eclampsia, at least not in western industrialized society.