[The significance of eicosanoids in gestosis]

Eicosanoids, especially prostaglandins and other arachidonic acid metabolites, play an important role in gestosis. Experimental and clinical evidence suggest prostacyclin deficiency, enhanced platelet reactivity and increased production of thromboxane A2 as possible reasons for gestosis. In addition, pathological interactions between cyclooxygenase-derived products and the renin-angiotensin- and kallikrein-kinin systems may exist and contribute to hypertension and reduced fetoplacental blood flow. Moreover, pregnancy-induced hypertension appears to be also related to lipoxygenase products and enhanced lipid peroxidation. In general, little is known about the regulation of arachidonic acid metabolism in gestosis. It is also unknown whether altered activities of mediators and hormones are cause or effect of pregnancy-induced hypertension. This is particularly relevant to the site of eicosanoid formation, i.e. platelets, the trophoblast or endothelial cells. At this time, it is not possible to give therapeutical recommendations, which are specifically designed to correct changes in eicosanoid production in gestosis. Antihypertensive therapy alone is insufficient, particularly with regard to the fetal situation. Preventive treatment with low-dose acetylsalicylic acid may have a protective effect against pregnancy-induced hypertension. Presently, more selective antagonists of thromboxane generation and/or action are being developed and might provide fresh insights both into the pathology of the disease and improved drug treatment.