MULTIFACTORIAL INTERACTIONS IN THE ETIOPATHOGENESIS OF EPH-GESTOSIS -A HYPOTHESIS

The aetiopathogenesis of EPH-Gestosis or pre-eclampsia-eclampsia is st ill not clear. Although many hypotheses implicating environmental, nut ritional, immunological, and genetic factors have been put forward, no hypothesis provides the scientific basis for the early spiral arteria l degenerative changes, and incomplete physiological trophoblastic inv asion of the spiral arteries, leading to a high utero-placental resist ance with reduced blood flow remains unexplained. To get an insight in to the basic pathogenesis of EPH-Gestosis, the following hypothesis ha s been proposed. The hypothesis considers an abnormal proliferation of the spiral vessels as the key factor in the pathogenesis of the high uteroplacental resistance and the endothelial dysfunctions in EPH-Gest osis. Further it is proposed that this proliferation is on account of the enhanced polymerization of the deficient DNA triggered by the high steroidal level and relatively low micronutrient level in EPH-Gestosi s during the early formative stages of the placental circulation. Ster oidal hormone helps in polymerization of the DNA, micronutrients exert a controlling influence through DNA synthesis on cell proliferation. A critical balance of hormone-micronutrients such as vitamin A, B-12, folic acid, etc., therefore, seems necessary for normal cellular proli feration. It appears therefore that there probably exists an imbalance with a high estrogen and a relatively low micro-nutrient level in EPH -Gestosis, triggering off a process of abnormal spiral vessel prolifer ation. These abnormal vessels with a deranged endothelial function may prevent the second wave of normal trophoblastic invasion assumed to b e important for the establishment of the low resistance uteroplacental circulation. They may also start off a chain of altered interaction w ith the trophoblasts leading to a condition of EPH-Gestosis, character ized by endothelial dysfunction and high uteroplacental resistance and reduced flow. Since it is known that hypobaric-hypoxic condition incr eases blood circulation probably by opening up collateral channels, it is suggested that in case of EPH-Gestosis too, a controlled hypobaric hypoxic exposure may increase uteroplacental flow to reduce the onset of the adverse consequences of EPH-Gestosis.