Multifactorial interactions in the aetiopathogenesis of EPH-Gestosis--a hypothesis.
The aetiopathogenesis of EPH-Gestosis or pre-eclampsia-eclampsia is still not clear. Although many hypotheses implicating environmental, nutritional, immunological, and genetic factors have been put forward, no hypothesis provides the scientific basis for the early spiral arterial degenerative changes, and incomplete physiological trophoblastic invasion of the spiral arteries, leading to a high utero-placental resistance with reduced blood flow remains unexplained. To get an insight into the basic pathogenesis of EPH-Gestosis, the following hypothesis has 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-Gestosis. 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-Gestosis during the early formative stages of the placental circulation. Steroidal 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, B12, folic acid, etc., therefore, seems necessary for normal cellular proliferation. 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 proliferation. These abnormal vessels with a deranged endothelial function may prevent the second wave of normal trophoblastic invasion assumed to be important for the establishment of the low resistance uteroplacental circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Sengupta
A
A
Centre for Biomedical Engineering, Indian Institute of Technology, New Delhi.
Guha
S K
SK
D000818:Animals; D005260:Female; D006801:Humans; D008954:Models, Biological; D011225:Pre-Eclampsia / Q000209:etiology* / Q000378:metabolism; D011247:Pregnancy