Genetics

Numerous studies suggest a genetic susceptibility to pre-eclampsia. The genetic defect may result from dysfunction of the normal maternal immunological adaptation to the presence of a foreign antigenic load (the fetus) during pregnancy. Insufficient maternal production of 'blocking antibodies' or the production of autoantibodies may initiate abnormal placentation. The incidence of pre-eclampsia is five times higher in blood relatives of women affected by eclampsia than in a control population of their non-blood relatives. Two kinds of genetic models have been suggested: a simple recessive model with genes acting in the mother, or a dominant model with

50 per cent penetrance. The recessive model appears to fit best but is questioned by the reported lack of concordance in monozygous twins. Further evidence of a genetic basis in pre-eclampsia is suggested by the following observations:

1. pre-eclampsia is more common with hydatidiform moles, where chromosomes are paternally derived;

2. multiparous women with no previous history of pre-eclampsia may develop the condition when pregnant to a new partner;

3. the incidence of eclampsia is higher in women born of eclamptic pregnancies than in their sisters born of non-eclamptic pregnancies;

4. there are ethnic differences in the incidence of pre-eclampsia;

5. pre-eclampsia is associated with some HLA types;

6. Caucasian and Japanese women with the T235 molecular variant of the estrogen-related angiotensinogen gene have a higher incidence of pre-eclampsia. Abnormal trophoblast invasion and placental pathology

The placenta is central to the pathogenesis of pre-eclampsia. The disease occurs in the absence of a fetus in molar pregnancy. Its incidence correlates with placental mass, being higher in twin pregnancy, molar pregnancy, and hydrops fetalis. The condition is cured by placental removal. Reduced uteroplacental perfusion has been demonstrated using radio-isotope and Doppler techniques. Ultrastructural studies of biopsy specimens from the placental bed have shown that, during normal placental development, endovascular trophoblast invades the decidual portion of the spiral artery at about 4 to 6 weeks of pregnancy and migrates along the lumen of the vessel wall, reaching the deciduomyometrial junction at 8 weeks. By 15 to 18 weeks, endovascular trophoblast can be found in the deeper parts of the myometrial segments of the spiral arteries. During this wave of migration, trophoblast penetrates the endothelium and replaces the intima and media by a fibrinoid material. The destruction of the tunica media results in distension of the spiral artery.

There is evidence that in pre-eclampsia, endovascular trophoblast migration and invasion is limited to the decidual segments of the spiral arteries ( Pinenb.org et..ML

1991). Absence of physiological invasion of the myometrial segments results in their remaining muscular, undilated, and responsive to vasomotor influences. This failure to convert the placental vasculature into a high-volume low-resistance system at least partially accounts for the decreased uteroplacental blood flow in pre-eclampsia. An additional lesion seen in some cases of pre-eclampsia is 'acute atherosis' in which there is fatty change in intimal cells, necrosis of the vessel wall, and luminal occlusion by aggregates of fibrin, platelets, and lipid-laden macrophages. This lesion may also contribute to reduced uteroplacental blood flow.

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