The twostage model of preeclampsia Figure

The two-stage model of pre-eclampsia, originally proposed more than a decade ago (Redman, 1991) and described elsewhere in this volume, envisages that pre-eclampsia arises in various ways including from placental ischemia secondary to deficient placentation. Whereas some consider abnormal placentation to be the start and invariable cause of pre-eclampsia, it is much more likely that it is a completely separate but predisposing condition (Redman and Sargent, 2000). Placentation is described elsewhere in this volume and may be abnormally shallow in pre-eclampsia, such that the spiral arteries are maladapted and unable to meet the perfusion needs of the second and third trimester fetoplacental unit. The mechanisms, which involve invasion of the placental bed by extravillous cytotrophoblasts and their close association with large granular lymphocytes in the decidua, remain to be defined. It is a local process, without evidence that systemic inflammatory

Preeclampsia Stages

Figure 7.2 The two possible stages of evolution of pre-eclampsia with different contributions from the maternal immune system in each stage. Other types of pre-eclampsia that do not depend on poor placentation but excessively large placentas or increased maternal susceptibility to the inflammatory stresses of an otherwise normal pregnancy (Redman and Sargent, 2000) will not depend on the first stage as depicted here.

Figure 7.2 The two possible stages of evolution of pre-eclampsia with different contributions from the maternal immune system in each stage. Other types of pre-eclampsia that do not depend on poor placentation but excessively large placentas or increased maternal susceptibility to the inflammatory stresses of an otherwise normal pregnancy (Redman and Sargent, 2000) will not depend on the first stage as depicted here.

responses are involved. There are, however, important data, described in chapter 6, which suggest that maternal immune recognition of trophoblast in the decidua may control placentation and, if deficient, cause poor placentation. The proposal is for a novel form of immune recognition, of paternally expressed genes on trophoblast by decidual natural killer cells. If such immune mechanisms operate they could explain particular features of pre-eclampsia, such as its first pregnancy preponderance and apparent partner specificity (Li and Wi, 2000; Lie et al., 1998).

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