Vascular defects in different disorders of pregnancy

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In the years immediately following the discovery of failed physiological changes in pre-eclampsia, it was assumed that this histopathological defect could be considered as pathognomonic for the disease. It was thereby thought that in other hypertensive disorders, such as essential or chronic hypertension, trophoblast invasion occurred normally, as long as no pre-eclampsia was superimposed on the pre-existing hypertension (Brosens, 1977). The finding that the physiological change of spiral arteries could also be impaired in intrauterine growth restriction without hypertension, was initially somewhat of a surprise and led to animated debates between different investigators (Brosens et al., 1977; Robertson et al., 1986; Sheppard and Bonnar, 1976, 1981). Especially the occurrence of acute atherosis, another putative pathognomonic feature, in non-hypertensive cases of intrauterine growth restriction (IUGR) was under discussion. One of the difficulties was how to distinguish true foam cells from senescent tropho-blasts with lipid changes, and in the long run this problem could only be solved after the introduction of immunohistochemical staining techniques. Later reports confirmed restricted physiological change in spiral arteries associated with non-hypertensive IUGR (Gerretsen et al., 1981; Khong et al., 1986), with occasional occurrence of acute atherosis (Hanssens et al., 1998; Khong, 1991).

An issue we always return to is the need for properly defining the patient populations under study, and particularly to distinguish the different categories of pregnancy-associated hypertension. Part of the problem is, of course, the ignorance of the real nature and underlying causes of the disease, and the uncertainty whether the hypertension-related symptoms represented only one or different diseases. Based upon a more extensive classification system (Davey and MacGillivray, 1988) a study on placental bed biopsies from a wide range of patients was performed (Pijnenborg et al., 1991). In this series, acute atherosis was indeed limited to cases of proteinuric hypertension (classical pre-eclampsia as well as pre-eclampsia superimposed on chronic hypertension), confirming previous claims. Unexpectedly, in women with chronic hypertension (without superimposed pre-eclampsia) several cases with non-invaded spiral arteries, i.e. without physiological changes, were found. Various degrees of hyperplasia of the vascular smooth muscle layer were observed in all categories of hypertensive women. Unfortunately, the group of non-proteinuric gestational hypertensives was under-represented in this particular study. In a different series it was shown later that acute atherosis is not really restricted to pre-eclampsia, and can also occur in non-proteinuric pregnancy-induced hypertension (Hanssens et al., 1998). In a small series, Frusca and colleagues (1989) found inadequate physiological change in three out of five chronic hypertensive women, one of them showing acute atherosis. A separate, more recently defined category of hypertensive pregnancy is the so-called HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome. It is to be expected that in such cases histopathological findings overlap with observations in ''classical'' pre-eclampsia (Aardema et al., 2001). In our own series, 7 out of 10 HELLP cases showed acute atherosis, which is a much higher incidence than observed in pre-eclampsia, and also the incidence of atherosis in myometrial segments (5 out of 10 cases) was unexpectedly high, compared with 8% in the pre-eclamptic group (unpublished results). These observations are compatible with the concept that the HELLP syndrome forms part of severe pre-eclampsia. It could be speculated that extension of this lesion over a longer distance of a vessel may compromise vascular function even further, also leading to an increased release of cytotoxic cytokines into the blood and surrounding tissues.

Defects in placental bed development have also been described in other groups of patients, including women with antiphospholipid antibody syndrome. Placentas of such cases may show severe infarction, and acute atherosis was observed in the attached decidual fragments (De Wolf et al., 1982; Magid et al., 1998). However, the only systematic study so far on placental bed biopsies from this particular group of patients showed higher concentrations of inflammatory cells, but absence of atherosis (Stone et al., 2006). Recently, disturbed invasion and defective physiological changes were also found in cases of pre-term pre-labor rupture of membranes, but less frequently than in pre-eclampsia (Kim et al., 2002). In diabetic women without hypertension, atherotic lesions with foam cells were described by Emmrich and colleagues (1975). In contrast, Bjork and colleagues (1984) mentioned ''intramural fibrosis'' as the only placental bed lesion in diabetes without hypertension, but their illustrated case is clearly an example of intimal thickening, described above as a normal event. Also Pinkerton (1963) and Khong (1991) failed to detect obvious placental bed defects in such women. Also in a recent study, Jauniaux and Burton (2006) only noted disturbed spiral artery conversion in diabetic pregnancies which were complicated by chronic hypertension or pre-eclampsia. Finally, it has to be mentioned that also in some apparently normal pregnancies with normal fetal growth, defective physiological changes and pathologic lesions, even including atherosis, have been observed (Aardema et al., 2001; Hanssens et al., 1998).

In summary, the results of all these studies indicate that the former black-and-white picture has been replaced by the more subtle concept of a spectrum of histopathological changes that may occur throughout different disorders of pregnancy. Such a concept is also more in line with present ideas on the complexity of pregnancy-associated diseases (Brown et al., 2000), which may represent different patterns of maternal pathophysiological response to early implantation or placentation defects (Roberts and Lain, 2002). In an extreme situation, when the mother cannot cope with defective early placentation, spontaneous early miscarriage would occur. Indeed, specimens of spontaneous miscarriage often show defective trophoblast invasion and physiological change in spiral arteries (Hustin et al., 1990; Khong etal., 1987), and this has also been shown to be the case for early pregnancy losses in women with antiphospholipid syndrome (Sebire etal., 2002).

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