Achados placentários na pré-eclâmpsia pré-termo e a termo: Uma revisão integrativa da literatura

Pietro, Luciana; Guida, José Paulo de Siqueira; Nobrega, Guilherme de Moraes; Antolini-Tavares, Arthur; Costa, Maria Laura

doi:10.1055/s-0041-1730292

Luciana Pietro

Institute of Health Sciences, Universidade Paulista, Campinas, SP, Brazil

Department of Obstetrics and Gynecology, Universidade Estadual de Campinas, Campinas, SP, Brazil

https://orcid.org/0000-0002-8511-2196

José Paulo de Siqueira Guida

Department of Obstetrics and Gynecology, Universidade Estadual de Campinas, Campinas, SP, Brazil

https://orcid.org/0000-0002-3648-6159

Guilherme de Moraes Nobrega

Department of Obstetrics and Gynecology, Universidade Estadual de Campinas, Campinas, SP, Brazil

https://orcid.org/0000-0001-9406-4256

Arthur Antolini-Tavares

Department of Pathology, Universidade Estadual de Campinas, Campinas, SP, Brazil

https://orcid.org/0000-0001-5964-4407

Maria Laura Costa

Department of Obstetrics and Gynecology, Universidade Estadual de Campinas, Campinas, SP, Brazil

https://orcid.org/0000-0001-8280-3234

Address for correspondence Maria Laura Costa, Department of Obstetrics and Gynecology The University of Campinas, 101 Alexander Fleming St, Campinas, SP, Brazil (e-mail: mlaura@unicamp.br).

Conflict of Interests

The authors have no conflict of interests to declare.

Figuras (4)
Tabelas (1)

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Fig. 1
Definition of preeclampsia and classification according to the moment of diagnosis

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Fig. 2
Diagrammatic representation of the effects of spiral artery remodeling on the inflow of maternal blood into the intervillous space in normal and pathological pregnancies (poor placentation)

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Fig. 3
Underlying conditions of placental insufficiency leading to preeclampsia and fetal growth restriction. Numerous factors are involved in the development of the placenta under physiological conditions: pro- and antiangiogenic factors, pro- and anti-inflammatory cytokines, and pro- and antiapoptotic factors. Under pathological conditions, the expression of many of these factors is altered Source: Courtesy of A. Antolini-Tavares, São Paulo, Brazil.

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Fig. 4
Representative morphological findings in placentas at term and early onset preeclampsia (EOP) cases – Hematoxylin and Eosin (H/E) analysis. In A, we can observe the invasion of the trophoblast (*) to transform maternal vessels (mv) from high pressure to low pressure, with physiological formation of fibrin (f), at the beginning of pregnancy (HE, 20x objective). In B, it is possible to observe the vessels of the decidua (d) with an evident and thick (hypertrophic) smooth muscle layer, with small intramural deposits of fibrinoid material (fm) (HE, 20x objective). In C, we observe the decidual vessel with extensive destruction of the muscle layer (necrosis) and replacement with fibrinoid material (fm) (HE, 20x objective). In D, it is possible to observe the vessel with necrosis of the muscle layer and inflammatory recruitment of macrophages (foamy cytoplasm) (arrows) in the middle of fibrinoid material (fm), characterizing atherosis (HE, 20x objective). In E, we observed a normal placenta at term, without distal villous hypoplasia (HE, 2.5x objective). In F, a case of EOP, we have a panoramic view of thin and elongated chorionic villi, with small and miniaturized terminal villi (within the square), with fewer vessels inside (usually one or two), in relation to mature villi (about three vessels in each terminal villus), characterizing distal villous hypoplasia (HE, 4x objective). In G, a case of EOP, it is possible to observe infarction centrally located in the placental parenchyma, due to hypertension in the vascular bed of the intervillous space, associated with the interaction between trophoblast and deficient uterine vessels: it is observed that, on the right, the villi are agglutinated (decreasing the distance between them due to an abrupt decrease in blood in the intervillous space) and a more eosinophilic color (pink) with less distinction of cell morphology (necrosis), and that, in the lower left corner, the villi have a more mature pattern, as if there were a “penumbra” of hypoxia that was not able to cause ischemic cell death (HE, 4x objective). And in H, a case of EOP, we observed another feature of hypertensive placental infarction, this time associated with a hematoma inside (hematoma infarction) (HE, 10x objective).

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Chart 1
Summary of the main changes in pathophysiological and anatomopathological findings when comparing placentas of early and late onset preeclampsia

Author/year	N° participants	Evaluated cases/groups	Main Findings
Shchegolev et al. (2016)⁴⁷47 Shchegolev AI, Lyapin VM, Tumanova UN, Vodneva DN, Shmakov RG. [Histological hanges in the placenta and vascularization of its villi in early- and late-onset preeclampsia]. Arkh Patol. 2016;78 (01):13-18. Doi: 10.17116/patol201678113-18 https://doi.org/10.17116/patol201678113-...	138	28 control group26 EOP84 LOP	Preponderance of branching angiogenesis in the preeclamptic chorionic villi and an increase in the number of syncytial nodules in EOP and microcysts in the septae in LOP. Morphometric analysis of immunohistochemical placental specimens established increased signs of placental hypoxia in EOP.
Orabona et al. (2016)⁴⁸48 Orabona R, Donzelli CM, Falchetti M, Santoro A, Valcamonico A, Frusca T. Placental histological patterns and uterine artery Doppler velocimetry in pregnancies complicated by early or late preeclampsia. Ultrasound Obstet Gynecol. 2016;47(05):580-585. Doi: 10.1002/uog.15799 https://doi.org/10.1002/uog.15799...	177	105 EOP72 LOP	Increased incidence of distal villous hypoplasia, decidual arteriolopathy, syncytiotrophoblast ‘knots’, microcalcification, villous infarcts, perivillous fibrosis, intervillous thrombi and nonspecific inflammatory lesions in the EOP
Khodzhaeva et al. (2016)⁴⁹49 Khodzhaeva ZS, Kogan YA, Shmakov RG, Klimenchenko NI, Akatyeva AS, Vavina OV, et al. Clinical and pathogenetic features of early- and late-onset pre-eclampsia. J Matern Fetal Neonatal Med. 2016;29(18):2980-2986. Doi: 10.3109/14767058.2015.1111332 https://doi.org/10.3109/14767058.2015.11...	150	50 control group50 EOP50 LOP	Greater remodeling of spiral arteries in EOP; with increased incidence of sclerosed blood vessel and lower incidence of intact vessels and smooth muscle cells in EOP compared to LOP. The degree of compensation of chronic hypoxia tissue in the area of the placental site was typical for LOP and was absent of an EOP.
Zhang et al. (2015)⁵⁰50 Zhang X, Jia H, Wang Y, Xie J, Gu Y. [Early and late onset severe preeclampsia: a clinicopathologic study of 178 placentas]. Zhonghua Bing Li Xue Za Zhi. 2015;44(12):879-883	178	54 EOP124 LOP	Decidual vascular disease, placental infarction, abruptio placentae and placental villi dysplasia were seen in both groups. The incidence of decidual vascular disease and placental villi dysplasia was higher in EOP, and the incidence of placental infarction was lower when compared with LOP.
Kovo et al. (2012)⁵¹51 Kovo M, Schreiber L, Ben-Haroush A, Gold E, Golan A, Bar J. The placental component in early-onset and late-onset preeclampsia in relation to fetal growth restriction. Prenat Diagn. 2012;32(07): 632-637. Doi: 10.1002/pd.3872 https://doi.org/10.1002/pd.3872...	130	37 EOP93 LOP	EOP had higher rates of FGR and lesions of maternal vascular supply. Within the LOP group, cases with FGR had higher rates of maternal vascular supply lesions than those without FGR, but similar rates of fetal vascular supply lesions
Ogge et al. (2011)⁵²52 Ogge G, Chaiworapongsa T, Romero R, Hussein Y, Kusanovic JP, Yeo L, et al. Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia. J Perinat Med. 2011;39(06):641-652. Doi: 10.1515/jpm.2011.098 https://doi.org/10.1515/jpm.2011.098...	19.041		Prevalence of lesions consistent with maternal underperfusion in EOP and LOP, but in EOP groups had a significantly higher frequency of placental lesions when compared with LOP.
Van der Merwe et al. (2010)⁵³53 van der Merwe JL, Hall DR, Wright C, Schubert P, Grové DAre early and late preeclampsia distinct subclasses of the disease-what does the placenta reveal? Hypertens Pregnancy. 2010;29(04): 457-467. Doi: 10.3109/10641950903572282 https://doi.org/10.3109/1064195090357228...	100	50 control group25 EOP25 LOP	EOP presented increased incidence of pathological infarction and chorionic plate thrombosis, however the LOP presented more incidence of decidual arteriopathy.
Egbor et al. (2006)⁵⁴54 Egbor M, Ansari T, Morris N, Green CJ, Sibbons PD. Morphometric placental villous and vascular abnormalities in early- and lateonset pre-eclampsia with and without fetal growth restriction. BJOG. 2006;113(05):580-589. Doi: 10.1111/j.1471-0528.2006.00882.x https://doi.org/10.1111/j.1471-0528.2006...	69	9 EOP11 LOP	EOP presented hipoplasic villi volume and impairment of total surface area of the terminal villi, while in LOP there was impact on peripheral villi or vasculature features

[1] Address for correspondence Maria Laura Costa, Department of Obstetrics and Gynecology The University of Campinas, 101 Alexander Fleming St, Campinas, SP, Brazil (e-mail: mlaura@unicamp.br).

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Achados placentários na pré-eclâmpsia pré-termo e a termo: Uma revisão integrativa da literatura

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