Association between maternal and perinatal outcomes and histological changes in the placenta of patients with Covid-19: A cohort study.

Although studies evaluated placental involvement in Covid-19 patients, few have assessed its association with clinical repercussions. The study aimed to determine the association between the clinical status and maternal and perinatal outcomes of patients with Covid-19 at delivery and changes in placental histology. It is so far the largest cohort evaluating placentas of patients infected by the SARS-CoV-2. A secondary analysis was conducted of a database from which a cohort of 226 patients, who tested real-time polymerase chain reaction-positive for Covid-19 at delivery and whose placentas were collected and submitted to pathology, was selected for inclusion. One or more types of histological changes were detected in 44.7% of the 226 placentas evaluated. The most common abnormalities were maternal vascular malperfusion (38%), evidence of inflammation/infection (9.3%), fetal vascular malperfusion (0.8%), fibrinoid changes and intervillous thrombi (0.4%). Oxygen use (P = .01) and need for admission to an intensive care unit (ICU) (P = .04) were less common in patients with placental findings, and hospital stay was shorter in these patients (P = .04). There were more fetal deaths among patients with evidence of inflammation/infection (P = .02). Fetal death, albeit uncommon, is associated with findings of inflammation/infection. Oxygen use and need for admission to an ICU were less common among patients with placental findings, probably due to the pregnancy being interrupted early. None of the other findings was associated with maternal clinical status or with adverse perinatal outcome.

Placental growth disorders and perinatal adverse outcomes in Brazilian HIV-infected pregnant women.

Fetal and placental growth disorders are common in maternal human immunodeficiency virus (HIV) infection and can be attributed to both the infection and comorbidities not associated with HIV. We describe placental growth disorders and adverse reproductive outcomes in HIV-infected pregnant women whose delivery occurred between 2001-2014 in Vitoria, Brazil. Cases with gestational age (GA) ≥ than 22 weeks validated by ultrasonography, with placental and fetal weight dimensions at birth, were studied. Outcomes were summarized as proportions of small (SGA), appropriate (AGA), and large (LGA) for GA when the z-score values were below -1.28, between -1.28 and +1.28, or above +1.28, respectively. Of 187 fetal attachment requisitions, 122(65.2%) women and their newborns participated in the study. The median maternal age was 28 years and 81(66.4%) underwent ≥ 6 prenatal visits. A total of 81(66.4%) were diagnosed before current pregnancy; 68(55.7%) exhibited criteria for acquired immunodeficiency syndrome (AIDS); 64(52.4%) had detectable viral load; 25(20.5%) cases presented SGA placental weight and 6(4.9%) SGA placental thickness. SGA placental area was observed in 41(33.6%) cases, and among the SGA placental weight cases 12(48%) were also SGA fetal weight. Preterm birth (PTB) occurred in 15.6%(19/122) of cases; perinatal death in 4.1%(5/122) and HIV vertical transmission in 6 of 122 (4.9%). Women, ≥36 years old, were 5.7 times more likely to have PTB than those under 36. Also, patients with AIDS-defining criteria were 3.7 times more likely to have PTB. Prenatal care was inversely associated with PTB. Statistically significant associations were observed between AGA placental area and Protease Inhibitor usage and between SGA placental weight and SGA area. We found a prevalence of placental growth disorders in HIV-infected pregnant women and values higher than international reference values. The restriction of placental growth was a common disorder, possibly attributed to virus effects or a combination of antiretroviral regimens.

Placental infection by Zika virus in French Guiana.

OBJECTIVES: To describe placental findings on prenatal ultrasound and anatomopathological examination in women with Zika virus (ZIKV) infection, and to assess their association with congenital ZIKV infection and severe adverse outcome, defined as fetal loss or congenital Zika syndrome (CZS). METHODS: This was a prospective study of pregnancies undergoing testing for maternal ZIKV infection at a center in French Guiana during the ZIKV epidemic. In ZIKV-positive women, congenital infection was defined as either a positive reverse transcription polymerase chain reaction result or identification of ZIKV-specific immunoglobulin-M in at least one placental, fetal or neonatal sample. Placental ZIKV-infection status was classified as non-exposed (placentae from non-infected women), exposed (placentae from ZIKV-infected women without congenital infection) or infected (placentae from ZIKV-infected women with proven congenital infection). Placentae were assessed by monthly prenatal ultrasound examinations, measuring placental thickness and umbilical artery Doppler parameters, and by anatomopathological examination after live birth or intrauterine death in women with ZIKV infection. The association of placental thickness during pregnancy and anatomopathological findings with the ZIKV status of the placenta was assessed. The association between placental findings and severe adverse outcome (CZS or fetal loss) in the infected group was also assessed. RESULTS: Among 291 fetuses/neonates/placentae from women with proven ZIKV infection, congenital infection was confirmed in 76 cases, of which 16 resulted in CZS and 11 resulted in fetal loss. The 215 remaining placentae from ZIKV-positive women without evidence of congenital ZIKV infection represented the exposed group. A total of 334 placentae from ZIKV-negative pregnant women represented the non-exposed control group. Placentomegaly (placental thickness > 40 mm) was observed more frequently in infected placentae (39.5%) than in exposed placentae (17.2%) or controls (7.2%), even when adjusting for gestational age at diagnosis and comorbidities (adjusted hazard ratio (aHR), 2.02 (95% CI, 1.22-3.36) and aHR, 3.23 (95% CI, 1.86-5.61), respectively), and appeared earlier in infected placentae. In the infected group, placentomegaly was observed more frequently in cases of CZS (62.5%) or fetal loss (45.5%) than in those with asymptomatic congenital infection (30.6%) (aHR, 5.43 (95% CI, 2.17-13.56) and aHR, 4.95 (95% CI, 1.65-14.83), respectively). Abnormal umbilical artery Doppler was observed more frequently in cases of congenital infection resulting in fetal loss than in those with asymptomatic congenital infection (30.0% vs 6.1%; adjusted relative risk (aRR), 4.83 (95% CI, 1.09-20.64)). Infected placentae also exhibited a higher risk for any pathological anomaly than did exposed placentae (62.8% vs 21.6%; aRR, 2.60 (95% CI, 1.40-4.83)). CONCLUSIONS: Early placentomegaly may represent the first sign of congenital infection in ZIKV-infected women, and should prompt enhanced follow-up of these pregnancies. Copyright © 2019 ISUOG. Published by John Wiley & Sons Ltd.

[Ultrastructural analysis of placentas with villitis. Retrospective study]. / Análisis ultraestructural de placentas con villitis. Estudio retrospectivo.

A villitis is a focal or multifocal inflammatory reaction of chorionic villi with infiltration of mononuclear cells and usually is associated with fibrinoid necrosis. The aetiology of villitis could be a transplacental infection of the fetus, especially with virus (VIV), in normal placentae however, the presence of villitis is referred as villitis of unknown ethiology (VED). This study was designed to characterize villitis lesions of 11 placentae, four VIV and seven VED, ultrastructural descriptive comparisons of both types of villitis are discussed. Biopsies were processed with the conventional optic and electronic microscopy techniques. Our ultrastructural observations confirmed the presence of virus in four placentae whereas no virus or bacteria were found in seven placentae. Microvilli were absent or markedly diminished, this finding was associated to the presence of fibrinoid necrosis in the stroma and clinically to intrauterine growth retardation, 4 preterm pregnancies and one obitus. Trophoblast alterations were found in both types of villitis, basal membrane thickness, is some cases associated to electrodense material similar to calcium deposites, vascuolization and the presence of edema in the stroma was observed. In some cases we noted the presence of focal fibrin deposits associated to necrosis zones in the stroma, calcium precipitates and mielinic bodies. Fetal vessels obliteration and intravascular thrombi were found in the syncitiotrophoblast placentae with viral particles CMV or rubivirus associated to an increment in Hofbauer cells and basal membrane calcifications. From our ultrastructural observations, we conclude that both types of villitis are associated to a typic immunologic reaction that induce lose of trophoblast microvilli, mononuclear infiltration and edema. This placental alterations reduce dramatically the maternofetal exchange of gases, nutrients and other active peptides and could be the cause of fetal growth retardation, inmadurity or death.