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SARS-CoV-2 infection can cause severe placental lesions leading rapidly to intra uterine fetal death (IUFD). From August 2020 to September 2021, in the pathology Department of Toulouse Oncopole, we analyzed 50 placentas from COVID-19 positive unvaccinated mothers. The purpose of our study is to describe the clinicopathological characteristics of these placental damages and to understand the pathophysiology. Ten of them (20%) showed placental lesions with positive immunohistochemistry for SARS-CoV-2 in villous trophoblast. In five cases (10%), we observed massive placental damage associating trophoblastic necrosis, fibrinous deposits, intervillositis as well as extensive hemorrhagic changes due to SARS-CoV-2 infection probably responsible of IUFD by functional placental insufficiency. In five other cases, we found similar placental lesions but with a focal distribution that did not lead to IUFD but live birth. These lesions are independent of maternal clinical severity of COVID-19 infection since they occur despite mild maternal symptoms and are therefore difficult to predict. In our cases, they occurred 1 to 3 weeks after positive SARS-CoV-2 maternal RT-PCR testing and were observed in 2nd and 3rd trimesters of pregnancies. When these lesions are focal, they do not lead to IUFD and can be involved in intra-uterine growth restriction. Our findings, together with recent observations, suggest that future pregnancy guidance should include stricter pandemic precautions such as screening for a wider array of COVID-19 symptoms, enhanced ultrasound monitoring as well as newborn medical surveillance.

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We report a case of twin anemia-polycythemia sequence (TAPS) CASE REPORTA 41-year-old woman was referred to our center at 16 + 2 weeks' gestation for twin-to-twin transfusion syndrome (TTTS). After it was diagnosed as Quintero Stage II, we selectively photocoagulated the communicating vessels by laser at 16 + 6 weeks. The recipient had a maximum vertical pocket of 9 cm, and the donor almost no amniotic fluid; the latter's bladder could not be visualized. Both had normal findings on umbilical artery, middle cerebral artery (MCA) and ductus venosus Doppler. The placenta was inserted posterolaterally, on the right. The site of fetoscope entry was on the left side, and three arteriovenous and two venoarterial anastomoses were coagulated. The procedure, conducted with epidural anesthesia, took 45 min.Weekly sonographic surveillance confirmed complete regression of TTTS, but twin anemia-polycythemia sequence (TAPS) was suspected at 18 weeks. From 18 to 24 weeks, sonographic surveillance was performed weekly. At 24 weeks, the suspected TAPS worsened, reaching Lopriore Stage 2; the former donor became polycythemic, with an MCA peak systolic velocity (PSV) < 0.8 multiples of the median (MoM) (16.6 cm/s = 0.52 MoM), and the former recipient became anemic, with an MCA-PSV > 1.7 MoM (80 cm/s = 2.60 MoM)1 . After counseling the parents regarding the different options available (expectant management, intrauterine transfusion (IUT) and laser coagulation), we jointly decided to perform a second laser photocoagulation, which was carried out at 24 + 5 weeks. The site of fetoscope entrance was on the right side of the umbilicus, and a single small arteriovenous anastomosis was coagulated. The procedure took 20 min. One week later we noted an improvement, with the MCA-PSV of the anemic twin decreasing to 58 cm/s (1.72 MoM). The MCA-PSV of the polycythemic twin, 21 cm/s (0.62 MoM), increased more slowly. At 30 weeks, the MCA-PSV had returned to normal for both: 48 cm/s (1.18 MoM) for the previously anemic and 36 cm/s (0.88 MoM) for the previously polycythemic twin (Figure 1).The pregnancy continued normally thereafter. Magnetic resonance imaging was performed at 33 weeks' gestation and showed no cerebral anomaly in either fetus. A prophylactic Cesarean delivery was performed at 36 + 3 weeks. The previous donor/polycythemic twin had a birth weight of 2000 g, Apgar score of 10 at both 1 and 5 min, hemoglobin of 20.2 g/dL and a reticulocyte

Extracellular vesicles (EVs) have increasingly been recognized as key players in a wide variety of physiological and pathological contexts, including during pregnancy. Notably, EVs appear both as possible biomarkers and as mediators involved in the communication of the placenta with the maternal and fetal sides. A better understanding of the physiological and pathological roles of EVs strongly depends on the development of adequate and reliable study models, specifically at the beginning of pregnancy where many adverse pregnancy outcomes have their origin. In this study, we describe the isolation of small EVs from a histoculture model of first trimester placental explants in normal conditions as well as upon infection by human cytomegalovirus. Using bead-based multiplex cytometry and electron microscopy combined with biochemical approaches, we characterized these small EVs and defined their associated markers and ultrastructure. We observed that infection led to changes in the expression level of several surface markers, without affecting the secretion and integrity of small EVs. Our findings lay the foundation for studying the functional role of EVs during early pregnancy, along with the identification of new predictive biomarkers for the severity and outcome of this congenital infection, which are still sorely lacking.

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