No abstract

Background/Aims: Universal screening for thyroid diseases during pregnancy is controversial. Targeted screening does not identify all women with thyroid dysfunction. Furthermore, antithyroid peroxidase antibodies (TPOAb) are suspected to be associated with an increased risk of fetal loss, premature delivery and hypothyroidism. The aim of our study was to assess the rationale behind universal screening and propose thyroxine treatment in particular cases. Methods: Between January 2008 and May 2009, 537 consecutive iodine-supplemented women with a singleton pregnancy [441 TPOAb– controls and 96 TPOAb+ women (47 nontreated and 49 treated)] were evaluated using thyroid and obstetric parameters. According to our algorithm for thyroid screening in pregnancy, if thyroid-stimulating hormone (TSH) exceeded 1 mU/l in TPOAb+ women, 50 µg of levothyroxine (L-T4) was prescribed. Results: The miscarriage rate was significantly higher in the nontreated TPOAb+ group compared with the treated group (16 vs. 0%; p = 0.02). Compared to the control group, TSH in TPOAb+ patients was higher at the first prenatal visit prior to L-T4 treatment (p < 0.01), while free thyroxine was higher than in the control group after the 20th week (p < 0.05). Conclusions: Our study supports the potential benefit of universal screening and L-T4 treatment for autoimmune thyroid disease during pregnancy. Efforts are still needed to further decrease miscarriage rates.

Despite occasional reports of SARS-CoV-2 vertical transmission during pregnancy, the question of placental infection and its consequences for the newborn remain questionable. Here, we analyzed the placentas of 31 COVID-19-positive mothers by RT-PCR, immunohistochemistry and in situ hybridization. We only detected one case of placental infection, which was associated with intrauterine demise of the fetus. We then isolated and differentiated primary trophoblasts from non-pathological human placentas at term, and exposed them to SARS-CoV-2 virions. Unlike for positive control cells Vero E6, we were not able to detect the virus inside cytotrophoblasts and syncytiotrophoblasts or in the supernatant four days after infection. As a mechanism of defense, we hypothesized that trophoblasts at term do not express ACE2 and TMPRSS, the two main host membrane receptors for SARS-CoV-2 entry. The quantification of these proteins in the placenta during pregnancy confirmed the absence of TMPRSS2 at the surface of the syncytium. Surprisingly, a transiently induced experimental expression of TMPRSS2 did not allow the entry or replication of the virus in differentiated trophoblasts. Altogether, these results underline that trophoblasts are not likely to be infected by SARS-CoV-2 at term, but the reported case raises concern about preterm infection.