ABSTRACT
Background: The infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV- 2), the causal agent of coronavirus disease 2019 (COVID-19), is associated with coagulation abnormalities, in which endothelial injury/dysfunction may be a key pathogenic mechanism. Endothelial dysfunction triggers tissue factor (TF) expression. Activated factor VII-antithrombin (FVIIa-AT) complex is a potential biomarker of prothrombotic diathesis reflecting FVIIa-TF interaction. Aim(s): To evaluate FVIIa-AT plasma levels in subjects with COVID-19 pneumonia. Method(s): FVIIa-AT plasma levels were assessed in 40 subjects (30 males and 10 females;64.8 +/- 12.3 years) admitted for COVID-19 pneumonia during the first pandemic wave in Italy (April 2020). FVIIa-AT levels were compared with those of two sex-and age-matched groups of hospitalized subjects without COVID-19, with or without laboratory signs of systemic inflammation. The concentration of FVIIa-AT was measured by ELISA on frozen citrate plasma samples. Data of coagulant activities of factor II (FII:c), factor V (FV:c), and factor VIII (FVIII:c) were available in a subgroup of subjects. Result(s): Hospitalized COVID-19 patients had FVIIa-AT levels significantly higher than sex-and age-matched no COVID-19 subjects (Table 1), either with or without inflammation (p = 0.013 and p = 0.017 by ANOVA with Tukey post-hoc comparison, respectively). No difference in FVIIa-AT levels was observed between no COVID-19 subjects with or without inflammation (p = 0.995). The association between COVID-19 and FVIIa-AT levels in the whole study sample remained significant by linear regression analysis adjusted for sex, age, C reactive protein, estimated glomerular filtration rate, fibrinogen, prothrombin time, and activated partial thromboplastin time (B coefficient 0.322 with standard error 0135, p = 0.019). In sub-analysis COVID-19 patients showed also lower FII:c, FV:c, and FVIII:c levels (Table 1). Conclusion(s): Our results indicate that SARS-CoV2 infection, at least during the first pandemic wave, was characterized by increased FVIIa-AT levels, thereby suggesting an increased FVIIa-TF interaction, which may be consistent with increased TF expression/activation due to SARS-CoV2 -induced endotheliopathy.
ABSTRACT
The almost relentless worldwide diffusion of severe acute respiratory syndrome coronavirus (SARS-CoV-2) is deeply engaging the minds of many scientists, clinicians and laboratory professionals, who struggle to identify the possible short- and long-term consequences of coronavirus disease 2019 (COVID-19) in the general population, as well as in specific cohorts of individuals, who may display peculiar features of infection. Pregnant women represent one of these categories, since the biological implications of SARS-CoV-2 infection extend far beyond those caused to the mother, involving also the fetus. Several lines of evidence now attest that although mother-to-child SARS-CoV-2 transmission is relatively rare (<2% of all pregnancies), the consequences on maternal-fetal-neonatal interface of COVID-19 can be very serious. To this end, some important questions raise, such as "is COVID-19 a risk factor for complications in pregnancy?", "which laboratory tests are more predictable of unfavorable pregnancy outcomes?", "how efficacious is COVID-19 vaccination in pregnancy?" and, last but not least, "what evidence supports laboratory monitoring of COVID-19 vaccination immunogenicity in pregnancy?". In this opinion paper, we will attempt to provide an overview of the current biological, clinical and laboratory evidence of SARS-CoV-2 infection in pregnancy, trying also to provide reliable answers to the aforementioned questions. Copyright © 2022 Biomedia. All rights reserved.